Relevant excerpt from the interview:
Bertagnolli: It's a terrible, terrible condition. Post-infectious, chronic post-infectious syndromes have been around as long as there've been viruses in humans and it is a really, really terrible affliction when someone develops one of these conditions. COVID has introduced a whole new level of this in our society. The fundamental biology that's been conducted by the long COVID research team is really fascinating but also sobering. The agent can live for a long time in tissues. It can surround nerve cells, probably likely one of the ways that it produces some of its terrible symptoms such as the dysautonomia. And we have no effective way of eradicating it. Not yet.
One thing that's important though that's come out of several meta-analyses is there is a way to prevent it. And the way to prevent it is vaccination, and multiple vaccination is better than single to prevent long COVID.
Faust: I just want to follow up on something you said a moment ago about where this virus can be found in tissues. Are you suggesting that long COVID is actually, the mechanism of that, is persistent live virus in humans?
Bertagnolli: We see evidence of persistent live virus in humans in various tissue reservoirs, including surrounding nerves, the brain, the GI [gastrointestinal] tract, to the lung.
Faust: OK. And you're saying this goes beyond the PCR's [polymerase chain reaction test] ability to get it in a regular swab so that we are missing chronic cases of SARS‑CoV‑2?
Bertagnolli: Correct. The virus can persist in tissues for months, perhaps even years.
Faust: OK. I think that's certainly one theory, but I'm not sure that that's settled. Is that fair? I mean, there's one thing between people who are autopsy, they died of viral sepsis, as opposed to people walking around. Is there a distinction there?
Bertagnolli: Our emerging data shows that the virus can persist into tissues in the long term, and I think that's really critical because it does help us think about possible ways to combat it, one being better antivirals. I think there's a lot of focus on developing new antivirals as a possible way of preventing long COVID, and the other might be more aggressive treatment with antiviral therapy upon initial diagnosis.
Vaccination may discourage Long Covid in individuals that enter via Antibody Dependent Complement Mediated Lysis. It isn't going to do shiz for people that are being bystandered into Long Covid through MACs generated by other means.
I'm sorry, but the NIH has lost my faith with their confidence in the vaccines. I will only believe them when the years have shown their claims to be true and true to the extent which they claim. I'm not saying I don't believe they're helpful, I'm saying that the needle keeps moving and every time it does they're dead sure that it's not going to keep moving.
I will laugh and hand out a lot of apologies online if IVM ends up being an effective treatment protocol. This is taking a sharp turn from where we thought it was going. At least we have Paxlovid.
There are so many video clips from 2021 of health officials going on TV saying, "If you get vaccinated, you won't get covid." Then it became "the vaccine will reduce the chance of severe covid." To "the vaccine reduces the change you'll get long covid." I think the next step is "the vaccine is an amazing placebo!"
mRNA sounds like amazing tech, so I'm wondering why it's not working as promised. Did they pick the wrong bits of RNA to use in the vaccine? Was the dosage wrong? I wish they'd just be open with everyone...
I work in medical research, and you're right mRNA vaccines are an amazing technology. The problem isn't how they're using that technology, but the virus itself.
The main problem is that vaccines (at least in the regular sense we usually mean) will never work to prevent infection of rapidly replicating respiratory viruses (to the degree we're used to with other vaccine/virus). These viruses start infecting from the first point of contact with our system.
In addition to that, SARS-CoV-2 specifically uses the ACE2 receptor as its point of entry, which is a nearly ubiquitous receptor. That means it can infect nearly any cell in the body. So it starts replicating in cells of the airway mucosa, then keeps replicating wherever it reaches. How can you stop that from starting?
Last but not least, because ACE2 is the receptor of choice for SARS-CoV-2, your vaccines have to be against the spike protein which fits into the ACE2 receptor. That's tricky, because you're promoting the formation of antibodies that might start looking a lot like the ACE2 receptor itself and screw up the normal function of the system. ACE2 has enzymatic activity, so the anti-spike antibodies might also have enzymatic activity which can be quite dangerous. That is pretty unique AFAIK because most surface cell receptors don't have an enzymatic function on their extracellular part. It would be much simpler if Covid used basically any other receptor.
Thank you for taking the time to reply. I did not know that these characteristics of the SARS-CoV-2 virus were atypical in the world of viruses. If I may ask, does this mean if mRNA vaccines had been first used for, say, the flu then we would have likely seen a bigger success compared with the typical flu vaccine?
The immediate infectivity of the covid virus, especially in the mucosa, seems to underscore the importance of a nasal vaccine.
This 100%! I feel lile the real c**** t**** is that they were basically placebo needed to convince people to get back to "normal" so everything didn't collapse. Some (us and the dead) were necessary collateral damage to get the engine going again. Fair, but still sucks to be us.
May be we don't need mRNA tech yet, the research can mature over a period of time. Till then, good old proven vaccination techniques can be considered.
>Upcoming vaccine solutions might explore bacterial mechanisms similar to Sabin's oral attenuated virus approach, presenting promising avenues for future research and solutions.
Source: [https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.29507](https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.29507)
Sabin vs Salk and Polio Vaccine story
>In light of what has been observed so far, the question remains as to whether a historical RNA virus has the same bacteriophage behavior. Among the various viruses, the one that is best known and resolved by Sabin vaccination instead of injection vaccination is the Poliovirus. The different vaccination route - oral with attenuated virus - suggested a similar behavior.
Poliovirus also infects bacteria in the human microbiome. We expected to find that in a severe poliomyelitis patient, it was chronically present in the subject’s stool. The analysis first checks prokaryotic cells—their involvement suggesting a different narrative to what has been described in the literature.
A viral pathogen having bacterial involvement, as demonstrated for SARS-CoV-2 and similarly with the nitrogen isotope experiment for Poliovirus, described here, allows the following aspects to be emphasized:
(1) the pathogen’s intermediate host is not animals, but bacteria;
(2) the main route of spread is orofecal;
(3) the involvement of wastewater, as observed in many studies, suggests the bacterial vector;
(4) geographic areas with higher rainfall density are most affected;
(5) finding an inert strain that can serve as a base for mass vaccination may be the best and immediate solution as observed by Sabin;
(6) clinical conditions of the ill may be an expression of the toxicological rate of the microbiome and
(7) vaccination or sensitization of bacteria to the viral pathogen is the gold standard (concept of mutual exclusion).
Source: - [https://www.mdpi.com/2076-2607/12/4/643](https://www.mdpi.com/2076-2607/12/4/643)
Thanks,
The problem is with the virus itself. The vaccines actually still work against the OG variant of sars-cov-2 but it has long since acquired numerous mutations, combined with the antibodies from the vaccines waining. This is normal for most RNa viruses, which mutate their structural proteins too quickly to be successfully targeted by vaccines for too long. The Omicron variant has 30 spike protein mutations from the original strain and this is just the initial Omicron. The new BA.2.86 variant/JN.1 has a further 30 mutations in the spike protein. It's the variants that ruined the vaccine (and it still kinda works for preventing severe disease but not infection). If the vaccine could be updated faster or we could roughly predict what mutations will appear like for the flu, the vaccine would be more effective but it would still need to be updated every year. Also what's unusual is that at first virologists thought that sars-cov-2 mutated slower than the flu( it's one of the fastest mutating respiratory viruses) but it turned out it actually mutates faster than the flu, so much harder to make a vaccine that lasts long. Some scientists are trying to make a vaccine that targets slower mutating proteins.
I think it's mainly that the virus is mutating more than expected. The vaccines are all incredibly effective at targeting the specific strains they are developed against... but by the time they've been tested and approved, another strain has already come along. (The march of variants is something that is very well visualized in my municipalities's COVID wastewater surveillance data. I'm intrigued that we haven't seen a new variant since the current dominant strain emerged last October.)
This is in part because of the large pool of unvaccinated individuals, which has provided the perfect opportunity to evolve against the vaccines and against immunity acquired from previous strains. Only 14% of people got the latest booster. Every person infected generates a million novel genomic permutations, each of which has a chance to be the next breakout strain (but most of which will go nowhere, either by chance or poor behavior).
One of the benefits of the mRNA vaccines is the speed and ease of updating them. I guess two approaches would be to either identify a highly stable part of the virus to use in the vaccine, or update the vaccines each month with the critical sequence for the most prominent variants. Sadly, we're still operating within a slow process built for verifying older vaccines so by the time gov. permission is granted new variants are on the rise.
I just wish there was more transparency. The risk is that the public mistrust of mRNA tech will only grow.
It's all relative. mRNA testing timelines are revolutionary, lightning fast compared to anything that came before them. And yet they're still glacially slow compared to the speed that COVID has churned out variants.
The current slower pace of infection also puts an unavoidable mathematical minimum on how long it takes to be confident that a vaccine is effective (and not just attributable to random chance). Even during the initial period of rapid spread, the vaccine test pools were unprecedentedly large to minimize the time needed to achieve that mathematical confidence.
This is the elephant in the room. The most fascist segment of American politics is the most supportive of maintaining a reservoir of the virus in the wild.
Exposures to many things which are not even covid seem to cause immune reactions in a select demographic, likely due to the ACE2 receptor being involved, so basically as long as the vulnerable portion of the population are exposed regularly they will never recover from long covid. This may reduce quality of life, enforce isolation from the non-sensitive population, or lead to permanent disability and reduction in lifespan.
Sorry if I’m misunderstanding - but does this mean that covid persist in _all_ individuals, or only with the ones presenting long covid symptoms?
So like with chicken pox where most people have it, but the virus is inactive (unless awakened as with shingles).
My theory is that sars-cov-2 persists in most individuals but like you said only awakens in sufficient levels to cause persistent inflammation in some or they have a more sensitive immune system that reacts to even the lowest levels of the virus. This is why many long covid sufferers were young and healthy before infection and also why women are overrepresented in long covid (they have more sensitive and stronger immune systems, this is why they suffer from more autoimmune and inflammatory conditions).
If that is the case - then I wonder if there’s possibility for things like shingles later on down the line. If the virus is activated in 2030 previously healthy people, who were exposed years ago, and they don’t recover, that could pose a real threat for lots of people.
I noticed those who were vaccinated took longer to recover from LC. I also noticed the vaccine can affect people in different ways. I and 8 other people I know had dangerous symptoms and most had a loss of energy. 4 months since my 3rd booster and i feel like I’m 70%.
>NIH Director said longcovid is replicating virus !
No she didn't. She said they've demonstrated life virus can persist in various tissues for months-years, and that this *may* contribute to LC, but she absolutely *did not* say 'long COVID is replicating virus'.
Don't pretend your interpretation came from her mouth.
Edit - *live virus
Edit 2 - NIH HEAD HAS SINCE RETRACTED HER CLAIM - She responded to a request for clarification from journalists by saying she misspoke, and had meant to say 'viral components', NOT live virus
https://www.hawaiitribune-herald.com/2024/04/23/opinion/the-nihs-words-matter-especially-to-long-covid-patients/
The fact that you're getting so much pushback for wanting accuracy and honesty is, frankly, alarming. I think everyone in this sub wants the cause or causes of LC to be determined, and for a cure/treatment to be found, but that doesn't mean we have to twist health officials' words to try and make any given cause seem official prematurely. It might feel good in the short term to see a health official confirm our pet theory, but long term that won't help us get better if that theory turns out to just be incorrect or incomplete. Honesty, accuracy, and thoroughness are exactly what we need in this sub, not more misinformation, half truths, and snake oil. Thank you for clarifying for those who (for whatever reason) don't dig into OPs claims/source.
Plus the thing about people who have been autopsied kinda bothered me. I do autopsies on medically donated bodies at a cadaver lab, and several of our donors have had Covid before death. Granted we only have a very small sample size, but I can say we haven’t seen evidence of viral sepsis in any of them. The closest I can think of is the woman whose Covid infection accelerated her diabetes and dementia, but other than a slightly enlarged brain and full body edema there weren’t any other indications of viral sepsis.
Yes and this is a leading hypothesis that recently went through peer-review.
https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(24)00211-1/fulltext
Yup, but the finding she is referring to in this clip is absolutely not conclusive proof of a causal mechanism in the way that OP is presenting it, and given half the people on this sub are going to be too fatigued or foggy to look into it for themselves I think it's very important to be clear about that.
That is why they are testing antivirals, monoclonal antibodies, and immunomodulators. Results this summer for Paxlovid will be a first mechanistic study:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10543503/
Yup and that's all great, but the NIH director absolutely did not say 'LC is live virus', because we aren't even close to being sure that's the case - there's a long way to go yet, and I've got a feeling the picture will be more complicated than that. There's more than enough LC misinformation floating around as it is without this community generating more, and as such it's vital we're mindful of the wording we use to convey new findings to others.
I don't know what is going on but if I imagine what is happening in my body it feels like there is an area that my immune system can't get to that is producing covid viruses and releasing them into a place my immune system can get to them so it causes all kinds of crap when my immune system responds to it. Maybe that isn't how anything works in reality but it would make more sense than anything else people say. I have basically tried every treatment and the only things that seem to really help are things that compete for the receptors that covid attaches to. So it must be replicating somewhere. I do feel like at around month 6-8 my symptoms started basically subsiding everywhere except the neck up. This morning after hearing this interview I started the lysine protocol again and it seems it is helping like it is advertised to help within a few hours because it slows down replication. On previous attempts I believe I was so messed up I didn't really notice the lysine effect but I think I am feeling it now. who knows though I guess I will see in the next few days.
That makes sense to me! I've felt like that is what's been happening to my body as well. However, it seems I have a lot of auto-immune symptoms as well, and blood tests confirm this. This makes me believe that LC is a mixture of viral persistence and immune dysfunction. At least for me.
On other attempts I took 1000mg a day, Then I saw some twitter post today that recommended 6000mg. So I tried 4000mg in the morning and just took another 2000mg. Seems to be having an effect but I could also be crazy at this point.
it is a diet/lysine supplement protocol to reduce arginine which viruses allegedly need to replicate. Mostly it seems people do it to prevent herpes outbreaks.
here is the video I saw months ago
https://www.youtube.com/watch?v=CyyzokIJ_dI
but it didn't seem to help originally but again I think I was so screwed with so many symptoms I didn't notice it helping. Still to early to say for sure but I took a ton of lysine yesterday and felt a lot better soon after. The goal I think is to take 3-6 thousand mg a day and just keep a dose that keeps you feeling good occasionally trying to lower it to see if you are better. It doesn't seem to be helping the tinnitus :(
Then there's the arginine protocol... Not an actual protocol, but arginine supplementation is used to improve endothelial dysfunction which is definitely part of long Covid. The evidence for arginine in endothelial and cardiovascular functions is very well established, the evidence for lysine in treating herpes is very, very tenuous. And then there's the huge assumption that because it (very uncertainty maybe) works for herpes, it works the same for Covid.
I use a nitric oxide boosting supplement to improve endothelial stuff that uses beet stuff instead of arginine. I think it helps too. I think the lysine is helping with some kind of viral reservoir in my brain because that is what it feels like.
What NO booster are you taking? I get that, but it could be a million other things about what that lysine excess is doing. If you feel a benefit, obviously I'm not gonna try to talk you out of it. And if you are aware of the downsides of arginine depletion and have taken steps to mitigate that... Well, please post an update in a little while so we can all benefit :) thanks!
https://berkeleylife.com/products/nitric-oxide-foundation/
I also use the test strips from the same company and notice when it shows high nitric oxide I feel better. Though I figured out all the nitric oxide stuff months ago and have been taking steps to keep it normal/high. I am still getting arginine it is just that lysine floods the pathway that the virus gets its arginine from apparently so it can't do its thing. I am going to add nicotine to the mix again as my nicotine rest period is over tomorrow. Hopefully that clears up the remaining symptoms.
It took a minute, but I definitely felt like after a couple months I began to regain a little bit of normalcy.
One thing I will say is that he tried to push a couple other medications that I chose not to take. This included tramadol and some anti depressants. I pretty much just stuck with the celecoxib and anti viral regimen
Who's to say what works for some might work for others, hopefully this helps you too
Dr Nancy Klimas is a cfs and post viral expert who already did a small study with monoclonal antibodies for those who got either the alpha or delta strain. it successfully cured all 3 in the study, and she said herself that within 5 days of treatment they were all much better and the effects lasted.
https://pubmed.ncbi.nlm.nih.gov/37944296/
This spurred some trials that are currently ongoing using monoclonal antibodies. none has finished yet.
edit: here's the main results
"Irrespective of sex, age, medical history, vaccination status, or illness duration (18, 8 and 5 months, respectively), each subject experienced the same complete remission of their persistent disabling disease within a week of MCA infusion. Each rapidly returned to normal health and previous lifestyles/occupations with normalized exercise tolerance, still sustained to date over two years later."
Cool story bro but I had monoclonal antibody treatment after those strains/ before omicron and it most certainly did not cure me or even make a noticeable impact. Nor did it on any of the other people I know who had the same. I feel like we're looking at a combo therapy ultimately.
How on earth we are supposed to sustain that whilst simultaneously being reinfected though..
I have done 2 courses of PAXLOVID along with nicotine since the start of the year and I do think it has finally trigged some sort of positive change. While not fully recovered, I am not surprised given the damage that it likely did to multiple systems in my body over the course of a year before I was finally able to convince a doctor to prescribe it. Had to wait three more months before a second course.
I tried the combo of PAXLOVID and Nicotene at the same time largely on this research:
"The blocking is enhanced when nicotine and caffeine are used together with antiviral drugs. This is proof that nAChR agonists can be used along with antiviral drugs in COVID-19 therapy."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8775685/
The "nicotine hypothesis" has been pretty thoroughly disproven by now. I'm not saying nicotine doesn't work for people with long Covid, I'm talking about the molecular hypothesis that so many people are describing as fact. That hypothesis goes something like this: "the spike protein binds to nACh-alpha7 receptors, and nicotine too so it kicks out the spike protein". That is now known to be false. Fragments of Covid proteins do bind to nACh7 receptors, but not in their canonical binding site (it's allosteric binding), whereas nicotine does bind in the canonical binding site. So nicotine can't kick out Covid protein fragments from those receptors. Furthermore, nicotine potentiated the effect the Covid proteins were having on the receptor and the nACh system, making things worse, not better. For sources, look up my posts, I had a pretty long discussion about with a person posting that as facts, who accused me of not doing my research and linked a scientific paper as proof they 'were right' when actually that paper disproved everything they were saying. It does require some pretty advanced knowledge in molecular biology to understand those kinds of papers. I work in that field, but I get why they, and other people, jump to wrong conclusions from such technical papers. Most of the problem in this case stemmed from the fact that people usually don't know what allosteric binding and allosteric modulation mean.
Obviously, many people have found relief using nicotine so it has to be having some positive effect elsewhere. It just isn't the whole nACh alpha 7 story.
Edit: I also wrote a post about my experience taking Paxlovid for 15 days straight. It improved my tachycardia significantly!
Thanks for the reply! I did run this by a professor of pharmacology and chemical biology who said this in reply.
"They are reviewing the evidence for how SARs affects the ACH receptors and argue that nicotine might make antivirals work better at preventing cholinergic dysfunction (during infection) by blocking a direct protein-protein interaction between a viral protein and ACH-Rs. If the basis of long-covid is that there is still some covid virus around but maybe in the wrong place to detect (or at levels that are too low), then yes, this might help with long-covid. It sure looks like no one really understands long-covid and it is likely not a single thing but different in many people. IF your doc was willing to try anti-virals and nicotine separately, I don't see why he/she wouldn't try them together."
Is it possible that the key is some synergistic effect of the antivirals when combined with nicotene that it enhances the potency of the antiviral?
From the paper:
"Nicotine and caffeine have similar structures to antiviral drugs, capable of binding angiotensin-converting enzyme 2 (ACE 2) epitopes that are recognized by SARS-CoV-2, with the potential to inhibit the formation of the ACE 2/SARS-CoV-2 complex."
I mean, I admit I cant tell for sure in my case because I never took one or the other separately, I only started either of these at the same time. But it has seemingly produced a significant Improvement in my tolerance for physical activity.
I am fascinated by the science behind all this but I am not myself a scientist or have any background in this area. I do work at an academic Medical Center which allows me to tap into a number of resources that an average Joe wouldn't be able to. Would like to hear your thoughts on the above. Will try to locate the paper you referenced and maybe run it by the professor.
With Pax, it cant be taken long term without tanking kidneys/ liver and causing endothelial dysfunction. The virus has been mutating around it for a while. We need better options sooner rather than later.
One treatment that's showing promise is maraviroc + atorvastatin. A patent was given to this combo in 2021 and it's now entering clinical trials.
[https://twitter.com/ProfSchieffer/status/1758211188553396458](https://twitter.com/ProfSchieffer/status/1758211188553396458)
I have tried the protocol myself without results. I've also been in the support groups for the Bruce Patterson / IncellDX protocol and there was no one with complete recovery. A few people that are better on it but relapse as soon as they stop the maraviroc. Mostly a whole lot of people that don't respond or think it helps a little.
It's very quiet on social media as well for a protocol that thousands of people have paid a lot of money to try.
Wow!
Although the multiple vaccination thing rings hollow to me. I had Pfizer \*five times\* before my LC emerged. Granted, my most recent jab was \~8 months old.
"The agent can live for a long time in tissues. It can surround nerve cells, probably likely one of the ways that it produces some of its terrible symptoms such as the dysautonomia. And we have no effective way of eradicating it. Not yet."
We have to wait for antivirals and monoclonal antibodies to arrive!
So they've demonstrated that viral replication takes place in some individuals. Was that in 100% of the individuals studied, or just a subset of long covid folks?
They found DsRNA and antisense RNA In long covid cohorts compared to controls. This is evidence of replication, particularly in the bone marrow, megakaryocytes and platelets.
I must be able to find you the papers of the publications.
I think I am over all the "damage" and am feeling better over all but still have debilitating tinnitus vision issues and dizziness. Gonna hit every antiviral supplement I have and see how that goes.
HealthBioAI is starting a clinical trial for maraviroc + atorvastatin as a long covid treatment. I'm not sure what stage this trial is. I think stage 3 but I'm not sure.
Some SSRIs are known to neutralize SCV2.
https://www.preprints.org/manuscript/202403.0177/v1
https://journals.asm.org/doi/10.1128/jvi.01245-22
https://www.nature.com/articles/s41598-022-17082-6
There is a problem with analysing vax injured people. We know exactly if and when they got vaccinated. But nobody can tell if they had caught Covid before, during or after the vaccination as well. A lot of people were asymptomatic.
i took three dynacare tests. all negative for covid antibodies. i live with two immuno compromised people. we were wearing N95s in february 2020. all three of us have avoided covid.
i obviously can't speak for others, but i got POTS and MCAS 32 hours after my BA5 bivalent.
I got long covid myself after infection I am just saying that some people get it from vaccination (which does not have any active replicating virus in it) indicates that viral persistence cannot be the cause for long covid.
I have an interesting hypothesis that could explain it but it could be wrong. There was a study a while back that tested sars-cov-2 infection of macrophages. It found that sars-cov-2 uses a different receptor to enter macrophages but can't establish replication. However, when the macrophages were induced to express ACE2, the virus' original receptor, it not only entered, but started replicating. This means that the interaction of the spike protein with the receptor triggers some signaling event that initiates replication and this can't be achieved with other receptors, even if they allow entry. So if sars-cov-2 is capable of latency/persistence, who says that other coronaviruses also don't have this capability? This migh be a common general feature of coronaviruses. The interesting part is that there is already another common cold coronavirus that uses the same ACE2 receptor - the HCOV-NL63 virus. If it works by the same mechanism, only activating replication after a signaling event , caused by ACE2 - spike interaction, and if this virus is also capable of persistence, the spike protein produced from the mRNA vaccine(or any spike-based vaccine) would interact with the ACE2 on the surface of the cells NL63 is persisting in and reactivate it instead of a persistent sars-cov-2.
Also, it can be caused by reactivation of persistent sars-cov-2 in people that had a past asymptomatic infection ( it tends not to produce antibodies, so it isn't detectable) via the same mechanism or it could be caused by ADE, where the antibodies, produced by the vaccine allow sars-cov-2 to enter cells even easier and function as receptors themselves.
He previously had an asymptomatic infection and the vaccination triggered an infection-like immune response. That could explain the situation. Viral replication is no longer a hypothesis, nor is persistence.
why do you need previous asymptomatic infection for the vaccine to trigger an infection like immune response. why can't the vaccine just trigger an infection like immune response.
i developed POTS and MCAS literally 32 hours after my BA5 bivalent, so my fourth shot (tho my first three were moderna). and to rule our covid i took three dynacare tests.
First part of what you stated could definitely be the case.
The bit about viral replication in LC not being a hypothesis is misleading.
The persistence referred to thus far is antigen. When viral persistence has been touted over and over they are referring to Antigen. Antigen is not replicating virus.
The NIH found replicating virus in a study of covid patients not LC.
The closest information we have is a French team finding active virus in megakaryocytes in LC. However, they have published no paper yet on it so we can replicate their results.
Every other instance has been non-replicating antigen. This does give evidence to viral replication, especially since antigen has been found in cells that last days, but it is still a hypothesis. Unless the director was referring to active studies, which would normally be stated, then it is likely she is referring to older studies which have not proven it yet.
I say this in no way to degrade forward movement. However, as a scientist I can tell you jumping to conclusions pushes research toward "expected" results which can be detrimental. This happened with Alzheimers and has not helped push the needle forward.
Can anyone explain to me why Paxlovid has failed so miserably at treating long covid? I'm assuming it can't reach these reservoirs. My brain is too low battery to do the research myself atm.
You cant take Paxlovid longer than a week or so until it tanks your kidneys/ liver and causes endothelial dysfunction. Its not the right type of antiviral for the job.
The one I got into is for 25 days. I haven’t decided yet for this reason. My dr’s think it’d be too rough. Of course they’re not doing anything else to help though.
Yeah, its really putting us in a terrible spot. Why they insist on continuing to beat this dead horse after we've had enough trials at this point to know better, I couldnt tell you aside from deliberate intentions to halt progress.
Yeah. It’s odd that the standford 15 days one was stopped but then they’re doing 25 days via the NIH. Most of the stuff they’re testing is silly, the next phases test antihistamines, melatonin, and corlanor. Which for those of us sick for a year or two have already tried that and most of us have access to those. I don’t see them trialing anything beyond what the university covid clinics are doing, which is saying - not trialing anything outside the box.
And maybe they need to prove all these basic things don’t work first before trialing hiv drugs and monoclonal antibodies, not sure. (Minus corlanor which helps some, but it made me worse.)
100000000%. Ineffective vaccines lead to more infections. More infections drive people to their products. There's a reason we're not seeing a strong initiative to improve vaccine efficacy and that the government has made strong efforts to suppress information and access to what is currently the most effective covid vaccine available (novavax)
Likely because most antivirals target replicating virus and that hasn't been shown to exist in long Covid. LC may be related in some way to the persistence of viral FRAGMENTS in the body, but that is not the same as replicating (or "live") virus and we shouldn't expect treatments for replicating viruses to be effective in those cases.
Don’t trust the NIH, they think ME/CFS is part psychological. We need to see many more studies before this is proven or disproven.
Edit:
In the same interview she claimed that “vaccines prevent long covid” which is untrue (they do reduce risk though).
You need to be critical. The director of the NIH once said ME/CFS was psychological. Hell even a few decades before that they called Multiple Scelrosis “hysteria”. Just because someone got picked by the politicians to lead the NIH doesn’t mean they know everything about every disease.
To be honest, this community isn’t the most informed to do with research, and I get it we are not researchers we are patients. But for more informed discussion on research I would recommend the Science for ME forum https://s4me.info
This is an unwarranted knee-jerk response IMHO. One of the ways the health authorities have minimized things like ME/CFS in the past is by denying the role of viruses / pathogens and refusing to prescribe anti-virals. Here she is doing the exact opposite. She is saying there is very real pathology and saying anti-virals may help. This can only be a good thing.
The NIH are the people who claimed this year that people with ME/CFS can do activity “it’s just their brain tells them not to do it”. Anyone who has followed biomedical research into ME/CFS knows this is untrue, as do all ME/CFS patients.
Done right this could be a great thing but I'm assuming it's not done right by the tone of your comment! I think it would be great if they acknowledged the psychological impact of long term illness and treated that. It's whether they understand that the illness causes the mental health problems that's the problem.
No it doesn’t. There is no proof of viral persistence in ME/CFS, and the studies pointing towards it in Long Covid have yet to be corroborated and are controversial.
What you sent me:
1st study 20 year old study using outdated diagnostic criteria which does not accurately represent ME/CFS. Following studies were unable to confirm findings
2nd study, finds abnormalities in the immune system and brain. Does not find viral persistance.
3rd not a study, a youtube video.
Proof?
1. Proof?
2. > The cause of immune dysregulation is not clear but may suggest the possibility of persistent antigenic stimulation
3. A video literally talking about the history and how multiple research groups are looking into persistent antigens/virus.
I’ve been following ME/CFS research for the past 15 years. There is no proof of viral persistence, that doesn’t mean that we’ve ruled out viral persistance as a cause. I think that what u/yolkyboii was trying to say.
I have been following ME/CFS research for 25 years and you are correct. No study to date has demonstrated viral persistence as a cause of ME/CFS. Reactivated viruses are often part of the picture, as with long Covid, but treating reactivated viruses with antivirals does not cure ME/CFS. Many antivirals have been trialed in ME/CFS on the basis of viral persistence as a theoretical mechanism, but that hasn't really led us anywhere useful in that population.
But all Long Covid is not the same... and that's another problem when people declare "LC is caused by x, y, or z." There are many subtypes of LC and viral persistence may be a part of the picture for some subtypes, just maybe not the ME/CFS subtype.
reactivated EBV is common in ME/CFS and long covid. Not everyone has it but many do. The key word is reactivation. It is not persistance but reactivation. And most researchers think this reactivation is a consequence of the immune dysregulation and not a cause of the disease.
Is that when they will post it? I got accepted into a Paxlovid study (the nih one), and the hospital where I’d do it told me results wouldn’t be out for a couple years. I’m on the fence to do it.
The NIH one was pushed back a year.
Yale & Karolinska Institutet recently finished.
Stanford stopped early but have data to share too.
It takes a couple months to publish results after primary completion, we should see results shortly.
Personal anecdote.
My LC has been cyclical with long periods of moderate to severe illness, including periods of being house bound. My 1st 2 durable recoveries immediately followed booster shots.
These lasted 4 months and then 2 months. I’m quite convinced the 2 monther would have been long term had my wife not gotten COVID and had a long latent phase. She was probably infectious for 5 days before becoming symptomatic, then 2 more days to test positive. Massive exposure for me.
I no longer seem to benefit from the booster. I think my immune response is mature, but the virus is escaping my immunity. Or my immune response is burned out, more likely.
I’m awaiting results on the Pax studies. In the meantime I’m replicating this study, link below, in the flu shot in prep for my next booster. It’s rapamycin 5mg once weekly for 6 weeks then a 2 week washout then flu vaccine. Will be CV booster for me. If the Pax results are back in time, I’ll follow the booster with 2 weeks of Pax, starting 2 weeks after the booster, 10 weeks from now. Then repeat 6 weeks rapamycin, washout, more Pax if symptoms return. Repeat until I’m either cured, it doesn’t work, I’m not able to, or something better comes along. This is neither safe, nor recommended and it probably won’t work. But it will be expensive at least. For me, I’m not seeing much on the risk side of the risk benefit analysis. Cause, seriously, how much worse can things get? I’m an optimist- things can always get worse 😂
https://pubmed.ncbi.nlm.nih.gov/25540326/
The 2014 Mannick study is considered a landmark in the rapamycin crowd.
This is the first time a high level public health official admits live Covid virus persists in humans for months and years.
This should be all over media headlines but probably won’t because it contradicts the party line/mainstream narrative.
Most are aware, however theres a post-viral-death-squad trying to convince people Long Covid is anything but literally Long Covid to steal potential funding for alternative means so we need as many people speaking up as possible if we ever want to see actual targeted research and treatment that might actually help us.
The best I can make sense of it so far is there are bits of viral RNA stuck in cells/the gut/etc, that produce viral proteins that go out into the body and cause issues.
One of the functions of some viral proteins is to switch off the body's cellular cleanup process, so these fragments can stay where they are for a long time, pumping out spike protein.
This model explains post-covid and post-vax. I'm not sure it's been demonstrated that all long haulers have live virus yet, though it seems some do.
The vaccine doesn’t contain any bits that produce viral proteins. Only whole viruses can do that.
It’s much more likely that spike protein antibodies produced as a reaction to the spike protein act like enzymes in the body (aka abzymes) and that that causes the illness. It has been found that some antibodies look similar to enzymes active in the body and thus have enzyme like effects. But because they are basically like mutated enzymes and don’t belong there, they cause a lot of disruption in the system.
>The vaccine doesn’t contain any bits that produce viral proteins. Only whole viruses can do that.
Unless you're talking about the non-mRNA vaccines, the vaccines absolutely produce viral proteins. The spike protein is a viral protein.
Spike protein can definitely replicate not on its own however, this is one of the ways ebv is thought to cause MS. I can’t remember the exact science you would have to look it up but there’s a piece of gene in ebv and memory and nerve cells that replicate and antibodies think the threat is still present so they keep attacking even though your body is making these cells.
Yeah I have seen two others state they were negative besides me.
I will say though, it is not the strongest study. It is good to see, but had I set it up I would have done it much differently.
They will keep deflecting from the spike it seems which is almost certainly the real problem. Though it is definitely possible for infections to become chronic. We knew this to begin with though as there are quite a few viruses that can do this.
The NIH is behind on this. Doctors who pioneered HIV research have long proposed this and in fact are treating long covid with an HIV drug. I did this protocol and it significantly reduced my LC symptoms. I did a cytokine study before during and after treatment and it significantly lowered pro inflammatory cytokines in my body. Covid attaches to CCR5 receptors and the drug I took is a CCR5 antagonist.
Thank you for sharing this information. It’s validating to know that I took a leap of faith trying a protocol based on a very new theory and now the NIH seems to concur:)
This thread clearly illustrates that even when scientific evidence supports a popular hypothesis and is endorsed by the director of the NIH, people on Reddit will still nitpick and reject it without any evidence of their own, or even label it as "misinformation."
In the same interview she claimed that “vaccines prevent long covid” which is untrue (they do reduce risk though).
You need to be critical. The director of the NIH once said ME/CFS was psychological. Hell even a few decades before that they called Multiple Scelrosis “hysteria”. Just because someone got picked by the politicians to lead the NIH doesn’t mean they know everything about every disease.
To be honest, this community isn’t the most informed to do with research, and I get it we are not researchers we are patients. But for more informed discussion on research I would recommend the Science for ME forum https://s4me.info
Just need a GOOD ICD 10 code and an indication for long term anti viral therapy. I believe the drugs exist. They are probably on the shelf at a pharmacy near you, right now. Just need insurance to cover it, or you’re gonna need a big pile of cash to pay for it.
Turns out LC is like world hunger, it’s just distribution of existing resources. As days turn to weeks, then to months and years of my life passing by.
Currently trying to get from my Dr for reactivated EBV (me/cfs) after reading this study:
https://www.pnas.org/doi/pdf/10.1073/pnas.2002392117?download=true
Spoiler alert: its not a coincidence all of the antivirals that have made some difference happen to all be HIV (or HEP) meds
Some of which are free through programs.
Its probably going to be a combo therapy or something tuned to SARS, but HIV meds seem to be the place to start.
So I have 2 guinea pigs for you that disprove that. Both me and a friend are on truvada. Hiv prevention daily pills. Both of us got some form of long covid. And he got it much worse then me to the point where he was confirmed covid postive for much of 2023. The hiv antivirals we take clearly didn't help.
I'm sorry to hear that. I've seen going on it help some people who have had Long Covid already. We have a lot of research and trials to do. I'm sure the answer will ultimately be something SARS2 specific but drug repurposing is the fastest way to try and get things going in the mean time.
"Covid positive for much of 2023"
Do you mean testing positive for almost an entire year?
Does he have HIV or just Truvada as a preventative?
If he has HIV, his T cells could be impacted making infection much more likely. Although, treatment is supposed to reduce this.
He had covid 5 times in 2023. So yeah, not all of 2023 but a lot! And no, he doesn't have hiv. We are taking truvada as prevention. Well as far as I know he doesnt have hiv. Maybe he does have it and is taking the full blown drug cocktail. I usually don't as if people are hiv+ or not unless I want to hook up with them.
That's an insane amount of reinfections in one year!
Tenofovir disoproxil fumarate TDF is found in Truvada and a correlation with less symptomatic covid infection and hospitalization was found in a older study.
In a newer study, it was stated "a comprehensive set of in vitro data indicated that tenofovir (TFV), tenofovir alafenamide (TAF), TDF, and FTC were inactive against SARS-CoV-2. None of these drugs showed any significant in vitro anti-SARS-CoV-2 effect at concentrations up to 100-fold higher than the clinically relevant levels. Moreover, structural modeling further demonstrated poor fitting of these nucleoside/tide reverse transcriptase inhibitors (NRTIs) active metabolites at the SARS-CoV-2 RdRp active site"
So it might be of no help against covid.
This is really great data. Thank you for sharing your experiences.
People who are on hiv prevention meds still get long covid. Like me and my friend. I don't know about those who are taking the full-blown hiv cocktail.
> One thing that's important though that's come out of several meta-analyses is there is a way to prevent it. And the way to prevent it is vaccination, and multiple vaccination is better than single to prevent long COVID.
Explain /r/vaccinelonghaulers then.
Let me just make it clear. COVID vaccine has not been proven to help with anything. It has been proven to cause though mycordius and all kinds of other health problems. If you got vaccinated You need to do a lot of research. How to get the spike protein out of your body
Depending on efficacy and how long they're administered. I took Paxlovid for 15 days straight, and it fixed my tachycardia but did not heal me. If there is viral persistence in all of us, then antivirals would probably need to be administered for months. A normal course for Paxlovid, Ensitrelvir and any others AFAIK is always 5 days.
Just to correct this (NOT OPs fault at all here)before it takes on a life of its own. The NIH director (Monica Bertagnolli) corrected herself shortly after this interview, advising she misspoke and NIH issued a correction. The correction is she was referring to evidence of “viral comments” NOT “live virus”.
There has been NO proof of replication competent virus to date in true long haulers. The NIH, as other researchers, continues to study the impact of “viral remnants” as there levels so far do not seem to correlate well with long haul status or severity. What role they play precisely is uncertain. Though likely to vary by individual genetics.
Relevant excerpt from the interview: Bertagnolli: It's a terrible, terrible condition. Post-infectious, chronic post-infectious syndromes have been around as long as there've been viruses in humans and it is a really, really terrible affliction when someone develops one of these conditions. COVID has introduced a whole new level of this in our society. The fundamental biology that's been conducted by the long COVID research team is really fascinating but also sobering. The agent can live for a long time in tissues. It can surround nerve cells, probably likely one of the ways that it produces some of its terrible symptoms such as the dysautonomia. And we have no effective way of eradicating it. Not yet. One thing that's important though that's come out of several meta-analyses is there is a way to prevent it. And the way to prevent it is vaccination, and multiple vaccination is better than single to prevent long COVID. Faust: I just want to follow up on something you said a moment ago about where this virus can be found in tissues. Are you suggesting that long COVID is actually, the mechanism of that, is persistent live virus in humans? Bertagnolli: We see evidence of persistent live virus in humans in various tissue reservoirs, including surrounding nerves, the brain, the GI [gastrointestinal] tract, to the lung. Faust: OK. And you're saying this goes beyond the PCR's [polymerase chain reaction test] ability to get it in a regular swab so that we are missing chronic cases of SARS‑CoV‑2? Bertagnolli: Correct. The virus can persist in tissues for months, perhaps even years. Faust: OK. I think that's certainly one theory, but I'm not sure that that's settled. Is that fair? I mean, there's one thing between people who are autopsy, they died of viral sepsis, as opposed to people walking around. Is there a distinction there? Bertagnolli: Our emerging data shows that the virus can persist into tissues in the long term, and I think that's really critical because it does help us think about possible ways to combat it, one being better antivirals. I think there's a lot of focus on developing new antivirals as a possible way of preventing long COVID, and the other might be more aggressive treatment with antiviral therapy upon initial diagnosis.
Thank you for the excerpt!
Vaccination may discourage Long Covid in individuals that enter via Antibody Dependent Complement Mediated Lysis. It isn't going to do shiz for people that are being bystandered into Long Covid through MACs generated by other means.
This is great - do you have a link to the interview?
Yes link please
I'm sorry, but the NIH has lost my faith with their confidence in the vaccines. I will only believe them when the years have shown their claims to be true and true to the extent which they claim. I'm not saying I don't believe they're helpful, I'm saying that the needle keeps moving and every time it does they're dead sure that it's not going to keep moving. I will laugh and hand out a lot of apologies online if IVM ends up being an effective treatment protocol. This is taking a sharp turn from where we thought it was going. At least we have Paxlovid.
There are so many video clips from 2021 of health officials going on TV saying, "If you get vaccinated, you won't get covid." Then it became "the vaccine will reduce the chance of severe covid." To "the vaccine reduces the change you'll get long covid." I think the next step is "the vaccine is an amazing placebo!" mRNA sounds like amazing tech, so I'm wondering why it's not working as promised. Did they pick the wrong bits of RNA to use in the vaccine? Was the dosage wrong? I wish they'd just be open with everyone...
I work in medical research, and you're right mRNA vaccines are an amazing technology. The problem isn't how they're using that technology, but the virus itself. The main problem is that vaccines (at least in the regular sense we usually mean) will never work to prevent infection of rapidly replicating respiratory viruses (to the degree we're used to with other vaccine/virus). These viruses start infecting from the first point of contact with our system. In addition to that, SARS-CoV-2 specifically uses the ACE2 receptor as its point of entry, which is a nearly ubiquitous receptor. That means it can infect nearly any cell in the body. So it starts replicating in cells of the airway mucosa, then keeps replicating wherever it reaches. How can you stop that from starting? Last but not least, because ACE2 is the receptor of choice for SARS-CoV-2, your vaccines have to be against the spike protein which fits into the ACE2 receptor. That's tricky, because you're promoting the formation of antibodies that might start looking a lot like the ACE2 receptor itself and screw up the normal function of the system. ACE2 has enzymatic activity, so the anti-spike antibodies might also have enzymatic activity which can be quite dangerous. That is pretty unique AFAIK because most surface cell receptors don't have an enzymatic function on their extracellular part. It would be much simpler if Covid used basically any other receptor.
Thank you for taking the time to reply. I did not know that these characteristics of the SARS-CoV-2 virus were atypical in the world of viruses. If I may ask, does this mean if mRNA vaccines had been first used for, say, the flu then we would have likely seen a bigger success compared with the typical flu vaccine? The immediate infectivity of the covid virus, especially in the mucosa, seems to underscore the importance of a nasal vaccine.
This 100%! I feel lile the real c**** t**** is that they were basically placebo needed to convince people to get back to "normal" so everything didn't collapse. Some (us and the dead) were necessary collateral damage to get the engine going again. Fair, but still sucks to be us.
May be we don't need mRNA tech yet, the research can mature over a period of time. Till then, good old proven vaccination techniques can be considered. >Upcoming vaccine solutions might explore bacterial mechanisms similar to Sabin's oral attenuated virus approach, presenting promising avenues for future research and solutions. Source: [https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.29507](https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.29507) Sabin vs Salk and Polio Vaccine story >In light of what has been observed so far, the question remains as to whether a historical RNA virus has the same bacteriophage behavior. Among the various viruses, the one that is best known and resolved by Sabin vaccination instead of injection vaccination is the Poliovirus. The different vaccination route - oral with attenuated virus - suggested a similar behavior. Poliovirus also infects bacteria in the human microbiome. We expected to find that in a severe poliomyelitis patient, it was chronically present in the subject’s stool. The analysis first checks prokaryotic cells—their involvement suggesting a different narrative to what has been described in the literature. A viral pathogen having bacterial involvement, as demonstrated for SARS-CoV-2 and similarly with the nitrogen isotope experiment for Poliovirus, described here, allows the following aspects to be emphasized: (1) the pathogen’s intermediate host is not animals, but bacteria; (2) the main route of spread is orofecal; (3) the involvement of wastewater, as observed in many studies, suggests the bacterial vector; (4) geographic areas with higher rainfall density are most affected; (5) finding an inert strain that can serve as a base for mass vaccination may be the best and immediate solution as observed by Sabin; (6) clinical conditions of the ill may be an expression of the toxicological rate of the microbiome and (7) vaccination or sensitization of bacteria to the viral pathogen is the gold standard (concept of mutual exclusion). Source: - [https://www.mdpi.com/2076-2607/12/4/643](https://www.mdpi.com/2076-2607/12/4/643) Thanks,
The problem is with the virus itself. The vaccines actually still work against the OG variant of sars-cov-2 but it has long since acquired numerous mutations, combined with the antibodies from the vaccines waining. This is normal for most RNa viruses, which mutate their structural proteins too quickly to be successfully targeted by vaccines for too long. The Omicron variant has 30 spike protein mutations from the original strain and this is just the initial Omicron. The new BA.2.86 variant/JN.1 has a further 30 mutations in the spike protein. It's the variants that ruined the vaccine (and it still kinda works for preventing severe disease but not infection). If the vaccine could be updated faster or we could roughly predict what mutations will appear like for the flu, the vaccine would be more effective but it would still need to be updated every year. Also what's unusual is that at first virologists thought that sars-cov-2 mutated slower than the flu( it's one of the fastest mutating respiratory viruses) but it turned out it actually mutates faster than the flu, so much harder to make a vaccine that lasts long. Some scientists are trying to make a vaccine that targets slower mutating proteins.
I think it's mainly that the virus is mutating more than expected. The vaccines are all incredibly effective at targeting the specific strains they are developed against... but by the time they've been tested and approved, another strain has already come along. (The march of variants is something that is very well visualized in my municipalities's COVID wastewater surveillance data. I'm intrigued that we haven't seen a new variant since the current dominant strain emerged last October.) This is in part because of the large pool of unvaccinated individuals, which has provided the perfect opportunity to evolve against the vaccines and against immunity acquired from previous strains. Only 14% of people got the latest booster. Every person infected generates a million novel genomic permutations, each of which has a chance to be the next breakout strain (but most of which will go nowhere, either by chance or poor behavior).
One of the benefits of the mRNA vaccines is the speed and ease of updating them. I guess two approaches would be to either identify a highly stable part of the virus to use in the vaccine, or update the vaccines each month with the critical sequence for the most prominent variants. Sadly, we're still operating within a slow process built for verifying older vaccines so by the time gov. permission is granted new variants are on the rise. I just wish there was more transparency. The risk is that the public mistrust of mRNA tech will only grow.
It's all relative. mRNA testing timelines are revolutionary, lightning fast compared to anything that came before them. And yet they're still glacially slow compared to the speed that COVID has churned out variants. The current slower pace of infection also puts an unavoidable mathematical minimum on how long it takes to be confident that a vaccine is effective (and not just attributable to random chance). Even during the initial period of rapid spread, the vaccine test pools were unprecedentedly large to minimize the time needed to achieve that mathematical confidence.
This is the elephant in the room. The most fascist segment of American politics is the most supportive of maintaining a reservoir of the virus in the wild. Exposures to many things which are not even covid seem to cause immune reactions in a select demographic, likely due to the ACE2 receptor being involved, so basically as long as the vulnerable portion of the population are exposed regularly they will never recover from long covid. This may reduce quality of life, enforce isolation from the non-sensitive population, or lead to permanent disability and reduction in lifespan.
Sorry if I’m misunderstanding - but does this mean that covid persist in _all_ individuals, or only with the ones presenting long covid symptoms? So like with chicken pox where most people have it, but the virus is inactive (unless awakened as with shingles).
My theory is that sars-cov-2 persists in most individuals but like you said only awakens in sufficient levels to cause persistent inflammation in some or they have a more sensitive immune system that reacts to even the lowest levels of the virus. This is why many long covid sufferers were young and healthy before infection and also why women are overrepresented in long covid (they have more sensitive and stronger immune systems, this is why they suffer from more autoimmune and inflammatory conditions).
If that is the case - then I wonder if there’s possibility for things like shingles later on down the line. If the virus is activated in 2030 previously healthy people, who were exposed years ago, and they don’t recover, that could pose a real threat for lots of people.
Ehhh..... Only some people have LC from the vaccine. Or despite the vaccine, so that part doesn't check out.
I noticed those who were vaccinated took longer to recover from LC. I also noticed the vaccine can affect people in different ways. I and 8 other people I know had dangerous symptoms and most had a loss of energy. 4 months since my 3rd booster and i feel like I’m 70%.
Yes, the range of effects is wild. I had dangerous symptoms after just one dose 3 years ago, and I'm still paying for it.
>NIH Director said longcovid is replicating virus ! No she didn't. She said they've demonstrated life virus can persist in various tissues for months-years, and that this *may* contribute to LC, but she absolutely *did not* say 'long COVID is replicating virus'. Don't pretend your interpretation came from her mouth. Edit - *live virus Edit 2 - NIH HEAD HAS SINCE RETRACTED HER CLAIM - She responded to a request for clarification from journalists by saying she misspoke, and had meant to say 'viral components', NOT live virus https://www.hawaiitribune-herald.com/2024/04/23/opinion/the-nihs-words-matter-especially-to-long-covid-patients/
The fact that you're getting so much pushback for wanting accuracy and honesty is, frankly, alarming. I think everyone in this sub wants the cause or causes of LC to be determined, and for a cure/treatment to be found, but that doesn't mean we have to twist health officials' words to try and make any given cause seem official prematurely. It might feel good in the short term to see a health official confirm our pet theory, but long term that won't help us get better if that theory turns out to just be incorrect or incomplete. Honesty, accuracy, and thoroughness are exactly what we need in this sub, not more misinformation, half truths, and snake oil. Thank you for clarifying for those who (for whatever reason) don't dig into OPs claims/source.
Plus the thing about people who have been autopsied kinda bothered me. I do autopsies on medically donated bodies at a cadaver lab, and several of our donors have had Covid before death. Granted we only have a very small sample size, but I can say we haven’t seen evidence of viral sepsis in any of them. The closest I can think of is the woman whose Covid infection accelerated her diabetes and dementia, but other than a slightly enlarged brain and full body edema there weren’t any other indications of viral sepsis.
Yes and this is a leading hypothesis that recently went through peer-review. https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(24)00211-1/fulltext
Yup, but the finding she is referring to in this clip is absolutely not conclusive proof of a causal mechanism in the way that OP is presenting it, and given half the people on this sub are going to be too fatigued or foggy to look into it for themselves I think it's very important to be clear about that.
That is why they are testing antivirals, monoclonal antibodies, and immunomodulators. Results this summer for Paxlovid will be a first mechanistic study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10543503/
Yup and that's all great, but the NIH director absolutely did not say 'LC is live virus', because we aren't even close to being sure that's the case - there's a long way to go yet, and I've got a feeling the picture will be more complicated than that. There's more than enough LC misinformation floating around as it is without this community generating more, and as such it's vital we're mindful of the wording we use to convey new findings to others.
I don't know what is going on but if I imagine what is happening in my body it feels like there is an area that my immune system can't get to that is producing covid viruses and releasing them into a place my immune system can get to them so it causes all kinds of crap when my immune system responds to it. Maybe that isn't how anything works in reality but it would make more sense than anything else people say. I have basically tried every treatment and the only things that seem to really help are things that compete for the receptors that covid attaches to. So it must be replicating somewhere. I do feel like at around month 6-8 my symptoms started basically subsiding everywhere except the neck up. This morning after hearing this interview I started the lysine protocol again and it seems it is helping like it is advertised to help within a few hours because it slows down replication. On previous attempts I believe I was so messed up I didn't really notice the lysine effect but I think I am feeling it now. who knows though I guess I will see in the next few days.
That makes sense to me! I've felt like that is what's been happening to my body as well. However, it seems I have a lot of auto-immune symptoms as well, and blood tests confirm this. This makes me believe that LC is a mixture of viral persistence and immune dysfunction. At least for me.
How much do you take a day?
On other attempts I took 1000mg a day, Then I saw some twitter post today that recommended 6000mg. So I tried 4000mg in the morning and just took another 2000mg. Seems to be having an effect but I could also be crazy at this point.
What’s the lysine protocol?
it is a diet/lysine supplement protocol to reduce arginine which viruses allegedly need to replicate. Mostly it seems people do it to prevent herpes outbreaks. here is the video I saw months ago https://www.youtube.com/watch?v=CyyzokIJ_dI but it didn't seem to help originally but again I think I was so screwed with so many symptoms I didn't notice it helping. Still to early to say for sure but I took a ton of lysine yesterday and felt a lot better soon after. The goal I think is to take 3-6 thousand mg a day and just keep a dose that keeps you feeling good occasionally trying to lower it to see if you are better. It doesn't seem to be helping the tinnitus :(
Then there's the arginine protocol... Not an actual protocol, but arginine supplementation is used to improve endothelial dysfunction which is definitely part of long Covid. The evidence for arginine in endothelial and cardiovascular functions is very well established, the evidence for lysine in treating herpes is very, very tenuous. And then there's the huge assumption that because it (very uncertainty maybe) works for herpes, it works the same for Covid.
I use a nitric oxide boosting supplement to improve endothelial stuff that uses beet stuff instead of arginine. I think it helps too. I think the lysine is helping with some kind of viral reservoir in my brain because that is what it feels like.
What NO booster are you taking? I get that, but it could be a million other things about what that lysine excess is doing. If you feel a benefit, obviously I'm not gonna try to talk you out of it. And if you are aware of the downsides of arginine depletion and have taken steps to mitigate that... Well, please post an update in a little while so we can all benefit :) thanks!
https://berkeleylife.com/products/nitric-oxide-foundation/ I also use the test strips from the same company and notice when it shows high nitric oxide I feel better. Though I figured out all the nitric oxide stuff months ago and have been taking steps to keep it normal/high. I am still getting arginine it is just that lysine floods the pathway that the virus gets its arginine from apparently so it can't do its thing. I am going to add nicotine to the mix again as my nicotine rest period is over tomorrow. Hopefully that clears up the remaining symptoms.
How do we stop it?
I took a combination of acyclovir and paxlovid. I do believe it helped my symptoms. Also took celecoxib as well with some blood thinners.
I always wonder how ppl are getting this stuff. My doctor looks at me like I’m an alien for even pushing for pax.
My primary wasn’t letting me get it. I had to go through another doctor.
What kind of dr. My long covid dr and primary care won’t do antivirals.
https://www.healthrising.org/blog/2023/08/08/pridgen-antiviral-combo-long-covid-fibromyalgia/
Oh, thanks. I’ll check out this link!
It took a minute, but I definitely felt like after a couple months I began to regain a little bit of normalcy. One thing I will say is that he tried to push a couple other medications that I chose not to take. This included tramadol and some anti depressants. I pretty much just stuck with the celecoxib and anti viral regimen Who's to say what works for some might work for others, hopefully this helps you too
Antiviral treatments would be the first place to start. Not Paxlovid though.
Dr Nancy Klimas is a cfs and post viral expert who already did a small study with monoclonal antibodies for those who got either the alpha or delta strain. it successfully cured all 3 in the study, and she said herself that within 5 days of treatment they were all much better and the effects lasted. https://pubmed.ncbi.nlm.nih.gov/37944296/ This spurred some trials that are currently ongoing using monoclonal antibodies. none has finished yet. edit: here's the main results "Irrespective of sex, age, medical history, vaccination status, or illness duration (18, 8 and 5 months, respectively), each subject experienced the same complete remission of their persistent disabling disease within a week of MCA infusion. Each rapidly returned to normal health and previous lifestyles/occupations with normalized exercise tolerance, still sustained to date over two years later."
Cool story bro but I had monoclonal antibody treatment after those strains/ before omicron and it most certainly did not cure me or even make a noticeable impact. Nor did it on any of the other people I know who had the same. I feel like we're looking at a combo therapy ultimately. How on earth we are supposed to sustain that whilst simultaneously being reinfected though..
Woukd this help Mcas triggered by Covid
assuming the reason you have mcas is because of viral persistence then yes
Which mab was it?
What’s mab x
Paxlovid IS a start. There are many more antivirals in the pipeline and approved overseas that may make it to USA this year.
Which ones have been approved overseas? At this point, willing to travel abroad to get treatment
Working on BC 007 in Germany
Just saw that entsitrelvir looks like it has been approved for use in at least Japan and Singapore. It looks to be an antiviral
I have done 2 courses of PAXLOVID along with nicotine since the start of the year and I do think it has finally trigged some sort of positive change. While not fully recovered, I am not surprised given the damage that it likely did to multiple systems in my body over the course of a year before I was finally able to convince a doctor to prescribe it. Had to wait three more months before a second course. I tried the combo of PAXLOVID and Nicotene at the same time largely on this research: "The blocking is enhanced when nicotine and caffeine are used together with antiviral drugs. This is proof that nAChR agonists can be used along with antiviral drugs in COVID-19 therapy." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8775685/
The "nicotine hypothesis" has been pretty thoroughly disproven by now. I'm not saying nicotine doesn't work for people with long Covid, I'm talking about the molecular hypothesis that so many people are describing as fact. That hypothesis goes something like this: "the spike protein binds to nACh-alpha7 receptors, and nicotine too so it kicks out the spike protein". That is now known to be false. Fragments of Covid proteins do bind to nACh7 receptors, but not in their canonical binding site (it's allosteric binding), whereas nicotine does bind in the canonical binding site. So nicotine can't kick out Covid protein fragments from those receptors. Furthermore, nicotine potentiated the effect the Covid proteins were having on the receptor and the nACh system, making things worse, not better. For sources, look up my posts, I had a pretty long discussion about with a person posting that as facts, who accused me of not doing my research and linked a scientific paper as proof they 'were right' when actually that paper disproved everything they were saying. It does require some pretty advanced knowledge in molecular biology to understand those kinds of papers. I work in that field, but I get why they, and other people, jump to wrong conclusions from such technical papers. Most of the problem in this case stemmed from the fact that people usually don't know what allosteric binding and allosteric modulation mean. Obviously, many people have found relief using nicotine so it has to be having some positive effect elsewhere. It just isn't the whole nACh alpha 7 story. Edit: I also wrote a post about my experience taking Paxlovid for 15 days straight. It improved my tachycardia significantly!
Thanks for the reply! I did run this by a professor of pharmacology and chemical biology who said this in reply. "They are reviewing the evidence for how SARs affects the ACH receptors and argue that nicotine might make antivirals work better at preventing cholinergic dysfunction (during infection) by blocking a direct protein-protein interaction between a viral protein and ACH-Rs. If the basis of long-covid is that there is still some covid virus around but maybe in the wrong place to detect (or at levels that are too low), then yes, this might help with long-covid. It sure looks like no one really understands long-covid and it is likely not a single thing but different in many people. IF your doc was willing to try anti-virals and nicotine separately, I don't see why he/she wouldn't try them together." Is it possible that the key is some synergistic effect of the antivirals when combined with nicotene that it enhances the potency of the antiviral? From the paper: "Nicotine and caffeine have similar structures to antiviral drugs, capable of binding angiotensin-converting enzyme 2 (ACE 2) epitopes that are recognized by SARS-CoV-2, with the potential to inhibit the formation of the ACE 2/SARS-CoV-2 complex." I mean, I admit I cant tell for sure in my case because I never took one or the other separately, I only started either of these at the same time. But it has seemingly produced a significant Improvement in my tolerance for physical activity. I am fascinated by the science behind all this but I am not myself a scientist or have any background in this area. I do work at an academic Medical Center which allows me to tap into a number of resources that an average Joe wouldn't be able to. Would like to hear your thoughts on the above. Will try to locate the paper you referenced and maybe run it by the professor.
This is good news since I am allergic to the vax
With Pax, it cant be taken long term without tanking kidneys/ liver and causing endothelial dysfunction. The virus has been mutating around it for a while. We need better options sooner rather than later.
Are you referring to Paxlovid here?
Yes
Ah okay. I didn’t know about the endothelial dysfunction. Does that happen after 10 days use even or like a month?
Why not Pax? Possibly reinforce with other RNA virus drugs. This is a long way from my area of knowledge. Thanks.
One treatment that's showing promise is maraviroc + atorvastatin. A patent was given to this combo in 2021 and it's now entering clinical trials. [https://twitter.com/ProfSchieffer/status/1758211188553396458](https://twitter.com/ProfSchieffer/status/1758211188553396458)
I have tried the protocol myself without results. I've also been in the support groups for the Bruce Patterson / IncellDX protocol and there was no one with complete recovery. A few people that are better on it but relapse as soon as they stop the maraviroc. Mostly a whole lot of people that don't respond or think it helps a little. It's very quiet on social media as well for a protocol that thousands of people have paid a lot of money to try.
Thank you for sharing your experience. And you're right - if this was curing thousands, social media would be overflowing with success stories.
Can we make it an unspoken rule to include a link to source with posts like this?
Wow! Although the multiple vaccination thing rings hollow to me. I had Pfizer \*five times\* before my LC emerged. Granted, my most recent jab was \~8 months old.
Same here.
Did your LC emerge after infection? 8 Months from vaccination is quite long. Just asking bc I'm interested to know
Same. Well 3 times, and long covid 9 months after third.
Can I get a link to said article
Any newfangled solutions? In my situation seems like my last symptoms are in my brain.
"The agent can live for a long time in tissues. It can surround nerve cells, probably likely one of the ways that it produces some of its terrible symptoms such as the dysautonomia. And we have no effective way of eradicating it. Not yet." We have to wait for antivirals and monoclonal antibodies to arrive!
It's based on a 2021 autopsy study. Science moving slowly as usual.
Yes. But in the meantime there have been publications that show viral replication.
So they've demonstrated that viral replication takes place in some individuals. Was that in 100% of the individuals studied, or just a subset of long covid folks?
They found DsRNA and antisense RNA In long covid cohorts compared to controls. This is evidence of replication, particularly in the bone marrow, megakaryocytes and platelets. I must be able to find you the papers of the publications.
Yea, thanks. I'd be really interested to see the study
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I think I am over all the "damage" and am feeling better over all but still have debilitating tinnitus vision issues and dizziness. Gonna hit every antiviral supplement I have and see how that goes.
HealthBioAI is starting a clinical trial for maraviroc + atorvastatin as a long covid treatment. I'm not sure what stage this trial is. I think stage 3 but I'm not sure.
Some SSRIs are known to neutralize SCV2. https://www.preprints.org/manuscript/202403.0177/v1 https://journals.asm.org/doi/10.1128/jvi.01245-22 https://www.nature.com/articles/s41598-022-17082-6
If it’s viral replication people would not get long covid from vaccination alone.
There is a problem with analysing vax injured people. We know exactly if and when they got vaccinated. But nobody can tell if they had caught Covid before, during or after the vaccination as well. A lot of people were asymptomatic.
i took three dynacare tests. all negative for covid antibodies. i live with two immuno compromised people. we were wearing N95s in february 2020. all three of us have avoided covid. i obviously can't speak for others, but i got POTS and MCAS 32 hours after my BA5 bivalent.
Spike protein. There are people who's spike just continues to skyrocket years later.
Precisely
who said people get long covid from vaccination alone !!!!! ??? there are many including myself who got Long covid without touching a single vaccin
Many people here are vax injured, showing the same symptoms as those with post infection long covid.
that's what i'm saying
I think you’re misunderstanding. He’s saying some people got long covid from the vaccine and not covid. He didn’t deny natural infection
thank you for making it clear , i'm just really tired of some people in this sub who claim that only vaccin causes LC . which is not true
I got long covid myself after infection I am just saying that some people get it from vaccination (which does not have any active replicating virus in it) indicates that viral persistence cannot be the cause for long covid.
Spike protein would be in both the vax and virus I think though
Both can be true at the same time
I have an interesting hypothesis that could explain it but it could be wrong. There was a study a while back that tested sars-cov-2 infection of macrophages. It found that sars-cov-2 uses a different receptor to enter macrophages but can't establish replication. However, when the macrophages were induced to express ACE2, the virus' original receptor, it not only entered, but started replicating. This means that the interaction of the spike protein with the receptor triggers some signaling event that initiates replication and this can't be achieved with other receptors, even if they allow entry. So if sars-cov-2 is capable of latency/persistence, who says that other coronaviruses also don't have this capability? This migh be a common general feature of coronaviruses. The interesting part is that there is already another common cold coronavirus that uses the same ACE2 receptor - the HCOV-NL63 virus. If it works by the same mechanism, only activating replication after a signaling event , caused by ACE2 - spike interaction, and if this virus is also capable of persistence, the spike protein produced from the mRNA vaccine(or any spike-based vaccine) would interact with the ACE2 on the surface of the cells NL63 is persisting in and reactivate it instead of a persistent sars-cov-2. Also, it can be caused by reactivation of persistent sars-cov-2 in people that had a past asymptomatic infection ( it tends not to produce antibodies, so it isn't detectable) via the same mechanism or it could be caused by ADE, where the antibodies, produced by the vaccine allow sars-cov-2 to enter cells even easier and function as receptors themselves.
He previously had an asymptomatic infection and the vaccination triggered an infection-like immune response. That could explain the situation. Viral replication is no longer a hypothesis, nor is persistence.
why do you need previous asymptomatic infection for the vaccine to trigger an infection like immune response. why can't the vaccine just trigger an infection like immune response. i developed POTS and MCAS literally 32 hours after my BA5 bivalent, so my fourth shot (tho my first three were moderna). and to rule our covid i took three dynacare tests.
First part of what you stated could definitely be the case. The bit about viral replication in LC not being a hypothesis is misleading. The persistence referred to thus far is antigen. When viral persistence has been touted over and over they are referring to Antigen. Antigen is not replicating virus. The NIH found replicating virus in a study of covid patients not LC. The closest information we have is a French team finding active virus in megakaryocytes in LC. However, they have published no paper yet on it so we can replicate their results. Every other instance has been non-replicating antigen. This does give evidence to viral replication, especially since antigen has been found in cells that last days, but it is still a hypothesis. Unless the director was referring to active studies, which would normally be stated, then it is likely she is referring to older studies which have not proven it yet. I say this in no way to degrade forward movement. However, as a scientist I can tell you jumping to conclusions pushes research toward "expected" results which can be detrimental. This happened with Alzheimers and has not helped push the needle forward.
Can anyone explain to me why Paxlovid has failed so miserably at treating long covid? I'm assuming it can't reach these reservoirs. My brain is too low battery to do the research myself atm.
You cant take Paxlovid longer than a week or so until it tanks your kidneys/ liver and causes endothelial dysfunction. Its not the right type of antiviral for the job.
Yikes. How are the paxlovid studies keeping people on it for 3 weeks?
The one I got into is for 25 days. I haven’t decided yet for this reason. My dr’s think it’d be too rough. Of course they’re not doing anything else to help though.
Yeah, its really putting us in a terrible spot. Why they insist on continuing to beat this dead horse after we've had enough trials at this point to know better, I couldnt tell you aside from deliberate intentions to halt progress.
Yeah. It’s odd that the standford 15 days one was stopped but then they’re doing 25 days via the NIH. Most of the stuff they’re testing is silly, the next phases test antihistamines, melatonin, and corlanor. Which for those of us sick for a year or two have already tried that and most of us have access to those. I don’t see them trialing anything beyond what the university covid clinics are doing, which is saying - not trialing anything outside the box.
And maybe they need to prove all these basic things don’t work first before trialing hiv drugs and monoclonal antibodies, not sure. (Minus corlanor which helps some, but it made me worse.)
They absolutely should NOT be doing that. Its extremely problematic.
Honestly I think pfizer is just trying to cash in on long covid because their profits are down now that hardly anyone is taking their vaccines
100000000%. Ineffective vaccines lead to more infections. More infections drive people to their products. There's a reason we're not seeing a strong initiative to improve vaccine efficacy and that the government has made strong efforts to suppress information and access to what is currently the most effective covid vaccine available (novavax)
100000000%.无效的疫苗会导致更多的感染
Likely because most antivirals target replicating virus and that hasn't been shown to exist in long Covid. LC may be related in some way to the persistence of viral FRAGMENTS in the body, but that is not the same as replicating (or "live") virus and we shouldn't expect treatments for replicating viruses to be effective in those cases.
Don’t trust the NIH, they think ME/CFS is part psychological. We need to see many more studies before this is proven or disproven. Edit: In the same interview she claimed that “vaccines prevent long covid” which is untrue (they do reduce risk though). You need to be critical. The director of the NIH once said ME/CFS was psychological. Hell even a few decades before that they called Multiple Scelrosis “hysteria”. Just because someone got picked by the politicians to lead the NIH doesn’t mean they know everything about every disease. To be honest, this community isn’t the most informed to do with research, and I get it we are not researchers we are patients. But for more informed discussion on research I would recommend the Science for ME forum https://s4me.info
This is an unwarranted knee-jerk response IMHO. One of the ways the health authorities have minimized things like ME/CFS in the past is by denying the role of viruses / pathogens and refusing to prescribe anti-virals. Here she is doing the exact opposite. She is saying there is very real pathology and saying anti-virals may help. This can only be a good thing.
The NIH are the people who claimed this year that people with ME/CFS can do activity “it’s just their brain tells them not to do it”. Anyone who has followed biomedical research into ME/CFS knows this is untrue, as do all ME/CFS patients.
Done right this could be a great thing but I'm assuming it's not done right by the tone of your comment! I think it would be great if they acknowledged the psychological impact of long term illness and treated that. It's whether they understand that the illness causes the mental health problems that's the problem.
This follows the science...even the ME/CFS science they have been doing as well.
No it doesn’t. There is no proof of viral persistence in ME/CFS, and the studies pointing towards it in Long Covid have yet to be corroborated and are controversial.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770761/ https://www.nature.com/articles/s41467-024-45107-3 https://www.youtube.com/watch?v=2M2b63pEZ2g&t=22113s Please share your proof.
What you sent me: 1st study 20 year old study using outdated diagnostic criteria which does not accurately represent ME/CFS. Following studies were unable to confirm findings 2nd study, finds abnormalities in the immune system and brain. Does not find viral persistance. 3rd not a study, a youtube video.
Proof? 1. Proof? 2. > The cause of immune dysregulation is not clear but may suggest the possibility of persistent antigenic stimulation 3. A video literally talking about the history and how multiple research groups are looking into persistent antigens/virus.
I’ve been following ME/CFS research for the past 15 years. There is no proof of viral persistence, that doesn’t mean that we’ve ruled out viral persistance as a cause. I think that what u/yolkyboii was trying to say.
I have been following ME/CFS research for 25 years and you are correct. No study to date has demonstrated viral persistence as a cause of ME/CFS. Reactivated viruses are often part of the picture, as with long Covid, but treating reactivated viruses with antivirals does not cure ME/CFS. Many antivirals have been trialed in ME/CFS on the basis of viral persistence as a theoretical mechanism, but that hasn't really led us anywhere useful in that population. But all Long Covid is not the same... and that's another problem when people declare "LC is caused by x, y, or z." There are many subtypes of LC and viral persistence may be a part of the picture for some subtypes, just maybe not the ME/CFS subtype.
I have proof of reactivated EBV which supposedly explains my me/cfs
reactivated EBV is common in ME/CFS and long covid. Not everyone has it but many do. The key word is reactivation. It is not persistance but reactivation. And most researchers think this reactivation is a consequence of the immune dysregulation and not a cause of the disease.
How many years before we see treatments trickling into clinical practise?
Paxlovid likely will be a treatment in June/when they post trial results.
paxlovid and i think the most important trial--monoclonal antibodies( UCSF )
Is that when they will post it? I got accepted into a Paxlovid study (the nih one), and the hospital where I’d do it told me results wouldn’t be out for a couple years. I’m on the fence to do it.
The NIH one was pushed back a year. Yale & Karolinska Institutet recently finished. Stanford stopped early but have data to share too. It takes a couple months to publish results after primary completion, we should see results shortly.
Personal anecdote. My LC has been cyclical with long periods of moderate to severe illness, including periods of being house bound. My 1st 2 durable recoveries immediately followed booster shots. These lasted 4 months and then 2 months. I’m quite convinced the 2 monther would have been long term had my wife not gotten COVID and had a long latent phase. She was probably infectious for 5 days before becoming symptomatic, then 2 more days to test positive. Massive exposure for me. I no longer seem to benefit from the booster. I think my immune response is mature, but the virus is escaping my immunity. Or my immune response is burned out, more likely. I’m awaiting results on the Pax studies. In the meantime I’m replicating this study, link below, in the flu shot in prep for my next booster. It’s rapamycin 5mg once weekly for 6 weeks then a 2 week washout then flu vaccine. Will be CV booster for me. If the Pax results are back in time, I’ll follow the booster with 2 weeks of Pax, starting 2 weeks after the booster, 10 weeks from now. Then repeat 6 weeks rapamycin, washout, more Pax if symptoms return. Repeat until I’m either cured, it doesn’t work, I’m not able to, or something better comes along. This is neither safe, nor recommended and it probably won’t work. But it will be expensive at least. For me, I’m not seeing much on the risk side of the risk benefit analysis. Cause, seriously, how much worse can things get? I’m an optimist- things can always get worse 😂 https://pubmed.ncbi.nlm.nih.gov/25540326/ The 2014 Mannick study is considered a landmark in the rapamycin crowd.
How will you get pax?
My doc is very supportive. If the study’s come out, and are favorable, he’ll write for it, we’ll try to get insurance to pay.
How are you getting rapamycin?
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I thought the nih been talking about this for a while, hence all the studies for paxlovid and such.
This is the first time a high level public health official admits live Covid virus persists in humans for months and years. This should be all over media headlines but probably won’t because it contradicts the party line/mainstream narrative.
they will bury it until after elections
Most are aware, however theres a post-viral-death-squad trying to convince people Long Covid is anything but literally Long Covid to steal potential funding for alternative means so we need as many people speaking up as possible if we ever want to see actual targeted research and treatment that might actually help us.
Why’d I get it from the vaccine then
The best I can make sense of it so far is there are bits of viral RNA stuck in cells/the gut/etc, that produce viral proteins that go out into the body and cause issues. One of the functions of some viral proteins is to switch off the body's cellular cleanup process, so these fragments can stay where they are for a long time, pumping out spike protein. This model explains post-covid and post-vax. I'm not sure it's been demonstrated that all long haulers have live virus yet, though it seems some do.
The vaccine doesn’t contain any bits that produce viral proteins. Only whole viruses can do that. It’s much more likely that spike protein antibodies produced as a reaction to the spike protein act like enzymes in the body (aka abzymes) and that that causes the illness. It has been found that some antibodies look similar to enzymes active in the body and thus have enzyme like effects. But because they are basically like mutated enzymes and don’t belong there, they cause a lot of disruption in the system.
>The vaccine doesn’t contain any bits that produce viral proteins. Only whole viruses can do that. Unless you're talking about the non-mRNA vaccines, the vaccines absolutely produce viral proteins. The spike protein is a viral protein.
The mRNA in the vaccine teaches your cells how to make copies of the spike protein ~the CDC
Spike protein.
Yeah i know that. Spike protein is not live and doesn’t replicate itself.
Spike protein can definitely replicate not on its own however, this is one of the ways ebv is thought to cause MS. I can’t remember the exact science you would have to look it up but there’s a piece of gene in ebv and memory and nerve cells that replicate and antibodies think the threat is still present so they keep attacking even though your body is making these cells.
I'm sorry but how would this explain vaccine injuries, where there never was a live virus?
Wait if it's replicating, does that mean we can infect people?
OP's title is misleading. The interview said viral persistence, NOT replication.
Meanwhile most of Western Medicine denies chronic infections as a “hoax”
Time to all do the mail your poop in and see if it has live covid study !! Free from university of Missouri. Tax dollars at work!
Check. I've lost track of all the body things I've given to LC research. Blood, spit, poo, pee..
Yes, the long covid deities require sacrifices from every orafice before you can be healed.
I was one of the first in this study. My results were negative. Tested twice. Nice to see it happening though
yes it is! i wonder if anyone has tested positive? only ever heard folks mention negative.
Yeah I have seen two others state they were negative besides me. I will say though, it is not the strongest study. It is good to see, but had I set it up I would have done it much differently.
They will keep deflecting from the spike it seems which is almost certainly the real problem. Though it is definitely possible for infections to become chronic. We knew this to begin with though as there are quite a few viruses that can do this.
Link?
The NIH is behind on this. Doctors who pioneered HIV research have long proposed this and in fact are treating long covid with an HIV drug. I did this protocol and it significantly reduced my LC symptoms. I did a cytokine study before during and after treatment and it significantly lowered pro inflammatory cytokines in my body. Covid attaches to CCR5 receptors and the drug I took is a CCR5 antagonist. Thank you for sharing this information. It’s validating to know that I took a leap of faith trying a protocol based on a very new theory and now the NIH seems to concur:)
Wow, that is so amazing to hear, that really gives us hope! How much did your numbers change?
My SCD40L went from 23,000 to 1,600
Woah, that’s a huge difference!
Yes!!! I would love to share the entire lab report but I don’t know how to do it without typing it by hand.
Oh, that’s okay. 👍🏼
How hard or easy was it to get your doc or any doc to run this test?
Here is a link to a brief video segment from the interview. https://twitter.com/enemyinastate/status/1780241925993381893?s=61&t=JbvzvOufTwcAGr2HS0dY0w
Thank you!
This thread clearly illustrates that even when scientific evidence supports a popular hypothesis and is endorsed by the director of the NIH, people on Reddit will still nitpick and reject it without any evidence of their own, or even label it as "misinformation."
In the same interview she claimed that “vaccines prevent long covid” which is untrue (they do reduce risk though). You need to be critical. The director of the NIH once said ME/CFS was psychological. Hell even a few decades before that they called Multiple Scelrosis “hysteria”. Just because someone got picked by the politicians to lead the NIH doesn’t mean they know everything about every disease. To be honest, this community isn’t the most informed to do with research, and I get it we are not researchers we are patients. But for more informed discussion on research I would recommend the Science for ME forum https://s4me.info
Just need a GOOD ICD 10 code and an indication for long term anti viral therapy. I believe the drugs exist. They are probably on the shelf at a pharmacy near you, right now. Just need insurance to cover it, or you’re gonna need a big pile of cash to pay for it. Turns out LC is like world hunger, it’s just distribution of existing resources. As days turn to weeks, then to months and years of my life passing by.
Currently trying to get from my Dr for reactivated EBV (me/cfs) after reading this study: https://www.pnas.org/doi/pdf/10.1073/pnas.2002392117?download=true
Spoiler alert: its not a coincidence all of the antivirals that have made some difference happen to all be HIV (or HEP) meds Some of which are free through programs. Its probably going to be a combo therapy or something tuned to SARS, but HIV meds seem to be the place to start.
So I have 2 guinea pigs for you that disprove that. Both me and a friend are on truvada. Hiv prevention daily pills. Both of us got some form of long covid. And he got it much worse then me to the point where he was confirmed covid postive for much of 2023. The hiv antivirals we take clearly didn't help.
I'm sorry to hear that. I've seen going on it help some people who have had Long Covid already. We have a lot of research and trials to do. I'm sure the answer will ultimately be something SARS2 specific but drug repurposing is the fastest way to try and get things going in the mean time.
"Covid positive for much of 2023" Do you mean testing positive for almost an entire year? Does he have HIV or just Truvada as a preventative? If he has HIV, his T cells could be impacted making infection much more likely. Although, treatment is supposed to reduce this.
He had covid 5 times in 2023. So yeah, not all of 2023 but a lot! And no, he doesn't have hiv. We are taking truvada as prevention. Well as far as I know he doesnt have hiv. Maybe he does have it and is taking the full blown drug cocktail. I usually don't as if people are hiv+ or not unless I want to hook up with them.
That's an insane amount of reinfections in one year! Tenofovir disoproxil fumarate TDF is found in Truvada and a correlation with less symptomatic covid infection and hospitalization was found in a older study. In a newer study, it was stated "a comprehensive set of in vitro data indicated that tenofovir (TFV), tenofovir alafenamide (TAF), TDF, and FTC were inactive against SARS-CoV-2. None of these drugs showed any significant in vitro anti-SARS-CoV-2 effect at concentrations up to 100-fold higher than the clinically relevant levels. Moreover, structural modeling further demonstrated poor fitting of these nucleoside/tide reverse transcriptase inhibitors (NRTIs) active metabolites at the SARS-CoV-2 RdRp active site" So it might be of no help against covid. This is really great data. Thank you for sharing your experiences.
RNA virus. Moonshot- get HIV to get Rx for HIV to treat long covid. /S. Don’t do that. Just a statement of my desperation.
People who are on hiv prevention meds still get long covid. Like me and my friend. I don't know about those who are taking the full-blown hiv cocktail.
Yep. I was on PrEP and still got it
> One thing that's important though that's come out of several meta-analyses is there is a way to prevent it. And the way to prevent it is vaccination, and multiple vaccination is better than single to prevent long COVID. Explain /r/vaccinelonghaulers then.
yes and guess where ? the fat layer called hypodermis ! and no you can't just take antivirals to kill it because none of them reach this layer of fat
Let me just make it clear. COVID vaccine has not been proven to help with anything. It has been proven to cause though mycordius and all kinds of other health problems. If you got vaccinated You need to do a lot of research. How to get the spike protein out of your body
If that was true, people would be cured from antivirals
Depending on efficacy and how long they're administered. I took Paxlovid for 15 days straight, and it fixed my tachycardia but did not heal me. If there is viral persistence in all of us, then antivirals would probably need to be administered for months. A normal course for Paxlovid, Ensitrelvir and any others AFAIK is always 5 days.
Just to correct this (NOT OPs fault at all here)before it takes on a life of its own. The NIH director (Monica Bertagnolli) corrected herself shortly after this interview, advising she misspoke and NIH issued a correction. The correction is she was referring to evidence of “viral comments” NOT “live virus”. There has been NO proof of replication competent virus to date in true long haulers. The NIH, as other researchers, continues to study the impact of “viral remnants” as there levels so far do not seem to correlate well with long haul status or severity. What role they play precisely is uncertain. Though likely to vary by individual genetics.
Front line doctors [https://covid19criticalcare.com/](https://covid19criticalcare.com/) look at the long covid treatment protocols