I keep seeing people say, "this is the sickest I've ever been, it's so much worse than COVID."

“If the cells are frequently turning over and they are still detecting viral persistence, what other plausible explanations are there for this other than replication?” That's a very good question, and it's one of the central puzzles in the field of viral persistence. Let’s see why: If a tissue contains cells that turn over relatively quickly (intestinal epithelium, immune cells, etc.), and viral RNA or proteins are still being detected months or years after an infection, then ongoing replication is the most intuitive explanation, but it is not the only one. Other reasonable options are: 1. Persistence in long-lived reservoir cells. The tissue as a whole may turn over, but a subset of cells may not. We know this happens for neurons, some endothelial cells, tissue macrophages, lymphocytes, and others. In this case, the virus isn't replicating continuously, but instead, a long-lived infected cell survives for months or years and continues to produce low levels of viral RNA or protein. This is essentially how the HIV reservoir works, for example. 2. Defective viral genomes. A cell can also contain incomplete viral genomes incapable of producing infectious viruses, so the genome may still produce RNA transcripts and some proteins. While this stimulates innate immunity (so enough to cause symptoms and pathology), it doesn’t generate new infectious virions. 3. Protein persistence without viral persistence. The virus itself may be gone but you can have lingering viral remnants like spike protein and nucleocapsid fragments that can persist inside phagocytic cells or in extracellular compartments. In this case, what is being detected is essentially debris rather than an active infection, but their presence is enough to induce immunological responses (and again, enough to produce symptoms/pathology). 4. Continuous release from another hidden reservoir. The tissue where detection occurs may not be the reservoir. Hidden reservoir can include gut, bone marrow and lymphoid tissue, while the released is being detected in blood or peripheral immune cells. In this model, the virus replicates (or persists) in one location, while viral products continually seed other compartments. 5. Cell-to-cell transfer without productive infection. Macrophages and other immune cells can acquire viral material from neighboring cells. These cells may test positive for viral RNA or viral proteins like spike, despite never being truly infected. So a positive signal does not necessarily mean productive viral replication. From a scientific perspective, the most reasonable model may actually be a combination of different situations, like a small reservoir that exists in a long-lived cell, which can induce low-level or intermittent replication. This can induce viral proteins and RNA to be continuously released. These products can then be captured by immune cells and distributed through the body. That model can explain why viral material remains detectable despite turnover, and why it is so hard for scientists to recover large amounts of infectious virus years later. One of the key unresolved question is whether the reservoir is producing new virus, or merely old viral products that are being recycled and retained. That's one of the areas where the field is still struggling to obtain definitive evidence. #LongCovid #MECFS

If the cells are frequently turning over and they are still detecting viral persistence, what other plausible explanations are there for this other than replication? (genuinely curious, have been wondering about this for a while)

Dr. Tim Henrich presented new findings surrounding long term persistence of SARS-CoV-2 proteins & RNA in Long COVID gut tissue at PolyBio’s recent Spring symposium. “We actually see [gut viral persistence] in both areas, the epithelium—which turns over every several days to week—to the lamina propria where you have long-lived myeloid immune cells… suggesting there may even be replication in some individuals,” said Henrich. Using a highly sensitive method of detecting viral RNA, “around 20-25% of the time, we see detection… all the way up until 3-4 years after initial infection” in Long COVID patients.

This thread from Alan is really embarrassing. I hope he keeps posting and further disgracing @WIRED for platforming him on a subject where he's so profoundly out of his depth.

Long COVID is an existential threat to all of the psychiatrists who have loudly attached themselves to pseudoscientific explanations for the illness. I've been saving quotes and have some funny (horrifying) ones, that I think are important to preserve for historical accuracy.

This article is behind a paywall, but even if it wasn't, the average person will not slog through it like I did. There is a very limited audience for this and while it's offensive, it's not worth getting annoyed at this low quality article.

I think 2026 is the year that sustaining denial becomes so absurd, that it tips into actually being funny when people say things like this…

Some of the conversations about #longcovid (LC) are delusional, frankly wrong and will actively harm people. Learn to think through the groups of possibilities first after loosely defining #longcovid as the sequeala of the acute infection (perceived as a respiratory infection with some extra stuff by most). For example, in the absence of concrete evidence to the contrary (no such evidence exists), LC includes phenotypes of 1) irreversible damage (think myocardial infarction/stroke both in the covid and in the non covid settings), 2) potentially reversible (think autoimmunity/inflammation/vascular involvement after the virus has left the body) and 3) reversible damage (vital persistence leading to inflammation as a localized continuation of the acute infection, think of a urinary tract infection). Therapies against: 🛑irreversible damage can never exist unless longevity/regenerative medicine research delivers in some unidentified time point after 2050, 💔potentially reversible autoimmune damage may exist but will probably require lifelong therapy unless CRISPR/CAR-T/CAR-NK deliver 🥳potentially reversible may exist, but will require prolonged and complex regimens that potentially vary according to local sites affected. Since no therapies have clearly been identified for any of the three and research has not even started for the feasible (2 and 3) categories, one is left with *prevention of infection* as the only mechanism to reduce the prevalence of #LongCovid after repeated infections at the societal level and time to heal (perhaps) the 💩 sequelae at the individual, hoping that the time to recovery will not be long enough to a) lose many productive years of one's life and b) potentially reversible damage to evolve to irreversible one (think of polyarteritis nodosa in chronic hepatitis B, cryoglobulinemic vasculitis and membranoproliferative glomerulonephritis in hepatitis C and liver cancer in both hepatitis B and C). If you are fine with hoping that you don't need to practice prevention against covid because therapies against #longcovid are just around the corner (this is the DELUSION), be my guest; after all #UDoU. But please don't peddle your copium to the gullible.

If you are able to, please help, I would really appreciate it.

People who tested positive for #COVID have a higher risk of being diagnosed with other infections in the following months. This has been shown for years and hundreds of publications in the topic. Covid has an impact on the immune system we still don't fully understand.

Symptomatic Long COVID is the tip of the iceberg. If you want to see below the surface, all you need to do is start reading studies. It's always been an everyone problem, even though everyone isn't ready to accept it.

For 6 years, I've been wondering what Mike Ryan frantically scribbled to Tedros and I think it might have been this.

Juste pour rappel, et pour énerver les rassuristes (running gag 😅) : si 28% des morts (recensés) de la covid auraient pu vivre encore >=5 ans s'ils n'avaient pas été infectés, cela veut dire qu'il y a bien actuellement un "effet moisson" dans la mortalité observée 🤷‍♂️ #maths