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Reply to "New Covid study from UK shows brain damage - what do you make of this?"
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[quote=Anonymous][quote=Anonymous][quote=Anonymous][quote=Anonymous][quote=Anonymous][quote=Anonymous][quote=Anonymous][quote=Anonymous]Neuroscientist here. So far I’ve only read the abstract. I’ll have to look for the full text version on a computer in the next few days. Does anyone who has read the full test know whether the participants in this study all experienced hyposmia or anosmia as a result of infection? Like was that a criterion for inclusion in the study? All of the brain areas the researchers looked at are part of the central olfactory pathways. Based on what we know so far omicron does not seem to cause hyposmia or anosmia at the same rate as previous variants. I am not convinced that results from studies using participants infected with earlier variants can be generalized to omicron which may not invade organ systems to the same extent. My whole family just had Covid and none of us (5 people) experiences more than very temporary hyposmia due to congestion , and certainly none of us experienced anosmia which is very distinct (total absence of smell). I think this is typical for many people who have been infected very recently or will be infected soon. I’m not sure we need to panic as these effects on the brain may be unique to those who experienced olfactory symptoms when infected with Covid. In general I am not sure anyone can realistically avoid negative neuropsychological effects from this pandemic whether infected or not. Social isolation and loneliness have very real detrimental effects on the brain and on cognition. Perhaps even more so during critical developmental periods. Never mind the stress that is caused by constant uncertainty. None of us are going to come out of this scot free in terms of neurobiological and epigenetic markers. Even if you think you are handling it all just fine — your brain and body know better. We don’t live in a risk free world. We all bear the marks of living on this planet and have to weigh the costs and benefits of different decisions that can be made at this time. I am not advocating for a “who cares” approach to Covid, by any means. But the reality is that this is going to affect all of us negatively in some way and that different people may make different decisions in light of the evidence. I am not convinced that the potential effects Covid has had on my brain or my children’s brains is necessarily worse than the effects of being out of school and away from peers, not participating in activities, etc for two years. Being a human being on planet Earth involves risk. We cannot run and hide from all of it. All we can do is mitigate it the best we can and not beat ourselves up if bad things happen anyway. [/quote] Mother of the Long COVID patient. My DC had mild illness without any loss of taste or smell, and yet, DC has real significant cognitive struggles. You are grasping at straws if you think that not having loss of senses protects you from Long COVID outcomes. There are many, many studies that have come out detailing the myriad of ways the body invades different body tissues and that the virus stays in the body for months even in patients who have mild infection. Like other viruses before it (flu, zika, ebola, HIV, HPV, Herpes), COVID is likely to have long term effects in at least some portion of the population and because of the millions of infected people, even if only 1% or 10% have long term issues, that’s still a ton of people. [/quote] It’s not grasping at straws to posit that previous variants that were more likely to produce olfactory symptoms may be more likely to affect olfactory related brain areas. It also stands to reason that people who get Covid after being vaccinated will not experience the same invasion of multiple organ systems. A lot of the data being published right now is from before vaccines were widely available. We should be concerned but not panicked, based on available evidence. Speaking of evidence, please point me to the studies showing that the virus stays in multiple organs of people who had a mild illness. The only studies. I have seen on that used patients who died from Covid. You can’t look at viral mRNA or RNA on tissues of people who are still alive. [/quote] The study that showed the persistence in the organs did include people that had mild cases. They died of something else and were autopsied. What was noticeably lacking was signs of inflammation despite signs of Covid, so many question if it will be lying dormant for years and possibly reactivated. Or not. I wish they had checked for Lewy bodies on those patients. [/quote] You should catch up on your reading, neuroscientist…. “ We show that SARS-CoV-2 is widely distributed, even among patients who died with asymptomatic to mild COVID-19, and that virus replication is present in multiple pulmonary and extrapulmonary tissues early in infection. Further, we detected persistent SARS-CoV-2 RNA in multiple anatomic sites, including regions throughout the brain, for up to 230 days following symptom onset. Despite extensive distribution of SARS-CoV-2 in the body, we observed a paucity of inflammation or direct viral cytopathology outside of the lungs. Our data prove that SARS-CoV-2 causes systemic infection and can persist in the body for months.” more: “ We show SARS-CoV-2 disseminates across the human body and brain early in infection 268 at high levels, and provide evidence of virus replication at multiple extrapulmonary sites during 269 the first week following symptom onset. We detected sgRNA in at least one tissue in over half of 270 cases (14/27) beyond D14, suggesting that prolonged viral replication may occur in extra- 271 pulmonary tissues as late as D99.” and “ Finally, a major contribution of our work is a greater understanding of the duration and 330 locations at which SARS-CoV-2 can persist. While the respiratory tract was the most common 331 location in which SARS-CoV-2 RNA tends to linger, ≥50% of late cases also had persistence in 332 the myocardium, thoracic cavity lymph nodes, tongue, peripheral nerves, ocular tissue, and in all 333 sampled areas of the brain, except the dura mater. Interestingly, despite having much lower 334 levels of SARS-CoV-2 in early cases compared to respiratory tissues, we found similar levels 335 between pulmonary and the extrapulmonary tissue categories in late cases. This less efficient 336 viral clearance in extrapulmonary tissues is perhaps related to a less robust innate and adaptive 337 immune response outside the respiratory tract. 338 We detected sgRNA in tissue of over 60% of the cohort. While less definitive than viral 339 culture23,24, multiple studies have shown that sgRNA levels correlate with acute infection and can 340 be detected in respiratory samples of immunocompromised patients experiencing prolonged 341 infection24. These data coupled with ISH suggest that SARS-CoV-2 can replicate within tissue 342 for over 3 months after infection in some individuals, with RNA failing to clear from multiple 343 compartments for up to D230. This persistence of viral RNA and sgRNA may represent infection 344 with defective virus, which has been described in persistent infection with measles virus – 345 another single-strand enveloped RNA virus—in cases of subacute sclerosing panencephalitis25. 346 The mechanisms contributing to PASC are still being investigated; however, ongoing 347 systemic and local inflammatory responses have been proposed to play a role5. Our data provide 348 evidence for delayed viral clearance, but do not support significant inflammation outside of the 349 respiratory tract even among patients who died months after symptom onset. Understanding the 350 mechanisms by which SARS-CoV-2 persists and the cellular and subcellular host responses to 351 viral persistence promises to improve the understanding and clinical management of PASC.” Cite: SARS-CoV-2 infection and persistence throughout the human body and brain DanielChertow (chertowd@cc.nih.gov). 12/20/21 https://assets.researchsquare.com/files/rs-1139035/v1_covered.pdf?c=1640020576 [/quote] Funny how you chose not to copy the info about the patient cohort. Most of the cases were from before vaccines were available and all of them were hospitalized and died of Covid. Extended Data Table 2 shows that the vast majority needed to be intubated. But go ahead and explain how this can be generalized to healthy, vaccinated adults with mild Covid. You can read all the studies you want but it won’t be worth much if you can’t properly interpret the findings. [/quote] PP is directly quoting the studies though - not interpreting them. Agree that most of the patients were very sick, but it's not the PP who wrote the part about mild and asymptomatic. It's directly from the abstract, so your beef is directly with NIH. [/quote] Again, quoting from the study, “ Our results collectively show while that the highest burden of SARS-CoV-2 is in the 313 airways and lung, [b]the virus can disseminate early during infection and infect cells throughout the 314 entire body, including widely throughout the brain[/b]. While others have posited this viral 315 dissemination occurs through cell trafficking11 due to a reported failure to culture virus from 316 blood3,22,[b] our data support an early viremic phase, which seeds the virus throughout the body 317 following pulmonary infection[b]. Recent work by Jacobs et al.22 in which SARS-CoV-2 virions 318 were pelleted and imaged from COVID-19 patient plasma, supports this mechanism of viral 319 dissemination. [/b]Although our cohort is primarily made up of severe cases of COVID-19, two 320 early cases had mild respiratory symptoms (P28; fatal pulmonary embolism occurred at home) or 321 no symptoms (P36; diagnosed upon hospitalization for ultimately fatal complications of a 322 comorbidity), yet still had SARS-CoV-2 RNA widely detected across the body, including brain, 323 with detection of sgRNA in multiple compartments. Our findings, therefore, suggest viremia 324 leading to body-wide dissemination, including across the blood-brain barrier, and viral 325 replication can occur early in COVID-19, even in asymptomatic or mild cases.[b] Further, [/b]P36 was 326 a juvenile with no evidence of multisystem inflammatory syndrome in children, suggesting 327 infected children without severe COVID-19 can also experience systemic infection with SARS- 328 CoV-2.[b] It is true that vaccinated individuals do not appear to be a part of this study; however, given the findings in mild, asymptomatic and juvenile patients, I think it’s wishful thinking to believe that vaccination and mild illness protects a patient fully from the early viremic seeding phase theorized in this paper. Do we know? No. Is vaccination at least partially protective? Probably. But this dissemination appears to happen in Wk1 even in those with mild illness, so I wouldn’t be surprised if we found out it is happening in vaccinated patients who have symptoms and test positive but recover in a week and never need medical care. [/quote]
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