The biology of coronavirus COVID-19 - including research and treatments

Somebody sent me this. I haven't read it, but I see it has 10,000 claps in one day so seems to be popular.
Link seems to be broken.

ETA: For some reason I needed to clear cookies for the site to work.
 
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New coronavirus losing potency, top Italian doctor says

“The swabs that were performed over the last 10 days showed a viral load in quantitative terms that was absolutely infinitesimal compared to the ones carried out a month or two months ago,” he told RAI television.

I would be wary of a top Italian doctor who says:
“We’ve got to get back to being a normal country,” he said. “Someone has to take responsibility for terrorizing the country.”

This guy has an axe to grind. Lower viral loads seems to me unlikely to mean much other than that people are being tested earlier in their illness.
 
yes, I also noticed that quote. This guy seems to think the government did the terrorizing, not the virus.
Not too sure when you look at that quote (unless he was quoted out of context) ...
Zangrillo said some experts were too alarmist about the prospect of a second wave of infections and politicians needed to take into account the new reality.

“We’ve got to get back to being a normal country,” he said. “Someone has to take responsibility for terrorizing the country.”
To me he seems to be saying that those warning of the severe consequences of Covid 19, were terrorizing people unnecessarily.

ETA: I realise that may be what you meant though @dave30th.
 
I doubt it.

There is also another study claiming that coronavirus immunity is not maintained. https://www.medrxiv.org/content/10.1101/2020.05.11.20086439v1

The serological findings suggest that where there is significant genetic variation of the antigenic proteins, immunity is not maintained (just like Influenza).
Their conclusion about short-lived immunity is also wrong because they don't seem to understand how the immune system works. The plasma cell/antibody kinetics they observed is typical of all short lived infections and vaccinations. Immune memory is based on memory T-cells and B-cells, not plasma cell kinetics, but I guess PhDs of virology and professors of epidemiology don't learn that anymore. :confused:

This paper is the one that talks about the immune response being there in uneffected people - I think because they are saying that there is some recognition of the spike proteins in some people from other infections. That is a different issue as to whether antibodies formed for SARS-CoV2 will maintain immunity as that would potentially be a different group of patients

https://www.cell.com/cell/fulltext/S0092-8674(20)30610-3#.XtUNRAVlzFA.twitter

Understanding adaptive immunity to SARS-CoV-2 is important for vaccine development, interpreting coronavirus disease 2019 (COVID-19) pathogenesis, and calibration of pandemic control measures. Using HLA class I and II predicted peptide “megapools,” circulating SARS-CoV-2-specific CD8+ and CD4+ T cells were identified in ∼70% and 100% of COVID-19 convalescent patients, respectively. CD4+ T cell responses to spike, the main target of most vaccine efforts, were robust and correlated with the magnitude of the anti-SARS-CoV-2 IgG and IgA titers. The M, spike, and N proteins each accounted for 11%–27% of the total CD4+ response, with additional responses commonly targeting nsp3, nsp4, ORF3a, and ORF8, among others. For CD8+ T cells, spike and M were recognized, with at least eight SARS-CoV-2 ORFs targeted. Importantly, we detected SARS-CoV-2-reactive CD4+ T cells in ∼40%–60% of unexposed individuals, suggesting cross-reactive T cell recognition between circulating “common cold” coronaviruses and SARS-CoV-2.
 
Preliminary findings concerning a potential treatment for T cell depletion in acute COVID-19.

Thymosin alpha 1 (Tα1) reduces the mortality of severe COVID-19 by restoration of lymphocytopenia and reversion of exhausted T cells.

Tα1 treatment significantly reduces mortality of severe COVID-19 patients (11.11% vs. 30.00%, p=0.044). Tα1 timely enhances blood T cell numbers in COVID-19 patients with severe lymphocytopenia (the counts of CD8+ T cells or CD4+ T cells in circulation lower than 400/μL or 650/μL, respectively).

Liu, Yue-Ping & Pang, Yue & Hu, Zhenhong & Wu, Ming & Wang, Chenhui & Feng, Zeqing & Mao, Congzheng & Tan, Yingjun & Liu, Ying & Chen, Li & Li, Min & Wang, Gang & Yuan, Zilin & Diao, Bo & Wu, Yuzhang & Chen, Yongwen. (2020).

Thymosin alpha 1 (Tα1) reduces the mortality of severe COVID-19 by restoration of lymphocytopenia and reversion of exhausted T cells. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 10.1093/cid/ciaa630. Background:
We previously reported that lymphocytopenia and T cell exhaustion is notable in acute COVID19 patients, especially in aged and severe cases. Thymosin alpha 1 (Tα1) had been used in the treatment of viral infections as an immune response modifier for many years. However, clinical benefits and mechanism of Tα1 supplement to COVID-19 are still unclear.

Methods:
We retrospectively reviewed the clinical outcomes of 76 severe cases with COVID-19 admitted into two hospitals in Wuhan from December 2019 to March 2020. The thymus output in peripheral blood mononuclear cells (PBMCs) from COVID-19 patients was measured by T cell receptor excision circles (TREC). The levels of T cell exhaustion markers PD-1 and Tim-3 on CD8+ T cells were detected by flow cytometry.

Results:
Compared with untreated group, Tα1 treatment significantly reduces mortality of severe COVID-19 patients (11.11% vs. 30.00%, p=0.044). Tα1 timely enhances blood T cell numbers in COVID-19 patients with severe lymphocytopenia (the counts of CD8+ T cells or CD4+ T cells in circulation lower than 400/μL or 650/μL, respectively). Under such conditions, Tα1 also successfully restores CD8+ and CD4+ T cell numbers in aged patients. Meanwhile, Tα1 reduces PD-1 and Tim-3 expression on CD8+ T cells from severe COVID-19 patients in comparison with untreated cases. It is of note that restoration of lymphocytopenia and acute exhaustion of T cells are roughly parallel to the rise of TRECs.

Conclusions:
Tα1 supplement significantly reduce mortality of severe COVID-19 patients. COVID-19 patients with the counts of CD8+ T cells or CD4+ T cells in circulation lower than 400/μL or 650/μL, respectively, gain more benefits from Tα1. Tα1 reverses T cell exhaustion and recovers immune reconstitution through promoting thymus output during SARS-CoV-2 infection.



PDF of the entire paper is available from here.
https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciaa630/5842185
 
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This paper is the one that talks about the immune response being there in uneffected people - I think because they are saying that there is some recognition of the spike proteins in some people from other infections. That is a different issue as to whether antibodies formed for SARS-CoV2 will maintain immunity as that would potentially be a different group of patients

https://www.cell.com/cell/fulltext/S0092-8674(20)30610-3#.XtUNRAVlzFA.twitter

CD4+ T-cells are supposed to have some degree of cross reactivity with the viral proteins, even without prior exposure, otherwise the adaptive immune system would never work correctly!

https://en.wikipedia.org/wiki/Naive_T_cell

But on the point I was making, the claim that there could be residual immunity due to prior exposure to other coronaviruses contradicts the claim that adaptive immune responses to (those other) coronaviruses are not long lived, as suggested by the authors in the paper I linked.
 
Somebody sent me this. I haven't read it, but I see it has 10,000 claps in one day so seems to be popular.
Just want to say that I may have had Covid toe. I treated it like gout, assuming that it was (haven't had it before) but it lasted longer than gout normally does. It lasted from early February to early March, and was painful enough to require paracetamol at first, and needed a dressing, which I had to change daily, and which was very difficult due to the skin sticking to the bandage. It was on the toe next to the big toe. Very relieved when it went!

Just want to add an 's' in case others have the problem I have in not being able to find words less than 4 letters long: toes.
 
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From Medscape: "For Experts Who Study Coronaviruses, a Grim Vindication"

The now prophetic words could be found buried at the end of a research paper published in the journal Clinical Microbiology Reviews in October of 2007: "The presence of a large reservoir of SARS-CoV-like viruses in horseshoe bats, together with the culture of eating exotic animals in southern China, is a time bomb."

The warning — made nearly 13 years ago and more than four years after a worrying first wave of severe acute respiratory syndrome, or SARS, killed nearly 800 people globally — was among the earliest to predict the emergence of something like SARS-CoV-2, the virus behind the current pandemic of Covid-19.

Many other warnings would follow.

Indeed, evidence of a looming and more deadly coronavirus pandemic had been building for years, but experts who specialize in coronaviruses — a large family of pathogens found especially in birds and mammals that can cross over from other mammals to humans and cause varying degrees of illness — struggled to convince a broader audience of the risk. Dogged by skepticism and inconsistent funding, these coronavirus researchers say they were stymied from developing treatments and vaccines for SARS — many of which could have been helpful in the current crisis. Much about what we learned about SARS would have applied now, according to Michael Buchmeier, a virologist at the University of California, Irvine. "The viruses are so similar."
 
(Pre-print)

The hypothalamus as a hub for putative SARS-CoV-2 brain infection
Most patients with COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), display neurological symptoms, and respiratory failure in certain cases could be of extra-pulmonary origin. With reports detecting SARS-CoV-2 in some post-mortem patient brains, the routes, targets and consequences of brain infection merit investigation. Hypothalamic neural circuits play key roles in sex differences, diabetes, hypertension, obesity and aging, all risk factors for severe COVID-19, besides being connected to brainstem cardiorespiratory centers. Here, human brain gene-expression analyses reveal that the hypothalamus and associated regions express angiotensin-converting enzyme 2 and transmembrane proteinase, serine 2, which mediate SARS-CoV-2 cellular entry, in correlation with several genes or pathways involved in physiological functions or viral pathogenesis. Immunolabeling in human and animal brains suggests that the hypothalamus could be central to SARS-CoV-2 brain invasion through multiple routes, and that sex hormones and metabolic diseases influence brain susceptibility.
https://www.biorxiv.org/content/10.1101/2020.06.08.139329v1
 
Is this the right thread to talk about trends, whether up or down, in the number of cases? If not, please move this. Thanks!

Some websites that report confirmed coronavirus cases also show a 7 day rolling average. Some show a 14 day rolling average.

I know the general reason for using a longer period of time to look for trends. A large single day increase/decrease might not have much significance. Maybe there were just more tests done that day, etc.

But I don't understand the pros and cons of using 7 days vs. 14 days. Is one better than the other?

Any thoughts?
 
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