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

COVID-19 immunology briefing note: What we know about long-term health consequences and priorities for research

https://www.immunology.org/news/covid-19-immunology-briefing-note-long-term-health-consequences

Direct link to briefing note, https://www.immunology.org/sites/default/files/BSI_Briefing_Note_August_2020_FINAL.pdf

 

I think it is possible to misinterpret what they are saying. Unless people are physically being turned away or never getting results, there are no functional capacity limits.

Note that in the link you provided, they state the local "capacity limit" was 48,000, which was lower than the number of tests over any of the time intervals. They point out that the "shortage" leads to delays, rather than an absence of test results.

 

Not sure if that has been discussed before

Virucidal Efficacy of Different Oral Rinses Against Severe Acute Respiratory Syndrome Coronavirus 2

"Several formulations with significant SARS-CoV-2 inactivating properties in vitro support the idea that oral rinsing might reduce the viral load of saliva and could thus lower the transmission of SARS-CoV-2."

From what I understand like with masks it's something to protect others, not myself.

 

The FDA approves a saliva-based test for Covid-19:

http://www.msn.com/en-gb/news/polit...as-major-game-changer/ar-BB180mvF?ocid=ASUDHP

 

Updates in thinking about immunity to Covid-19:

http://www.msn.com/en-gb/news/polit...-questions/ar-BB181VDK?li=AAnZ9Ug&ocid=ASUDHP

 

While I'm still hearing people talk vaguely about "strengthening the immune system" or "damping down overactive immune response", the picture that is emerging is much more complex. We have previously learned that this coronavirus, and probably others, manages to make the RNA it places in cells look like the cell's own mRNA, operating under a false flag as it were. The term RNA cap turns up in searches. More complexity seems likely.

Here's a financial press report on new work at Hong Kong University. The paper which triggered the interview was published in Immunity. This suggests that severe cases involve broad suppression of different types of immune cells: T-cells, dendritic cells, NK cells and monocytes. This is much more extensive than previous research has documented. In addition it affects both CD8+ "killer" T-cells and CD4+ "helper" T-cells.

The financial implications were that it may be more difficult to develop effective vaccines than commonly assumed, and harder to pick the eventual winner. This also means we need treatment options available before vaccines are effective and widely available.

This sounds a lot more like the mysterious immune disturbances seen in ME/CFS patients, though perhaps worse than most experience. We have virtually no studies of the acute infection which precipitates many ME/CFS cases, so I can't compare SARS-CoV 2 with these. None of us expected sequelae to last years when we first became ill, and many modern tests of immune function simply did not exist, for example during the Royal Free Hospital outbreak of 1955.

Sheer speculation on my part: I've long thought we were dealing with a "two-hit" pathogen. I was exposed to the "Punta Gorda Flu" in 1956, but was only mildly affected. In 1957 I had "the worst flu of my life" when the Asian flu hit. My father, who had survived the 1918 flu soon after he was born, was immune. There was some cross-immunity between H1N1 and H2N2. (I believe there was some H1N1 circulating prior to H2N2, but that epidemic was much smaller.) A disregulated immune system hit with a powerful ordinary pathogen could explain the wide range of severity patients experienced.

A personal note: the "Asian flu" was a prequel to our current pandemic. Despite being very ill, I never saw a doctor. Hospitals were overwhelmed. Prescriptions were made by telephone. Immunity came from surviving infection. There was little protective equipment. Most treatment was symptom-based and supportive. I don't believe there were any effective antivirals. The pandemic eventually burned itself out. There were 116,000 deaths in the U.S., which had a smaller population then (172 million), and 1.1 million deaths in the world. That last is probably an undercount.

 

Pre-print - Patient outcomes after hospitalisation with COVID-19 and implications for follow-up; results from a prospective UK cohort.

https://www.medrxiv.org/content/10.1101/2020.08.12.20173526v1

 

'Patients with COVID19 remain highly symptomatic at 12 weeks, however, clinical abnormalities requiring action are infrequent, especially in those without a supplementary oxygen requirement during their acute illness. This has significant implications for physicians assessing patients with persistent symptoms, suggesting that a more holistic approach focussing on rehabilitation and general wellbeing is paramount.'

So no logic again, then. Abnormalities requiring action were infrequent so they should all get rehabilitation.
With the clear implication that this is for 'holistic' reasons, i.e. touchy feely all makey-better drivel suitable for people with nothing wrong.

 

Hmm and what about the ones who didn't go to hospital - a lot of the " longhaulers" appear to those who did not go to hospital at all

 

Some discussion from one of the authors:

https://twitter.com/user/status/1294979418356670464

 

Why should effective strategy be an alternative to testing? Again no logic.
We may want strategies but that does not mean shunting people off to unproven 'rehab'.

 

We've entered a time warp. It's 1990 all over again.

 

I believe the late Douglas Adams covered this response with his invention of the "Somebody Else's Problem" cloaking field.

 

What is actually needed is research to understand what is going wrong so that it can be treated.

This pandemic has shown hat research can be done very rapidly when there is the will. So do the same for long covid and ME/CFS and stop wasting time trying to manage what you don't understand (or understand less well than the people who have it).

 

Not yet. But the serological tests have around a 90% sensitivity several months down the track. This can be due to, but isn't necessarily due to a lack of antibodies, but a failure of the assay to detect all types of antibodies to the pathogen.

When you have thousands of people with an illness, even 10% of those adds up.

 

Could people with lingering symptoms be having those symptoms because the virus is still there but is eluding the immune system so it thinks the bug is gone?

 

No. Regardless of whether the immune system thinks the bug is gone or not, there will still be IgG floating around (in circulation) due to the prior infection.

 

IgG doesn’t last forever, so surely after it has broken down there will be no more made if the infection is somehow hidden from the immune system. I guess its durability is the question here.

 

Even if the hypothetically becomes totally hidden, there are memory B cells that divide over time and mature into antibody secreting plasma-cells, this is how immunity is maintained for years post-infection.

Any infection initially serious enough to lead to noticeable symptoms will lead to such immunological memory.