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
The British Society for Immunology has published a new expert briefing note which rapidly reviews current research on the long-term immunological health consequences of COVID-19 and sets out the key recommendations for future research.

This briefing note has been produced by our Immunology and COVID-19 taskforce, an expert advisory group that aims to identify the immunology research priorities to guide future studies and treatments and inform public health measures to control the Coronavirus spread.
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
 
While the situation is better than it was in March, my understanding is that testing capacity remains a problem throughout much of the United States, especially in states mentioned by @anciendaze .

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.
 
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.
Background: COVID19 causes a wide spectrum of disease. However, the incidence and severity of sequelae after the acute infection is uncertain. Data measuring the longer-term impact of COVID19 on symptoms, radiology and pulmonary function are urgently needed to inform patients and plan follow up services.

Methods: Consecutive patients hospitalised with COVID19 were prospectively recruited to an observational cohort with outcomes recorded at 28 days. All were invited to a systematic follow up at 12 weeks, including chest radiograph, spirometry, exercise test, blood tests, and health-related quality of life (HRQoL) questionnaires.

Findings: Between 30th March and 3rd June 2020, 163 patients with COVID19 were recruited. Median hospital length of stay was 5 days (IQR 2 to 8) and 30 patients required ITU or NIV, 19 patients died. At 12 weeks post admission, 134 were available for follow up and 110 attended. Most (74%) had persistent symptoms (notably breathlessness and excessive fatigue) with reduced HRQoL. Only patients with disease sufficiently severe to warrant oxygen therapy in hospital had abnormal radiology, clinical examination or spirometry at follow up. Thirteen (12%) patients had an abnormal chest X-ray with improvement in all but 2 from admission. Eleven (10%) had restrictive spirometry. Blood test abnormalities had returned to baseline in the majority (104/110).

Interpretation: 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.
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.
 
'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.

I believe the late Douglas Adams covered this response with his invention of the "Somebody Else's Problem" cloaking field.
 
Several studies have found that most COVID-19 patients produce antibodies that recognize the new coronavirus, and that these molecules endure for months. Their presence should confirm whether a long-hauler was indeed infected. But there’s a catch: Most existing antibody studies focused on either hospitalized patients or those with mild symptoms and swift recoveries. By contrast, Putrino told me that in his survey of 1,400 long-haulers, two-thirds of those who have had antibody tests got negative results, even though their symptoms were consistent with COVID-19. Nichols, for example, tested negative for antibodies after twice testing positive for the coronavirus itself. “Just because you’re negative for antibodies doesn’t mean you didn’t have COVID-19,” Putrino said.

This is from a good article by Ed Yong that Slysaint posted on the Possibility of ME or PVFS after Covid-19 thread
https://www.theatlantic.com/health/...9-recognition-support-groups-symptoms/615382/

What do we know about the antibody test? How reliable is it? Is there any evidence that it's less reliable in people with lingering symptoms?
 
QoL and symptom burden are massive (#LongCovid ). We need effective strategies to manage these impacts of COVID-19 - on people - perhaps rather than performing lots of testing on patients who have had mild COVID-19.

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).
 
Last edited:
Is there any evidence that it's less reliable in people with lingering symptoms?

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.
 
By contrast, Putrino told me that in his survey of 1,400 long-haulers, two-thirds of those who have had antibody tests got negative results, even though their symptoms were consistent with COVID-19. Nichols, for example, tested negative for antibodies after twice testing positive for the coronavirus itself. “Just because you’re negative for antibodies doesn’t mean you didn’t have COVID-19,” Putrino said.

What do we know about the antibody test? How reliable is it? Is there any evidence that it's less reliable in people with lingering symptoms?

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.
 
IgG doesn’t last forever, so surely after it has been 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.
 
Back
Top Bottom