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4 Nov, 15 tweets, 8 min read
Denmark orders military to kill all mink in the country after mutated, mink-passaged SARS-CoV-2 strain with supposedly poor antibody response (details pending) spreads back to humans.

Extensive prior culling was unsuccessful in halting mink infections.

bt.dk/politik/mette-…
Discussion among virologists trying to get more data--



So far, no further details.
Another article states explicitly that there are scientific concerns about potential vaccine efficacy against mink-passaged SARS-CoV-2.

I see no preprints posted as yet. Solely relaying information from media sources.

Mutations acquired in mink passaging of SARS-CoV-2 are suspected to potentially pose efficacy problems for vaccines (was this actually tested somehow?) but show no clear increase in apparent clinical severity.
Source of antibodies used for testing in vitro is not currently clear. (Isolated from convalescent plasma? Just testing commercial mAbs? Some other mAb or mAbs?)

However, reduced efficacy has indeed been observed.

No info on T cells.

Discussion from the press conference in Denmark:



Goal is to prevent further divergence from strains which can be neutralized effectively by existing antibodies.
Earlier context on mink-passaged SARS-CoV-2 strains:



This was released weeks ago, before we had confirmation that existing antibodies are indeed less effective against them.
I am still waiting to see the experimental details of the antibody studies, however. The precise basis for this claim is not yet clear to me.
Further discussion of earlier sequencing results for the Danish mink-passaged mutant SARS-CoV-2 strains--



This work occurred before confirmation at today's press conference that antibody efficacy is impaired in vitro. Details not yet available.
English translation of key discussion from Danish mink culling press conference:



Assays appear to have used antibodies from human plasma.

This is worse than if they had just been mAbs. It implies some risk of weaker immunity, including from vaccines.
Danish version:

Translations from article on impact to Danish mink breeding and farming industry-- likely to be entirely destroyed:



Includes some terms for compensation schemes. Bonus for rapid culling.

Government is trying to halt passaging as quickly as possible.
Assay used antibodies extracted from serum of multiple individuals who had recovered from acute COVID-19.



Antibodies neutralized existing circulating strains of SARS-CoV-2, but were less effective against the mink strains recently transmitted to humans.
More details on the specific Danish mink-passaged SARS-CoV-2 strain that seems to be partly evading antibodies to existing circulating strains:

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More from @__ice9

ice9 Profile picture
23 Oct
Terguride (5-HT2A/B antagonist) for prevention of PAH and ventricular or pulmonary fibrosis in conditions of acutely elevated plasma 5-HT @farid__jalali

hindawi.com/journals/bmri/…

pubmed.ncbi.nlm.nih.gov/28821451/

researchgate.net/publication/51…
This might complement the effects of cyproheptadine and/or famotidine in the treatment of acute serotonin syndrome:

Precedex (dexmedetomidine) has also drawn favorable commentary recently for ICU cases, and likewise has a history of use in serotonin syndrome.

Read 5 tweets
ice9 Profile picture
23 Oct
@Longco191 That is a more complex question.

There are various possible post-acute COVID-19 symptoms.

Cardiorespiratory functional capacity may sometimes take a few weeks to months to recover.

Patients who experienced extensive clotting may have longer-lasting damage to affected areas.
@Longco191 There may be a risk of developing an autoimmune or autoinflammatory condition, such as a new joint or connective tissue disorder, potentially requiring assessment by a rheumatologist for diagnosis and treatment. Anecdotally, this often does appear to be treatable to some extent.
@Longco191 Some acutely recovered patients have reported fairly strong indicators of developing POTS, which is usually symptomatically treatable with appropriate medication by e.g. GPs familiarized with the issue. The underlying cause is usually harder to address and may be neurological.
Read 6 tweets
ice9 Profile picture
22 Oct
Further thoughts on post-viral ME/CFS after more literature review.

Initial suspicions about infected leukocytes were too narrow.

Persistently, latently, or formerly infected cells in tissues with low turnover are a more likely culprit.
Clearance of such cells in ME/CFS patients is impaired.

The secretome of such cells is often inflammatory (see first reference above) and has been shown to be metabolically disruptive for at least some viruses (more data on CoVs would be helpful):

Read 9 tweets
ice9 Profile picture
22 Oct
Mask tests, worst-case short-distance pure-aerosol:

- increased distance somewhat protective

- cotton and surgical masks somewhat protective if worn by spreader, limited if recipient

- N95 masks highly protective on spreader, moderately highly on recipient; fit also matters
Important:

- this is a worst-case test

- none of the masks fully protected

- hospital staff should use PAPR/CAPR if possible

- limit proximity/duration of contact

- if you think you may be infected, avoid others; wear good quality mask otherwise

msphere.asm.org/content/msph/5…
Real-world viral load in respiratory secretions is likely a couple orders of magnitude lower than the viral concentrations in the aerosols used in this test:

Read 7 tweets
ice9 Profile picture
22 Oct
First pass:

Converging evidence seems to indicate a common underlying mechanism for ME/CFS of specifically post-viral origin might result from DRP1-inducing warning signals from infected leukocytes.

Should be possible for any virus that can persistently infect leukocytes.
Not sure how to correct.

Perhaps more apoptosis? Steroids then.

May be more persistent if virus has reached bone marrow. Predict more chronic symptoms in patients w/ bone marrow infection.

Indirect remedial measures: mitochondrial antioxidants, co-factors, e.g. CoQ10, NADH.
Anyway this is still early and speculative. There are other theories too.

But it explains why steroids may help recent cases and not old ones, why rituximab helped in some studies, why mitochondrial ROS is high and glycolysis starts quickly, why ME/CFS plasma *causes it*, etc
Read 4 tweets
ice9 Profile picture
21 Oct
@GemzME @sickanddamned I mean yes you will end up with rhabdomyolysis if you push too hard at the limits of dysfunctional mitochondria in muscle tissue.

I will also predict considerable myalgia in ME/CFS patients after little exercise. And yes, this appears to be the case.
@GemzME @sickanddamned Questions:

- What is the mechanism of indomethacin-induced mitochondrial fragmentation and ROS increase, and does it occur in a relevant immune response also?

- What is mechanism of COVID-19 myalgia? Is it related?

- What about myalgia in other viruses, esp w/ high lactate?
@GemzME @sickanddamned Indomethacin activates PKCζ-p38-DRP1 pathway, causing rapid mitochondrial fission and risking apoptosis.
jbc.org/content/early/…

Blocked by mitochondrial fission inhibitor mdivi-1

DRP1 is also induced by p53 in some viral infections, interestingly.
solvecfs.org/hhv-6-mediated…
Read 59 tweets

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