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13 Nov, 4 tweets, 2 min read
Recent RCT demonstrates reduced viral load in patients treated with ivermectin.

papers.ssrn.com/sol3/papers.cf…

Along with the post-exposure prophylaxis trials, this further indicates genuine antiviral activity in vivo for ivermectin (not merely anti-inflammatory). ImageImage
See here for a few other relevant studies:

The only study in vitro for ivermectin against SARS-CoV-2 used Vero cells and did not pre-treat at all.



This made it difficult to infer much about the effect during an ongoing repository infection in humans. Initial estimates looked unhittable.
*"respiratory" typo

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More from @__ice9

ice9 Profile picture
4 Nov
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.
Read 15 tweets
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

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