ice9 Profile picture
13 Oct, 7 tweets, 2 min read
Pardon delayed responses. I seem to have contracted a respiratory virus after maintenance staff visited my residence.

On the bright side, treatments discussed seem to work. Mostly feeling better after ~2.5 days of nasal/throat irritation, myalgia, low fever, headache, fatigue.
First symptom was scratchy feeling in oropharynx, then recalcitrant headache and fever and fatigue, then intermittent burning feeling in nasal passages, but only partial loss of olfactory perception.

Still feel a bit unsteady and tired from past fever but otherwise no symptoms.
Used:
- alcoholic mouthwash gargling 3x/day, ended odd sensations in throat quickly
- vitamin D 2000 IU 2x/day
- vitamin C 1g 3x/day
- nitazoxanide 500mg 3x/day
- umifenovir 200mg 3x/day
- bromhexine 8mg 3x/day
- ambroxol 15mg 3x/day
- hydroxychloroquine 200mg 2x/day
...
...
- indomethacin 50mg once, helped with headache but likely worsened myalgia even with vit. C; do not mix with nitazoxanide
- loratidine 10mg 1x/day, cetirizine 10mg 1x/day, famotidine 40mg 2x/day during fever
- acetaminophen 500mg 2x/day during fever, finished off headache
...
...
- quercetin 500mg 2x/day
- zinc picolinate 50mg/day with some kind of meal
- GABA 500mg 1x/day during fever, seemed to improve sleep
- elderberry syrup 2x/day during initial throat issue
Apparent viral progress seemingly arrested in oropharynx as far as I can tell. Continuing measures to keep it that way.

Consequently, have not needed intensified measures designed to address LRTI or platelets. Low vWF personally regardless.

Switched to non-vented masks.
Incubation period ~6 days.

Suspect frequent use of mouthwash helpful in preventing LRTI. Rapid apparent effect.

Bromhexine and ambroxol as insurance.

Switched nitazoxanide for 300mg doxycycline today. Post-entry antiviral and anti-inflammatory effects. Do not combine them.

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More from @__ice9

29 Sep
"SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells... in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients"

"spike glycoprotein (S) directly binds to the CD4 molecule, which... also requires ACE2 and TMPRSS2"

Impairs adaptive immunity.
Note TMPRSS13 expression as well.

SARS-CoV-2 can use TMPRSS13 to cleave Spike and deploy FP with approximately equal efficiency to TMPRSS2.



It can also use certain TMPRSS11 subtypes, albeit more slowly.
Severe COVID-19, much like SARS, heavily damages the spleen and lymph nodes.

Read 7 tweets
26 Sep
Depletion of surfactant from the lungs of rats followed by mechanical ventilation is sufficient to cause infiltration by neutrophils, tissue damage, and pneumocyte apoptosis.

COX-2 expression was reduced, and treatment with COX-2 inhibitors further worsened the resulting damage.
Histological samples resemble autopsies from fatal COVID-19, with extensive alveolar exudates, epithelial cell apoptosis, and neutrophil infiltration.

SARS-CoV-2 destroys secretory cells, reducing surfactant production and thereby promoting the above. Replace the surfactant.
COX-2 inhibitors further increased the damage. Most aren't used often anymore, as they were infamously associated with cardiovascular disease.

The reason is likely their mitochondrial toxicity, especially harmful under conditions of intense stress.

sciencedirect.com/science/articl…
Read 6 tweets
23 Sep
Interesting.

ncbi.nlm.nih.gov/pmc/articles/P…

Some references for the hypothesis that post-acute COVID-19 might be partly an endocrine disorder.

Note treatment for Addison's disease is often corticosteroids as well.
Read 9 tweets
22 Sep
About 60 percent of severe COVID-19 patients in the ICU exhibit clinical symptoms that look essentially indistinguishable from serotonin syndrome.
This fits evidence provided earlier showing elevated plasma serotonin levels in COVID-19.

Consistent with observed platelet activation (platelets store most peripheral serotonin) and damage to pulmonary endothelium (clears it from plasma)

Cyproheptadine and famotidine have been noted as effective in the treatment of serotonin syndrome.

aafp.org/afp/2010/0501/…

ncbi.nlm.nih.gov/pmc/articles/P…

Famotidine performs well in trials for COVID-19. I do not see any for cyproheptadine, but it shows up in protocols regardless.
Read 4 tweets
22 Sep
@vikramml @RealVladivostok Stephen Chen is a sensationalist.

60°C for one hour is usually enough for roughly a 5-log reduction in PFU terms in CoVs (see my post above).

Hence, starting with >100,000 viral particles could still allow infecting cells afterward.
@vikramml @RealVladivostok Gross appearance need not be altered during thermal inactivation, which involves thermal denaturation of key proteins.

90°C for 10 minutes reliably inactivates CoVs, including SARS-CoV-2.
@vikramml @RealVladivostok I am unsure why the article even bothered mentioning that the Spike protein wiggles. All proteins wiggle.

Spike count varies. The D614G mutation increased it by roughly a factor of 5, increasing infectivity. It is now carried by the majority of SARS-CoV-2 samples.
Read 5 tweets
21 Sep
Cerebrospinal fluid of patients experiencing significant COVID-19 neurological symptoms contains high levels of inflammatory cytokines, often for weeks afterward.

Little evidence for any viral material in CNS tissue based on CSF samples at least.

Occasional vascular damage.
Overall, consistent with the view that post-acute COVID-19 neurological symptoms are likely mediated in large part by persistent inflammatory processes.
Evidence for both neutralizing and autoimmune origins:

medrxiv.org/content/10.110…
High frequency of cerebrospinal fluid autoantibodies in COVID-19 patients with neurological symptoms

biorxiv.org/content/10.110…
Immunologically distinct responses occur in the CNS of COVID-19 patients
Read 5 tweets

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