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.
...
- 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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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.
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.
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.
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