Doctors are coming out in droves saying hydroxychloroquine works

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For example, the article in post #1,522 is about glycosylation, which is a major prognostic factor. HCQ does change endosome pH, though the virus can switch from ACE2 receptors to TMPRSS2, and TMPRSS2 connects to a current suspect as intermediate host of COVID-19, the Yangtze finless porpoise. All of this links to the Wuhan-Pennsylvania connection, already mentioned on the snake meat thread:


Furthermore, it is dumb not to include zinc and azithromycin in arguing for the benefits of hcq: the Zelenko protocol.
 
Most doctors and scientists are saying that HCLQ doesn't provide any significant benefit. If I catch this thing, I hope they use Remdosivir or plasma transfusions to treat me. HCLQ is bullshit and doesn't really work.
 
It's obvious that post # 1,542 has not read Gold's white paper on hydroxychloroquine. The way forward is to test individual posters so that other readers can actually see who is clued up and who is not. Remdesivir and dexamethasone discourse should also be welcome, though the jury is still out on other treatments, such as the new Russian areplivir (based on favipiravir).

It's interesting that, even after Homo sapiens has learned the history of cocktails against HIV-1, it's still having trouble accepting complexities. It wants a once-and-for-all answer for itself.
 
It's obvious that post # 1,542 has not read Gold's white paper on hydroxychloroquine. The way forward is to test individual posters so that other readers can actually see who is clued up and who is not. Remdesivir and dexamethasone discourse should also be welcome, though the jury is still out on other treatments, such as the new Russian areplivir (based on favipiravir).

It's interesting that, even after Homo sapiens has learned the history of cocktails against HIV-1, it's still having trouble accepting complexities. It wants a once-and-for-all answer for itself.

You can always find some idiot to support your bullshit. Doesn't mean you are right. Remember when some doctors said that smoking is good for you back in the 50's and early 60's?
 
In addition, once the source of COVID-19 in nature is discovered, treatment should advance greatly, including vaccines (COVID-19 hamster model may be possible). Is there a valid reason for repeating the embarassing history of the source of ebola in nature?
 
What bullshit we're dealing with is 'god is my sensei' xian bigotry, scared shitless to go back to school.
 
In addition, once the source of COVID-19 in nature is discovered, treatment should advance greatly, including vaccines (COVID-19 hamster model may be possible). Is there a valid reason for repeating the embarassing history of the source of ebola in nature?

How in the hell is a hamster model going to work for a virus that originated in bats?
 
Post #1,548: If you would have read the snake meat thread, you'd know how the hamster model fits into the drama.
 
Anyone contemplating plasma in lieu of hydroxychloroquine should know about the D614G mutation that occurred in COVID-19 at least by Feb 2020.

COVID-19 / Convalescent Plasma

So we see the virus mutate towards alkalinity, because its original aspartic acid (D, pH 2.98, acidic) went higher, to glycine (G, pH 6.06, more basic), though hcq (also [italics]) increases alkalinity in endosomes. This hcq-induced alkalinity affects virus replication.
 
For example, the article in post #1,522 is about glycosylation, which is a major prognostic factor. HCQ does change endosome pH, though the virus can switch from ACE2 receptors to TMPRSS2, and TMPRSS2 connects to a current suspect as intermediate host of COVID-19, the Yangtze finless porpoise. All of this links to the Wuhan-Pennsylvania connection, already mentioned on the snake meat thread:


Furthermore, it is dumb not to include zinc and azithromycin in arguing for the benefits of hcq: the Zelenko protocol.

I'm not sure you actually read the paper you're referencing. For starters, it's not a paper about COVID 19. Second, there is no "switching from ACE2 to TMPRSS2" since TMPRSS2 is a protease and not a binding site.
 
At avian flu talk forum, they are hawking green tea as a zinc ionophore, because zinc is difficult to get into the cell. However, chloroquine is also a zinc ionophore.

Zinc / Chloroquine / Ionophore
'....using chloroquine as an ionophore while zinc inside the infected cell can stop SARS-CoV-2 replication.'
 
#1,552: You are incorrect. COVID-19 can use TPRSS2 as an alternate enzyme. It does not need ACE2.
 
The Conundrum of the Binding Site

Can COVID-19 gain cell entry without S priming/TMPRSS2?

TMPRSS2

Ap 2020 SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2
 
The article of post #1,555 continue, recalling that ebola vaccine is based on VSV:

'....Replication-defective VSV particles bearing coronavirus S proteins faithfully reflect key aspects of coronavirus host cell entry....All cell lines were readily susceptible to entry driven by the glycoprotein of the pantropic VSV (VSV-G), as expected....In order to determine whether SARS-CoV-2 can use CatB/L for cell entry, we initially employed ammonium chloride, which elevates endosomal pH and thereby blocks CatB/L activity....only TMPRSS2 activity is essential for viral spread and pathogenesis in the infected host whereas CatB/L activity is dispensable....Priming of coronavirus S proteins by host cell proteases is essential for viral entry into cells, and encompasses S protein cleavage as the S1/2 and S2' sites. The S1/2 cleavage site of SARS-CoV-2-S harbors several arginine residues (multibasic), which indicates high cleavability. Indeed, SARS-CoV-2 was efficiently cleaved in cells and cleaved S protein was incorporated into VSV particles. Notably, the cleavage site sequence can determine the zoonotic potential of coronaviruses, and a multibasic cleavage site was not present in RaTG13, the coronavirus most closely related to SARS-CoV-2. It will be interesting to determine whether the presence of a multibasic cleavage site is required for SARS-CoV-2 entry into human cells and how this cleavage site was acquired.'

Arginine (R) has the highest isoelectric pH, and we first mentioned RaTG13 in post #366 of the snake meat thread. RaTG13 was from the Yunnan bat. This zoonotic potential of the cleavage site may help pinpoint the intermediate COVID-19 host in nature.
 
In another thread, we have already mentioned lungworm of suspected COVID-19 intermediate host, Neophocaena and the swine lungworm as intermediate host of influenza virus. Thus for the TMPRSS2 investigative trajectory, there is an entry for bat-associated influenza and TMPRSS2:

Hemagglutinin of Bat-Associated Influenza Virus is Activated by TMPRSS2 for pH-Dependent Entry Into Bat but not Human Cells
 
We've already mentioned ebola, CatB/L and VSV. TMPRSS2 links ebola drugs such as remdesivir:

Ebola / Marburg / TMPRSS2

Chagas disease links a parasite (trypanosome) in comparison to hcq for malaria:

Chagas / Ebola / CatB/L
 
Nafamostat is promising and here also is mentioned remdesivir and chloroquine in comparison, remdesivir has a higher SI (selectivity index) than chloroquine, though we don't know the SI for hydroxychloroquine:

COVID-19 / Nafamostat / Remdesivir / Chloroquine
'....Notably, two compounds, remdesivir (EC50= 0.77 mM, SI 129.87) and chloroquine (EC50= 1.13 mM, SI 88.50) potently blocked virus infection at low micromolar concentration and showed high SI.'
 
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