3 ms·

> If there is no vaccine, or if the vaccine isn't very good, social-distancing and contact-tracing is the only way to win. I know I sound like a broken record

> If there is no vaccine, or if the vaccine isn't very good, social-distancing and contact-tracing is the only way to win. I know I sound like a broken record every time I say this on HN... but why no one thinks of pharmacological treatment? The first wave of (small) trials will end this June.

adrianN 6y ago
I'm moderately optimistic that plasma transfusions will help reduce the death toll, but evidence is mounting that even "mild" cases can leave the patients with severe lung damage. Having the contact data ready to start treatment earlier might help with that too.
- lbeltrame 6y ago
  I meant something far more aggressive towards disease treatment, from the repurposed drugs (which a few here say don't work, but I'm waiting for the results of the trials), then the specific ones like antibodies, soluble ACE2 receptors, and others. Plus I'm confident that the anti-inflammation drugs being tested can help with lung tissue damage.
  - adrianN 6y ago
    I'm no pharmacologist but I think we would be extremely lucky if one of existing antivirals also works here. I don't think that antibody drugs will be an important tool. They're extremely hard to manufacture (and hence very expensive). I don't think we could satisfy demand. It would be great though if one of those studies found an effective drug!
    - lbeltrame 6y ago
      > I'm no pharmacologist but I think we would be extremely lucky if one of existing antivirals also works here. Even if the results are bad, it also depends on what they were used for, since the little evidence we have tells us that the sooner we act, the better. Example: ritonavir was a letdown, but even in the NEJM paper the limitations of the study mention that the trial was done on people with rather severe sympthoms. At this point it was probably too late to make a dent in the infection. The data on remedisivir (which came from two suspended trials due to lack of enrollment, so no statistical power) showed an almost-identical mortality between the two groups, but I'd argue that those (at least one of them was) were done on patients in severe conditions, so once again late. Later trials which are ongoing are hopefully better designed (NIH's for remedisivir at least, Gilead's don't use a placebo IIRC) and will get us answers. IMO, even a small improvement on hospitalization rate would be a huge win for the ICUs. That said, remedisivir is i.v. so this limits applicability to hospitals.

adrianN 6y ago

I'm moderately optimistic that plasma transfusions will help reduce the death toll, but evidence is mounting that even "mild" cases can leave the patients with severe lung damage. Having the contact data ready to start treatment earlier might help with that too.

lbeltrame 6y ago
I meant something far more aggressive towards disease treatment, from the repurposed drugs (which a few here say don't work, but I'm waiting for the results of the trials), then the specific ones like antibodies, soluble ACE2 receptors, and others. Plus I'm confident that the anti-inflammation drugs being tested can help with lung tissue damage.
- adrianN 6y ago
  I'm no pharmacologist but I think we would be extremely lucky if one of existing antivirals also works here. I don't think that antibody drugs will be an important tool. They're extremely hard to manufacture (and hence very expensive). I don't think we could satisfy demand. It would be great though if one of those studies found an effective drug!
  - lbeltrame 6y ago
    > I'm no pharmacologist but I think we would be extremely lucky if one of existing antivirals also works here. Even if the results are bad, it also depends on what they were used for, since the little evidence we have tells us that the sooner we act, the better. Example: ritonavir was a letdown, but even in the NEJM paper the limitations of the study mention that the trial was done on people with rather severe sympthoms. At this point it was probably too late to make a dent in the infection. The data on remedisivir (which came from two suspended trials due to lack of enrollment, so no statistical power) showed an almost-identical mortality between the two groups, but I'd argue that those (at least one of them was) were done on patients in severe conditions, so once again late. Later trials which are ongoing are hopefully better designed (NIH's for remedisivir at least, Gilead's don't use a placebo IIRC) and will get us answers. IMO, even a small improvement on hospitalization rate would be a huge win for the ICUs. That said, remedisivir is i.v. so this limits applicability to hospitals.