FYI, your name came up at the Winnipeg in 2023 party at CapClave, as one of the organizers' personal virology expert.
As a nucleoside analog, I assume that molnupiravir will (like monoclonal antibodies) be useful mainly early in the course of disease, because once COVID-19 is severe the actual viral load is typically low and dropping. As I understand it, at that point you're dealing with the sequelae of the infection, especially the inflammatory response and collateral damage to otherwise-healthy tissues.
Merck has also said that the drug will be investigated for other RNA-viral diseases, which could be super-useful if it works.
Huh, glad to hear that my messages are making it out into the world. Thanks for letting me know. I wonder who it was, though I think I can guess.
On to the more COVID-19 related part of this: yes, I would suspect that molnupiravir will be at its most useful early in infection. This is true of most antiviral agents, for the reasons that you state--by the time you reach a few days into *most* viral infections, the virus has run its course and it's the immune response and tissue damage that you're really dealing with.
There are some notable exceptions, but they are mainly chronic infections, such as herpes virus infections, Hepatitis C virus infections, and HIV infections. In these cases the antiviral agents are able to control outbreaks, overcome sustained virus replication, or force other actions that help manage or even cure disease. In each of these cases, however, we have viruses that are *not* typically reined in by the action of the immune system.
I'm surprised, therefore, that molnupiravir works at all, really. I'm used to the model of influenza virus, where administration of antiviral agents later than a day or two into infection means they can do very little to control disease. But, SARS-CoV-2 is different, and so is molnupiravir. Coronaviruses do not have a high mutation rate per base of RNA copied, and perhaps they are less able to tolerate, even a bit later in infection, the errors that molnupiravir introduces. Perhaps molnupiravir introduces so many errors that it can effectively control virus infections to greater degree that older-generation antivirals. Either way, I am impressed that it works and so well.
I hope it does work for other virus infections. I can think of quite a few where it would be nice to be able to see these sorts of effects, but I'm hesitant to speculate without seeing more experimental data.
Hi, John.
FYI, your name came up at the Winnipeg in 2023 party at CapClave, as one of the organizers' personal virology expert.
As a nucleoside analog, I assume that molnupiravir will (like monoclonal antibodies) be useful mainly early in the course of disease, because once COVID-19 is severe the actual viral load is typically low and dropping. As I understand it, at that point you're dealing with the sequelae of the infection, especially the inflammatory response and collateral damage to otherwise-healthy tissues.
Merck has also said that the drug will be investigated for other RNA-viral diseases, which could be super-useful if it works.
Huh, glad to hear that my messages are making it out into the world. Thanks for letting me know. I wonder who it was, though I think I can guess.
On to the more COVID-19 related part of this: yes, I would suspect that molnupiravir will be at its most useful early in infection. This is true of most antiviral agents, for the reasons that you state--by the time you reach a few days into *most* viral infections, the virus has run its course and it's the immune response and tissue damage that you're really dealing with.
There are some notable exceptions, but they are mainly chronic infections, such as herpes virus infections, Hepatitis C virus infections, and HIV infections. In these cases the antiviral agents are able to control outbreaks, overcome sustained virus replication, or force other actions that help manage or even cure disease. In each of these cases, however, we have viruses that are *not* typically reined in by the action of the immune system.
I'm surprised, therefore, that molnupiravir works at all, really. I'm used to the model of influenza virus, where administration of antiviral agents later than a day or two into infection means they can do very little to control disease. But, SARS-CoV-2 is different, and so is molnupiravir. Coronaviruses do not have a high mutation rate per base of RNA copied, and perhaps they are less able to tolerate, even a bit later in infection, the errors that molnupiravir introduces. Perhaps molnupiravir introduces so many errors that it can effectively control virus infections to greater degree that older-generation antivirals. Either way, I am impressed that it works and so well.
I hope it does work for other virus infections. I can think of quite a few where it would be nice to be able to see these sorts of effects, but I'm hesitant to speculate without seeing more experimental data.