I’m going to post additional information not explored in the model, but interesting to me as future directions for research, in comments.
Drug resistance can be studied in viral kinetics/dynamics studies. These studies focus on two aspects of viral biology:
Mutations vs. drug resistance
Mutations vs. replication efficiency
One in vitro study found some baloxavir-resistant strains are generally less efficient at replication than wild type, though that’s not a universal for all contexts/viruses/cell types/metrics. Also, these studies typically control the genome of the virus, whereas in the wild, viruses can develop compensating mutations for the decreased fitness induced by the resistance-conferring mutation.
The mutations linked to resistance are currently rare (<1%) in flu patients. This study measured resistance in terms of cell death +/- baloxavir and viral yield +/- baloxavir at different concentrations of drug and different strain mixtures. In some cases, only small fractions of resistant strains were needed to reduce susceptibility. I’m curious if this may be because the resistant proteins are being “shared” among the population of resistant and non-resistant viruses in the cell, but don’t have enough knowledge of influenza biology to know if that’s plausible.
There are a whole bunch of interesting looking in vitro studies on various drugs/strains/cell types.
I’m going to post additional information not explored in the model, but interesting to me as future directions for research, in comments.
Drug resistance can be studied in viral kinetics/dynamics studies. These studies focus on two aspects of viral biology:
Mutations vs. drug resistance
Mutations vs. replication efficiency
One in vitro study found some baloxavir-resistant strains are generally less efficient at replication than wild type, though that’s not a universal for all contexts/viruses/cell types/metrics. Also, these studies typically control the genome of the virus, whereas in the wild, viruses can develop compensating mutations for the decreased fitness induced by the resistance-conferring mutation.
The mutations linked to resistance are currently rare (<1%) in flu patients. This study measured resistance in terms of cell death +/- baloxavir and viral yield +/- baloxavir at different concentrations of drug and different strain mixtures. In some cases, only small fractions of resistant strains were needed to reduce susceptibility. I’m curious if this may be because the resistant proteins are being “shared” among the population of resistant and non-resistant viruses in the cell, but don’t have enough knowledge of influenza biology to know if that’s plausible.
There are a whole bunch of interesting looking in vitro studies on various drugs/strains/cell types.