Deleterious mutations slow down flu's antigenic evolution, make it more punctuated in nature, and reduce the virus's genetic diversity.

Both within and between hosts, the key factor guiding whether increasing treatment strength will increase or decrease antibiotic resistance is whether inter-strain competition is effective, not whether it is present.

SARS-CoV-2 spike variants that resist neutralization by therapeutic antibodies or convalescent plasma can be generated in the laboratory and exist at low frequency in natural populations.

Antigenic drift in influenza’s major surface proteins, hemagglutinin and neuraminidase, contributes to variability in epidemic magnitude across seasons but is less influential than subtype interference in shaping annual outbreaks.

Comprehensive investigation reveals the variability and importance of the nuclear pore complex in HIV-1 infection and the activity of the antiretroviral protein, MX2.

Racial and ethnic disparities in SARS-CoV-2 infection rates can impact overall epidemic dynamics and herd immunity, underscoring the need to develop socially informed transmission models that account for population variability.

HIV co-infection does not affect Mycobacterium tuberculosis mutation rates and does not drive the emergence of antimicrobial resistance within patients in the largest outbreak of multidrug-resistant tuberculosis in Latin America to date.

Fitting a simple model of COVID-19 transmission to crowdsourced case report data allowed the estimation of mean cluster size and transmission rates in Canadian schools, as well as determining which interventions are most likely to limit transmission.