J. D. Bloom

The paper re-analyzes sequencing data from four studies to resolve discrepancies in estimates of viral genetic diversity during human influenza infections, identifying technical issues in one study as the source of inflated diversity measurements.

This study identifies alternate translation initiation sites in influenza virus-infected cells, revealing a truncated neuraminidase protein and host transcript initiation patterns.

The paper shows that sera from humans with narrowly focused influenza virus antibodies select for single HA escape mutations in ovo, reducing antibody binding.

The paper maps functional epitopes of antibodies targeting HIV Env fusion peptide by analyzing mutations affecting neutralization, revealing differences between vaccine- and infection-elicited antibodies.

The paper models site-specific amino-acid preferences to improve phylogenetic estimates of viral divergence times, finding longer branches for influenza virus hemagglutinin.

The paper experimentally measures the effects of all single amino-acid mutations in H3N2 influenza HA on viral growth and shows their correlation with evolutionary success in natural lineages.

The paper identifies and quantifies single amino-acid mutations that confer resistance to broad and narrow antibodies targeting H1 influenza hemagglutinin.

The paper quantifies how amino-acid mutations affect HIV Env protein fitness across two diverged viral strains, finding most sites have conserved preferences but some show shifted mutational tolerance.

The paper investigates whether a cooperative mutation in H3N2 influenza virus, observed in cell culture, is present in unpassaged clinical samples using deep sequencing.

phydms enables efficient phylogenetic analyses using substitution models informed by deep mutational scanning, allowing comparison of lab and natural selection pressures.

This study maps HIV-1 escape mutations from a broadly neutralizing antibody by quantifying the effect of all single amino-acid mutations on viral sensitivity.

This study maps viral escape mutations from neutralizing antibodies by creating all replication-competent variants and using deep sequencing to identify enriched mutations.