Correction for Ojwach et al., “Pol-Driven Replicative Capacity Impacts Disease Progression in HIV-1 Subtype C Infection”

Number of HIV-1 founder variants is determined by the recency of the source partner infection

“…However, it is important to note that even small differences between genotypes can have important clinical outcomes. For instance, single polymorphisms can affect replication capacity(21), or can lead to primary non-nucleoside reverse transcriptase inhibitor resistance with different amino acids changes at the same position conferring equivalent levels of resistance(22).Previous studies have disagreed over the extent to which the elevated risk of transmission during the acute stage of infection (reviewed in (23)) is driven by increased viral load, elevated per particle transmission probability or other behavioural factors such as high rates of sex partner change or concurrent partnerships(24)(25)(26)(27)(28)(29). Here, while we find strong evidence to support the fact that acute stage transmissions are characterised by more virus particles and variants founding infection, this result alone cannot disentangle virus-and host-related drivers of elevated transmission.…”

“…However, even small differences between genotypes can have important clinical outcomes. For instance, single polymorphisms can affect replication capacity (21) or can lead to primary non-nucleoside reverse transcriptase inhibitor resistance with different amino acid changes at the same position conferring equivalent levels of resistance (22).…”