The molecular epidemiology of respiratory syncytial virus (RSV) was studied over four consecutive seasons (1997–2000) in a single tertiary hospital in South Africa: 225 isolates were subgrouped by RT–PCR and the resulting products sequenced. Subgroup A predominated in two seasons, while A and B co-circulated approximately equally in the other seasons. The nucleotide sequences of the C-terminal of the G-protein were compared to sequences representative of previously defined RSV genotypes. South African subgroup A and subgroup B isolates clustered into four and five genotypes respectively. One new subgroup A and three new subgroup B genotypes were identified. Different genotypes co-circulated in every season. Different circulation patterns were identified for group A and B isolates. Subgroup A revealed more variability and displacement of genotypes while subgroup B remained more consistent.

Understanding HIV remission in rare individuals who initiated antiretroviral therapy (ART) soon after infection and then discontinued, may inform HIV cure interventions. Here we describe features of virus and host of a perinatally HIV-1 infected child with long-term sustained virological control. The child received early limited ART in the Children with HIV Early antiRetroviral therapy (CHER) trial. At age 9.5 years, diagnostic tests for HIV are negative and the child has characteristics similar to uninfected children that include a high CD4:CD8 ratio, low T cell activation and low CCR5 expression. Virus persistence (HIV-1 DNA and plasma RNA) is confirmed with sensitive methods, but replication-competent virus is not detected. The child has weak HIV-specific antibody and T cell responses. Furthermore, we determine his HLA and KIR genotypes. This case aids in understanding post-treatment control and may help design of future intervention strategies.

Significance: Levels of CC chemokine receptor 5 (CCR5) on T cells are a critical factor influencing HIV/AIDS susceptibility. DNA methylation is an epigenetic feature associated with lower gene expression. Here we show that the DNA methylation status ofCCR5 cis-regulatory regions (cis-regions) correlates inversely with CCR5 levels on T cells. T-cell activation induces demethylation ofCCR5 cis-regions, upregulating CCR5 expression. Higher vs. lower sensitivity ofCCR5 cis-regions to undergoing T-cell activation-induced demethylation is associated with increased vs. decreased CCR5 levels. Polymorphisms inCCR5 cis-regions that are associated with increased vs. decreased HIV/AIDS susceptibility are also associated with increased vs. decreased sensitivity to activation-induced demethylation. Thus, interactions among T-cell activation,CCR5epigenetics, and genetics influence CCR5 levels on T cells and, by extension, HIV/AIDS susceptibility.