Speaker
Description
Reductions in HIV infection rates in sub-Saharan Africa (SSA) do not fully reflect the increases in viral load suppression achieved through universal testing and treatment (UTT). Heterogeneities in risk and treatment uptake contribute to this disparity. In North America and Europe, HIV transmission is concentrated among key populations with frequent super spreading. The extent to which African HIV epidemics are similarly linked to key populations is poorly understood. Molecular epidemiology can shed light on these dynamics.
We analyzed phylogenetic clustering patterns using HIV-TRACE on HIV sequences from the PANGEA-HIV consortium. Clustering was compared across sites and investigated with agent-based simulations (PopART-IBM and EMOD-HIV). We also compared clustering between men who have sex with men (MSM) in the UK and Netherlands and heterosexual populations in SSA.
The distribution of clusters in SSA was more homonegenous and typically centred around a smaller average than in MSM populations in Europe, even when accounting for sampling fraction and epidemic phase. European MSM clusters are characterised by large overdispersion.
A simple branching process model shows that phylogenetic clustering is sensitive to the skewness of the transmission offspring distribution.The extent to which the dissimilarity in offspring distributions between MSM in Europe and heterosexual in SSA can be attributed to the degree distribution of sexual networks is investigated with a simple sexual network model.
Our findings align with agent-based simulations in which HIV transmission originates from the general population without necessarily significant contributions from key populations, with important implications for the future of HIV prevention in SSA.
