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The majority of HIV-infected This phenotype appears very similar to that observed in the non-human primate natural hosts of SIV (simian immunodeficiency virus) infection, such as sooty mangabeys and African Green monkeys, whose normal, healthy life-spans are associated with normal CD4 counts and low immune activation despite persistent high viral loads. The fact that a proportion of the mothers of these paediatric ‘non-progressors’ share the same phenotype suggests either a shared genetic mechanism and/or viral factors are involved. We have recently shown that HLA does not play a significant part in this phenotype, and diminished viral replicative capacity is also not the mechanism (Adland et al PLoS Path 2015). The strategy adopted by HIV-infected children to avoid disease in HIV infection is therefore entirely different from that observed in ‘elite controller’ adults, where HLA-mediated control of viral replication drives the virus down to undetectable levels.

In these studies we are comparing the innate immune response and adaptive immune response of paediatric non-progressors to age-matched progressor children, uninfected age-matched children, age-matched ART-treated children, and HIV-infected adults who are matched for CD4 count but who are putative progressors.