Polymorphisms of large effect explain the majority of the host genetic contribution to variation of HIV-1 virus load. PNAS
McLaren et al. combined the majority of available genome-wide genotyping data in HIV-infected populations to test for association between ∼8 million variants and set point HIV viral load (spVL) in 6’315 individuals of European ancestry. They observed strong associations between spVL and multiple alleles at HLA-A, -B, and -C over a broad range of effect sizes. A second genome-wide significant association signal was observed in the chemokine receptor gene cluster on chromosome 3. Heritability analysis demonstrated that common human genetic variation explains 25% of the variability in viral load.
In conclusion, the study results indicate that common variants of large effect explain the majority of the host genetic component of HIV viral load.