There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Considerable attention has been focused on how the APOL1/MYH9 locus determines susceptibility
to focal segmental glomerulosclerosis, including HIV-associated nephropathy (HIVAN).
Atta and colleagues found that homozygosity for APOL1 risk alleles was associated
with many, but not all, HIVAN cases, and that APOL1 variation failed to predict characteristics
of disease. Their work gives important impetus to identify other genetic and environmental
factors that may provide a 'second hit' linking HIV infection to HIVAN.