The variability in both the clinical progression and transmission of human immunodeficiency virus (HIV) infection has prompted a search for cofactors influencing replication of the virus. Although it is clear that host immune and genetic factors, as well as the replication kinetics of particular viral strains, influence the progression of HIV disease, a variety of exogenously acquired infectious agents also appear to influence the pace of HIV replication, the destruction of CD4+ T cells, and HIV transmission to infants and sexual partners. Transient bursts of HIV replication occur after vaccination and during episodes of acute systemic infection. More persistent elevations . . .
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Lawrence Corey (2007) studied this question.
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