The intimate relationship between the HIV-1 life-cycle and the activation state of cells supporting viral replication results in a dynamic interaction between coinfections and HIV-1 replication in dually infected people. The immunologic impact of recurrent coinfections has the potential to increase viral replication, viral genotypic heterogeneity and CD4 T lymphocyte loss, leading to accelerated decline in immune function, reduced survival and increased HIV-1 transmission risk. These effects may play a particularly significant role in the HIV-1 epidemic in sub-Saharan Africa. The mechanisms underlying these effects on virus-host dynamics are reviewed and data describing the impact of tuberculosis, malaria, schistosomiasis and genital ulceration on HIV-1 infection are presented.