Figure 2: Immune responses to concurrent infections such as malaria or HSV-2 provide a suitable environment for HIV infection and replication by the rise of certain modulators that promote cellular activation and the consequent increment in the pool of HIV target cells (1), and up-regulation of viral replication (2). Cellular activation also increases the concentration of modulators in the host cell that facilitate virus expression (3), and viruses such as HSV-2 have regulatory proteins that interact with the HIV LTR upregulating HIV replication (4).