In latent infections, overt disease is not produced, but the virus is not eradicated. The virus may exist in a truly latent noninfectious occult form, possibly as an integrated genome or an episomal agent, or as an infectious and continuously replicating agent, termed as a persistent chronic viral infection. Reactivation of a latent infection may be triggered by various stimuli, including changes in cell physiology, super-infection by another virus, and physical stress or trauma. Viruses that cause latent infections can persist at the same time in different cell types of one or more tissues or organs. This review summarizes the characteristics and mechanisms by which persistent infections are maintained by modulation of both virus and cellular gene expression and modification of the host immune response.
Keywords: DNA viruses, Latency, reactivation, herpesvirus, papillomavirus, retrovirus, HIV, EBV, VZV, HCV, HPV, HCMV, latency associated transcripts (LATS), major IE promoter/enhancer (MIEP), EBV nuclear antigen (EBNA1), Burkitt’s lymphoma, concatamers, dorsal root ganglion (DRG), CD4, CCR5, gutassociated lymphoid tissue (GALT), HAART.