Herpes Simplex Virus: The Interplay Between HSV, Host, and HIV-1.
Herpes simplex virus proteins interact with host (human) proteins and create an environment conducive for its replication. Genital ulceration due to herpes simplex virus type 2 (HSV-2) infections is an important clinical manifestation reported to increase the risk of human immunodeficiency virus type 1 (HIV-1) acquisition and replication in HIV-1/HSV-2 coinfection. Dampening the innate and adaptive immune responses of the skin-resident dendritic cells, HSV-2 not only helps itself, but creates a "yellow brick road" for one of the most dreaded viruses HIV, which is transmitted mainly through the sexual route. Although, data from clinical trials show that HSV-2 suppression reduces HIV-1 viral load, there are hardly any reports presenting conclusive evidence on the impact of HSV-2 coinfection on HIV-1 disease progression. Be that as it may, understanding the interplay between these three characters (HSV, host, and HIV-1) is imperative. This review endeavors to collate studies on the influence of HSV-derived proteins on the host response and HIV-1 replication. Studying such complex interactions may help in designing and developing common strategies for the two viruses to keep these "partners in crime" at bay.
Department of Virology, ICMR-National AIDS Research Institute , Pune, India .
Dipen Vijay
DV
Desai
Department of Virology, ICMR-National AIDS Research Institute , Pune, India .
Smita Shrikant
SS
Kulkarni
D060085:Coinfection / Q000473:pathology / Q000821:virology; D015497:HIV-1 / Q000502:physiology*; D018258:Herpesvirus 2, Human / Q000502:physiology*; D054884:Host-Pathogen Interactions; D006801:Humans; D007108:Immune Tolerance; D056265:Microbial Interactions; D014779:Virus Replication