Innate Immunity to Herpes Simplex Virus Type 2
- 1 December 2003
- journal article
- review article
- Published by Mary Ann Liebert Inc in Viral Immunology
- Vol. 16 (4) , 475-490
- https://doi.org/10.1089/088282403771926300
Abstract
Herpes simplex virus type 2 (HSV-2) is responsible for most cases of genital herpes and also can cause fatal disseminated disease in perinatally infected newborns. Sexually transmitted infections initiate in the skin or mucosa and quickly spread into peripheral nerves to establish latency. Innate immunity, the first line of defense during both primary and recurrent infection, is essential during this period of acute infection to limit initial viral replication and to facilitate an appropriate adaptive immune response. The innate immune response consists of a complex multilayered system of mechanical and secreted defenses, immediate chemokine and IFN responses, and rapidly recruited cellular defenses. HSV has devised equally elaborate strategies to evade or interfere with innate immunity. This review summarizes our current understanding of the innate immune responses to HSV-2 and the mechanisms by which HSV-2 can overcome these barriers. Newly emerging links between products of innate responses and the development of adaptive immune responses are also discussed.Keywords
This publication has 124 references indexed in Scilit:
- Local Delivery of CpG Oligodeoxynucleotides Induces Rapid Changes in the Genital Mucosa and Inhibits Replication, but Not Entry, of Herpes Simplex Virus Type 2Journal of Virology, 2003
- Cell Surface Major Histocompatibility Complex Class II Proteins Are Regulated by the Products of the γ134.5 and UL41 Genes of Herpes Simplex Virus 1Journal of Virology, 2002
- Participation of Type I Interferon in the Decreased Virulence of the UL13 Gene-Deleted Mutant of Herpes Simplex Virus Type 1Journal of Interferon & Cytokine Research, 2001
- The virus battles: IFN induction of the antiviral state and mechanisms of viral evasionPublished by Elsevier ,2001
- Splenic Marginal Metallophilic Macrophages and Marginal Zone Macrophages are the Major Interferon‐α/β Producers in Mice upon Intravenous Challenge with Herpes Simplex VirusScandinavian Journal of Immunology, 1999
- Herpes virus induced proteasome-dependent degradation of the nuclear bodies-associated PML and Sp100 proteinsOncogene, 1999
- Mapping the genetic region coding for herpes simplex virus resistance to mouse interferon /betaJournal of General Virology, 1993
- Natural killer cell-mediated lysis of herpes simplex virus-infected fibroblasts: Inability to detect soluble factors that contribute to lysisCellular Immunology, 1990
- Genetically Determined Difference in the Antiviral Action of /beta Interferon in Cells from Mice Resistant or Susceptible to Herpes Simplex Virus Type 2Journal of General Virology, 1986
- Glycoprotein C of herpes simplex virus 1 acts as a receptor for the C3b complement component on infected cellsNature, 1984