Herpes Simplex Virus
Herpes Simplex Virus Type 1 Infection at the Molecular Level
Research Paper
Virology
24 November 2008
Abstract Herpes simplex virus type 1 (HSV-1) infection is widespread and causes significant disease in humans. The structure, epidemiology, pathogensis and immune response are examined in this review, as well as specific ways to reduce and eliminate pathology and related diseases. The virus naturally infects mucosal areas and begins the search for its target host cell. Upon binding to the host cell membrane via teams of glycoproteins, the virion is then phagocytosed. Soon the nucleus is seized and all regular host cell mechanisms are shut off. Replication of HSV-1 is specific encoding immediate early, early and late genes. Once the virus replication process is complete the virus exits epithelial cells near the site of infection through a process known as cell lysis. Sensory neurons are the specific target of HSV-1, where it can then travel to the trigeminal ganglia (TG) stoma via neuronal microtubular networks. Both innate and adaptive immune systems respond to the infection with various antibodies, interleukins and interferons. Once the virion reaches the nervous system, the immune responses are unable to detect it although they try to contain it as best they can. HSV-1 enters a latent stage, usually via latent associated transcripts, not causing pathogenesis but unable to fight off by means of the host immune system. Following a stressful situation or similarly UV activation, HSV-1 travels back down nerve fibers to re-infect cells near the original site of infection. This process is known to continue throughout the lifespan of the infected individual, normally without fatalities. When the host immune response is unable to contain the virus in the TG, several associated diseases such as encephalitis and keratits result. Genes involved with virus replication and host genes, to eliminate the virus, have been maneuvered to cause reverse effects and are currently
Research Paper
Virology
24 November 2008
Abstract Herpes simplex virus type 1 (HSV-1) infection is widespread and causes significant disease in humans. The structure, epidemiology, pathogensis and immune response are examined in this review, as well as specific ways to reduce and eliminate pathology and related diseases. The virus naturally infects mucosal areas and begins the search for its target host cell. Upon binding to the host cell membrane via teams of glycoproteins, the virion is then phagocytosed. Soon the nucleus is seized and all regular host cell mechanisms are shut off. Replication of HSV-1 is specific encoding immediate early, early and late genes. Once the virus replication process is complete the virus exits epithelial cells near the site of infection through a process known as cell lysis. Sensory neurons are the specific target of HSV-1, where it can then travel to the trigeminal ganglia (TG) stoma via neuronal microtubular networks. Both innate and adaptive immune systems respond to the infection with various antibodies, interleukins and interferons. Once the virion reaches the nervous system, the immune responses are unable to detect it although they try to contain it as best they can. HSV-1 enters a latent stage, usually via latent associated transcripts, not causing pathogenesis but unable to fight off by means of the host immune system. Following a stressful situation or similarly UV activation, HSV-1 travels back down nerve fibers to re-infect cells near the original site of infection. This process is known to continue throughout the lifespan of the infected individual, normally without fatalities. When the host immune response is unable to contain the virus in the TG, several associated diseases such as encephalitis and keratits result. Genes involved with virus replication and host genes, to eliminate the virus, have been maneuvered to cause reverse effects and are currently
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