24 November 2008
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 used as antivirals. Although no vaccine has been approved for use against HSV-1, various attempts have been made. This research paper defines the virus infection at a molecular level as well as demonstrates modifications of the virus genes to cause reverse effects and investigates just a few of the diseases connected with HSV-1. Introduction
Herpes simplex viruses type 1 and 2 are well known members of the family Herpesviridae, subfamily Alphaherpesvirinae, which cause lifelong, latent infection in humans. Herpes simplex virus type 1 (HSV-1) typically remains the cause of cold sores, gingivostomatitis, and skin lesions in the orofacial area, as well as many rare but fatal conditions (1). Herpes simplex virus type 2 (HSV-2) is primarily associated with genital area infection. Worldwide, approximately one third of people display clinical manifestations of HSV-1 infection (2). HSV-1 is neurotropic, infecting multiple cell types but establishing latency in the trigeminal ganglia (TG). HSV-1 reactivates, in response to certain stimuli such as emotional or physical stress or UV light, and is transported along nerve fibers to mucosal or cutaneous regions (1). Infected cells show signs of the nucleus changing shape and nucleolus displacement with a formation of multinucleated giant cells. Cells degenerate, lyse and vesicles of fluid containing the virus locate between the epidermis and dermal layer of the skin forming a lesion (2). Although HSV-1 infects a large percentage of the population, few actually show symptoms of disease. HSV Structure and Genome
HSV-1 is an enveloped double stranded DNA (dsDNA) virus consisting of four elements. First, an outer envelope with glycoprotein spikes on its surface. Second, a tegument layer including several viral proteins important during HSV-1 infection. Third, an iscosahedral capsid surrounding the last compartment, the electron opaque core containing the dsDNA genome wrapped as a spool. The envelope is made up of 13...