Viral Structure Of Hsv
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HSV-1 and HSV-2 are two of the eight known viruses which comprise the HSV family. As with all herpes viruses, they are large, enveloped visions with an icosahedral nucleocapsid consisting of 162 capsomeres, arranged around a linear, double-stranded DNA core. The genome consists of two covalently linked components, designated L (long) and S (short).
Each component consists of a unique sequence flanked by inverted repeats. Additionally, the unique L and S components can invert relative to one another, yielding four linear isomers. Each intact HSV vision contains only one of these four isomers, and each of the four is equally virulent (functionally equivalent) in the host cell.
The DNAs of HSV-1 and HSV-2 are largely collinear, and considerable homology exists between the HSV-1 and HSV-2 genomes. These homologous sequences are distributed over the entire gnomic map, and most of the polypeptides specified by one viral type are antigenically related to polypeptides of the other viral type.
This results in considerable cross-reactivity between the HSV-1 and HSV-2 glycoproteins, although unique antigenic determinants exist for each virus. Viral surface glycoproteins mediate HSV attachment to and penetration into cells and provoke host immune responses. Eleven glycoproteins of HSV have been identified (gB, gC, gD, gE, gG, gH, gI, gJ, gK, gL, and gM).
In addition, a twelfth is predicted (gN). gD is the most potent inducer of neutralizing antibodies and appears related to viral entry into a cell, and gB also is required for infectivity. Antigenic specificity is provided by gG, with the resulting antibody response allowing for the distinction between HSV-1 (gG-1) and HSV-2 (gG-2).
Two biologic properties which directly influence human disease are latency and neurovirulence. During HSV infection, visions are transported by retrograde flow along axons that connect the point of entry into the body to the nuclei of sensory neurons. Viral multiplication occurs in a small number of sensory neurons, and the viral genome then remains in a latent state for the life of the host.
With periodic reactivation brought on by events such as physical or emotional stress, fever, UV light, and tissue damage, the virus is transported back down the axon to replicate again at or near the original point of entry into the body. Such reactivation can result in clinically apparent disease or clinically inapparent infection.
The mechanisms by which HSV establishes latency are being intensely investigated but remain incompletely understood. Neurovirulence refers to the affinity with which HSV is drawn to and propagated in neuronal tissue. This can result in profound disease with severe neurologic sequelae, as is the case with neonatal HSV central nervous system (CNS) disease and with herpes simplex encephalitis in older children and adults.
Sites on the HSV genome which mediate this propensity for neurovirulence have been mapped to the thymidine kinase gene as well as the termini of the L component. Of note, the gene is required for replication in central nervous system tissue and prevents apoptosis of infected neuronal cells. Genetically engineered HSV visions lacking the gene are currently being investigated as therapies for brain tumors.
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