Herpes simplex viruses (HSVs) are extremely host-adapted viruses that can cause a wide variety of illness in infected human hosts. There are two types of the HSVs: (a) herpes simplex virus type 1 (HSV-1) and (b) herpes simplex virus type 2 (HSV-2). Both the types are closely related in their DNA homology, anti-genic determinants, and tissue tropism and disease symptoms, but differ in epidemiology. HSV-1 is transmitted primarily by contact with infected saliva, whereas HSV-2 is transmitted by sexual contact or by genital tract infection to newborn from an infected mother.
Herpes simplex viruses show following features:
· The HSVs like other herpesviruses are large, enveloped, icosadeltahedral viruses.
· Both HSV-1 and HSV-2 are structurally and morphologically similar. They, however, are distinguished antigenically by using type-specific monoclonal antibodies, restriction endonuclease patterns of their genome DNA, and the site of lesions.
· The virus contains a dsDNA. The genomes of both HSV-1 and HSV-2 are similar in organization and show a higher degree of sequence homology. They, however, can be differentiated by restriction enzyme analysis of viral DNA.
· The unique feature of the DNA genome is that it encodes for as few as 80 polypeptides.
· Half of the proteins are required for replication of viruses, whereas other proteins help in interaction of the viruses with different host cells and immune response. HSV encodes for at least 11 glycoproteins that serve as (a) viral attachment proteins (gB, gC, gD, gH), (b) fusion proteins (gB), (c) struc-tural proteins, (d) immune escape proteins (gE, and gI), and (e) other fractions.
Herpes simplex virus (HSV) grows very rapidly in infected cells, requiring only 8–16 hours for completion. The virus infects most types of cells in human hosts and usually causes lytic infections of the fibroblasts and epithelial cells. After entry into the cell, the virion is uncoated, genome is released, and the genome DNA enters into the nucleus. The mRNA is tran-scribed by host cell RNA polymerase and then translated into early nonstructural proteins. Subsequently, the viral DNA poly-merase replicates the genome DNA, during which synthesis of early proteins is stopped but synthesis of late structural pro-teins begins. These late proteins are transported to the nucleus where assembly of virion occurs.
The virion acquires its envelope by budding through the nuclear membrane. It also causes latent infections of neurons by the presence of multiple copies of HSV-1 DNA in the cytoplasm of infected neurons.
Like other enveloped viruses, HSVs are sensitive to treatment with acid, fat solvents, detergents, and drying. They are readily inactivated in the conditions prevalent in the gastrointestinal tract.