Herpes simplex viruses type 1 HSV1 and type 2 HSV2

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There are several features which distinguish herpes viruses from other viruses. The genome is a linear double-stranded DNA ranging from 125 000 to 250 000 base pairs. The viron is composed of the DNA-containing core; an icosahedral capsid, which is about 100 nm in diameter and exhibits 162 morphological units (capsomeres) on its surface and an outer lipid-containing membrane or envelope. These viruses use both the nucleus and the cytoplasm of the host cell for their replication.

The pathology and epidemiology of herpes virus infections depend on the mode of viral replication, associated cytotoxicity as well as their capacity to cause latent infections. Clinically many of the infections caused by HSV-1 and HSV-2 are indistinguishable. Despite the fact that these strains are predominantly isolated from different anatomical sites, it is clear that strains of either type can initiate and establish infection at either genital or extragenital sites.

HSV rarely causes severe disseminated disease in adults, except when cell-mediated immunity is compromised. Among infected individuals who have no known immunologic defects, the responses to infection typically range from no clinical signs and symptoms to localized lesions. Mild to moderate systemic symptoms followed by periodic recurrence of localized lesions may occur. Asymptomatic genital infections are responsible for a significant number of transmissions. Genital HSV infections are a significant public health problem. It is estimated that 1 in 4 Americans are infected with HSV. Cell-mediated immune deficiency rather than antibody synthesis is associated with increased incidence of disseminated disease caused by HSV. It is likely that cell-mediated effector mechanisms are more important for preventing the spread of infections. Recurrent localized herpetic lesions can occur in the presence of high antiviral antibody titers. Despite this fact, antibodies are important. Many interrelated issues occur between cell-mediated immunity and the humoral immune response that regulate immediate antimicrobial effector responses.

It has been suggested by studies on protective immunity to HSV infections that the envelope glycoprotein antigens have the most likely potential to be protective. However, it has been difficult to predict which antigens are most important in inducing protective cell-mediated responses. Some of the viral glycoproteins expressed by HSV may not only induce immune responses but also modulate effector mechanisms in ways that have not been precisely defined. Immune responses to viral antigens can, in some instances, cause as much or more damage in affected tissues as the cytopathology associated with viral replication.

Live attenuated as well as subunit HSV vaccines have been studied. The disadvantage of live vaccines is that even an attenuated HSV strains can establish a latent infection. The study of subunit vaccines revolves around the myriad of viral proteins, which is the best immunogen for protective immunity and methods to present them to the host. Therefore, the promise of an effective vaccine is not immediately apparent.

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