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  Herspes Simplex Virus

Herspes Simplex Virus:

Herpes Simplex viruses are tremendously widespread and are extremely cytolytic. The Herpes Simplex viruses are accountable for a spectrum of diseases ranging from gingevostomatitis to keratoconjuctivits, encephalitis, genital diseases and infections of latest born. They establish latent infections in trigeminal and sacral nerve ganglia, and recurrences are ordinary.

Types:

There are two kinds of HSV viz., HSV 1 (i.e., HHV type 1) and HSV 2 (i.e., HHV type 2).  The two viruses cross retort serologically. They vary in their mode of transmission. HSV 1 spreads by direct contact, generally including infected saliva or droplet spread from cases or carriers. HSV 2 is transmitted sexually or from maternal genital infection to latest born. This outcome in various clinical features of human infection.

Pathogenesis:

Primary infection is generally acquired in early childhood among 2 to 5 years of age. Primary HSV infections are generally mild; in fact most of them are asymptomatic. HSV is transmitted by the contact of a vulnerable person with an individual excreting virus. The virus enters mucosal surfaces or wrecked skin, multiplies locally with cell to cell spread. After that it invades local nerve endings and is transported to the dorsal root ganglia. Then further replication in the ganglia, latency is established. Antibodies might not prevent recurrences however can decrease the severity of the clinical disease. Cell mediated immunity is more significant in resistance and recovery from HSV infections. HSV diseases are more common and rigorous in AIDS patients. Usually HSV 1 generates ‘above the waist’ and HSV 2 ‘underneath the waist’ lesions however the rule is not absolute. HSV 2 infection confers few protections against HSV 1 although not vice-versa.

Latent infection:

Following asymptomatic or symptomatic primary infection, virus resides in latently infected ganglia in a non-replicating situation for the life of the host. Appropriate provocative stimuli such as fever, stress, and exposure to UV and axonal injury can reactivate the virus from the latent state; the virus is transported back to the peripheral place and replication proceeds at the skin or mucous membranes.

 

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