subject: Nature Of Hsv Infection [print this page] Susceptible individuals develop primary infection after their first exposure to either HSV-1 or HSV-2. A recurrence of HSV is known as recurrent infection. Initial infection occurs when an individual with preexisting antibodies to one type of HSV experiences a first infection with the opposite virus type. Reinfection with a different strain of HSV can occur, albeit extremely uncommonly in healthy hosts, and is called exogenous reinfection.
The histopathologic characteristics of a primary or recurrent HSV infection reflect virus-mediated cellular death and associated inflammatory response. Viral infection induces ballooning of cells, with condensed chromatin within the nuclei of the cells, followed by degeneration of the cellular nuclei, generally within the parabasal and intermediate cells of the epithelium.
Infected cells lose intact plasma membranes and form multinucleated giant cells. When cell lysis occurs, a vesicular fluid containing large quantities of virus appears between the epidermal and dermal layers. The vesicular fluid contains cellular debris, inflammatory cells, and, often, multinucleated giant cells.
In dermal substructures there is an intense inflammatory response, usually in the corium of the skin and more intense with primary infection than with recurrent infection. When healing occurs, the vesicular fluid becomes pustular, with the recruitment of inflammatory cells and subsequent formation of scabs.
Scarring is uncommon. When mucous membranes are involved, the vesicles are replaced by shallow ulcers. The pathogenesis of human HSV disease depends on intimate, personal contact between a susceptible individual and an individual who is excreting HSV. Virus must come in contact with mucosal surfaces or abraded skin for infection to be initiated.
With viral replication at the site of infection, either an intact virion or, more simply, the capsid is transported retrograde by neurons to the dorsal root ganglia where, after another round of viral replication, latency is established. Although replication sometimes leads to disease and infrequently results in life-threatening infection, the predominant host-virus interaction leads to the establishment of latency.
After latency is established, a stimulus that can produce viral reactivation can cause the virus to again appear as skin vesicles or mucosal ulcers. Infection with HSV-1 generally occurs in the oropharyngeal mucosa. The trigeminal ganglion becomes colonized and harbors latent virus. Acquisition of HSV-2 results in infection at genital, perigenital, or anal skin sites, with seeding of the sacral ganglia.
The natural history of HSV infections is influenced by both specific and nonspecific host defense mechanisms. With the appearance of nonspecific inflammatory changes that parallel a peak in viral replication, specific host responses can be quantitated but vary between animal systems. Host responses in humans are delayed, developing approximately 7-10 days later.
Neutralizing and antibodydependent cellular cytotoxic antibodies generally appear 2-6 weeks after infection and persist for the lifetime of the host. Immunoblot and immunoprecipitation antibody responses have defined host response to infected cell polypeptides and have been correlated with the development of neutralizing antibodies.
Reactivity of lymphocyte blastogenesis develops within 4-6 weeks after the onset of infection, and sometimes as early as 2 weeks after infection. With recurrences, boosts in blastogenic responses can be defined; however, these responses decrease in intensity with time. Nonspecific blastogenic responses do not correlate with a history of recurrences.
Humoral immunity does not prevent either recurrences or exogenous reinfection. Thus, it is not surprising that antibodies acquired transplacentally from mothers are not totally protective against infection in newborns. Transplacentally acquired neutralizing antibodies may either prevent infection or ameliorate disease in exposed newborns, as do antibody-dependent cell-mediated cytotoxic antibodies.
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