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The herpesvirus family contains herpes simplex virus (HSV) types 1 and 2, varicella-zoster virus, cytomegalovirus, Epstein-Barr virus, and human herpesviruses 6 through 8.
HSV types 1 and 2 produce infections that are expressed in various clinical manifestations ranging from mild stomatitis to disseminated and fatal disease. The more common clinical conditions include gingivostomatitis, keratitis, encephalitis, vesicular skin eruptions, aseptic meningitis, neonatal herpes, genital tract infections, and disseminated primary infection. Infections with HSV types 1 and 2 can differ significantly in their clinical manifestations and severity. HSV type 1 is closely associated with infections of the mouth and lips, although genital infections can be common in some populations. HSV type 2 is the cause of the majority of urogenital infections and is almost exclusively found in adults.
Aiding in the diagnosis of infection with herpes simplex virus
A positive result (ie, the presence of IgM class herpes simplex virus [HSV] 1 and/or 2 antibodies) indicates recent infection. The presence of HSV 1 and/or 2 antibodies may indicate a primary or reactivated infection, but cannot distinguish between them. Specimens with positive results are automatically tested for IgM antibodies by a second method (immunofluorescence assay [IFA]).
The continued presence or level of antibody cannot be used to determine the success or failure of therapy.
The prevalence of HSV IgM antibodies can vary depending on a number of factors such as age, gender, geographical location, socio-economic status, race, sexual behavior, testing method used, specimen collection and handling procedures, and the clinical and epidemiological history of individual patients.
A negative result does not necessarily rule out a primary or reactivated infection since specimens may have been collected too early in the course of disease, when antibodies have not yet reached detectable levels, or too late, after IgM levels have declined below detectable levels.
Results obtained with this assay serve only as an aid to diagnosis and should not be interpreted as diagnostic in themselves.
In pregnant women, this test should not be used as the sole criterion for the diagnosis of current herpes simplex infection. The presence of herpes simplex virus (HSV) should be demonstrated by molecular methods, which detect viral DNA (ie, LHSV / Herpes Simplex Virus [HSV], Molecular Detection, PCR), or by isolation of live virus (ie, viral culture).
The performance characteristics of this test have not been established for plasma, or neonates and infants.
Due to commonly shared antigens, infections with one type of HSV, in the presence of antibody to the other type, may produce an amnestic response with the level of the pre-existing antibody becoming higher than the antibody titer of the current infection. Definitive diagnosis of HSV type should be made by PCR.
Heterotypic IgM antibody responses may occur in patients infected with Epstein-Barr virus and give false-positive results in HSV1 and 2 IgM enzyme immunoassay tests. A heterotypic rise in anti-HSV antibody level may also be observed in a primary or reactivated varicella-zoster virus infection.
Since rheumatoid factor (RF) binds to IgG in immunocomplexes, false-positive results may arise in specimens with RF and specific IgG. False-negatives may arise due to specific IgG competing with specific IgM. The goat antihuman IgG in the specimen diluent diminishes RF interference and minimizes competing specific IgG in test specimens. The specimen diluent removes most (>95%) of the IgG at levels up to 1,400 mg/dL. Specimens with IgG levels >1,400 mg/dL should be interpreted with caution.
The prevalence of the analyte will affect the assay's predictive value.
Results from immunosuppressed patients should be interpreted with caution.
Negative (reported as reactive or negative)
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2. Brown ZA, Selke S, Zeh J, et al: The acquisition of herpes simplex virus during pregnancy. N Engl J Med 1997;337:509-515
3. Lafferty WE, Coombs RW, Benedetti J, et al: Recurrences after oral and genital herpes simplex infection. N Engl J Med 1987;316:1444-1449
4. Whitley RJ: Herpes simplex viruses. In Fields Virology. Vol.2. Second Edition. Edited by BN Fields, DM Knipe. New York, Raven Press, 1990, pp 1843-1887