DNA banking in epidemiologic studies.
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Biomedical subjects
Publications and source records attributed to K C Sanderlin.
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Human herpesvirus-6 (HHV-6) and human immunodeficiency virus (HIV) are both tropic for CD4+ lymphocytes. To determine whether HHV-6 infection affects the susceptibility to or the course of HIV infection, HHV-6 titers were measured by an anticomplement immunofluorescence assay in serum of three groups of homosexual or bisexual men: (1) those with AIDS (n = 78), (2) those with HIV-associated lymphadenopathy (LAS; n = 81), and (3) those who were HIV-seronegative (n = 55). Early and late serum samples were available for 45 men with LAS (median interval 49 months). Men with early LAS did not differ from HIV-seronegative men in either the percentage that were HHV-6-seropositive or in the distribution of titers. There was a significantly lower percentage of seropositives in AIDS patients than in the other two groups (P less than .01). LAS patients who progressed to AIDS did not differ in percentage seropositivity or distribution of titers from nonprogressors. HHV-6 titers tended to decrease over time. HHV-6 titers late in LAS were similar to those in AIDS patients. These findings suggest that it is unlikely that previous exposure to HHV-6 either predisposes to or affects the course of HIV infection.
Experiments performed to optimize the growth conditions of HHV-6(Z29) revealed that the virus grows best in phytohemagglutinin-stimulated umbilical cord blood lymphocytes (CBL) cultured in media containing 32 units/ml interleukin-2 and 0.01 mg/ml hydrocortisone. The titer of maternal antibody in the plasma of the cord blood cells does not affect the ability of the cells to support virus growth. DEAE-dextran and polybrene do not increase virus growth in umbilical cord blood lymphocytes. Phorbol myristate acetate abolishes virus growth. The HHV-6(Z29) growth cycle in CBL was approximately 5 days; capsids were not seen before day 3, and mature virions were not seen before day 5.
Microtubule-like structures have been observed ultrastructurally in BHK-21/4 cells infected with herpes simplex virus type 2 (HSV-2) but not in cells infected with herpes simplex virus type 1 (HSV-1). BHK-21/4 cells were infected with two known strains of HSV-2 and one known strain of HSV-1, as well as with vesicular fluid from 50 clinical isolates (47 perioral, two penile, and one from the leg) in an examination of the accuracy of electron microscopy for differentiation between clinical isolates of HSV-1 and HSV-2. Cells infected with the known strains of HSV-2 or with material from the genital or leg lesions demonstrated microtubule-like structures. Cells infected by a known strain of HSV-1 or by material from perioral lesions did not show evidence of microtubule-like structures. Typing by indirect hemagglutination of these same 50 clinical isolates gave identical results.
Four fatal cases of neonatal herpes simplex infection occurred during a two-month period in the perinatal intensive care unit of a hospital. Virus isolation or serologic studies, or both, implicated herpesvirus hominis type 2 in all four cases. Three of the infants developed symptoms in the first week of life and were probably infected in utero or at delivery. The fourth infant did not develop signs of illness until age 6 weeks, an interval much longer than that expected with disease acquired at birth. An epidemiologic investigation indicated that the most likely source of this fourth infant's herpes infection was by indirect contact with one of the other three infected neonates. Nosocomial spread of herpes simplex virus within a hospital nursery, although uncommon, may pose an added risk to the newborn infant if nursery techniques among infants are compromised.