Replication of herpes simplex virus in human T lymphocytes: characterization of the viral target cell

Herpes simplex virus (HSV) replicated in mitogen-stimulated human T cells. Virus replication was obtained in highly enriched mitogen-stimulated T cells of the OKT 3+, OKT 4+, or OKT 8+ subtype, in stimulated B cells, and in macrophages precultured for 7 days. In contrast, no virus replication was ob...

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Veröffentlicht in:The Journal of immunology (1950) 1984-02, Vol.132 (2), p.914-919
Hauptverfasser: Braun, RW, Teute, HK, Kirchner, H, Munk, K
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Sprache:eng
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Zusammenfassung:Herpes simplex virus (HSV) replicated in mitogen-stimulated human T cells. Virus replication was obtained in highly enriched mitogen-stimulated T cells of the OKT 3+, OKT 4+, or OKT 8+ subtype, in stimulated B cells, and in macrophages precultured for 7 days. In contrast, no virus replication was obtained in unstimulated T or B cells, in macrophages grown in culture for 1 day, in Null/NK cells, or in granulocytes. Infectious center assays revealed that below 1% of the infected T cell subpopulations supported virus replication, whereas up to 42% of infected B cells and 80% of macrophages cultured for 1 wk were able to replicate HSV. By indirect double immunofluorescence studies, complement-mediated mass cytolysis, and positive selection experiments, it was shown that only T cells expressing Ia antigen actively replicated the virus. T cells activated in the mixed lymphocyte culture and with UV-inactivated HSV were also susceptible to HSV infection. Several human leukocyte cell lines were tested for their ability to support virus replication and were tested for a correlation with the expression of Ia antigen. Only cell lines expressing Ia antigen on more than about 5% of the total population produced new progeny virus. Ia-expressing T cells that spontaneously replicated HSV without any mitogenic prestimulation were found to occur in variable numbers in human cord blood. It is suggested, that such T cells, permissive for HSV replication, might contribute to an outspread of viral infection in vivo.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.132.2.914