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Human immunodeficiency virus type 1-specific cytotoxic T lymphocytes (CTL), virus load, and CD4 T cell loss: evidence supporting a protective role for CTL in vivo.
Greenough, T C; Brettler, D B; Somasundaran, M; Panicali, D L; Sullivan, J L.
Afiliación
  • Greenough TC; Program in Molecular Medicine, University of Massachusetts Medical School, Medical Center of Central Massachusetts-Memorial Hospital, Worcester 01605, USA.
J Infect Dis ; 176(1): 118-25, 1997 Jul.
Article en En | MEDLINE | ID: mdl-9207357
The relationships between primary human immunodeficiency virus type 1 (HIV-1) Gag-specific cytotoxic T lymphocyte (CTL) frequency, virus load, and CD4 T cell loss were evaluated in a group of 46 HIV-1-infected persons with hemophilia. Freshly isolated peripheral blood mononuclear cells in limiting dilution assays were used to measure HIV-1 Gag-specific CTL frequencies. Concurrent measurements of virus load and lymphocyte surface markers were obtained. No correlation between Gag-specific CTL frequency and concurrent CD4 cell count was observed. A significant inverse relationship was observed between HIV-1 Gag-specific CTL frequency and provirus load as measured by polymerase chain reaction. Subjects with higher CTL frequencies were found to have more stable CD4 cell counts over time. These results provide additional evidence to support the concept that the predominant role of this virus-specific cellular immune response is to limit viral replication and CD4 cell loss in HIV-1 infection.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos T Citotóxicos / VIH-1 Límite: Adolescent / Adult / Child / Humans / Male / Middle aged Idioma: En Revista: J Infect Dis Año: 1997 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos T Citotóxicos / VIH-1 Límite: Adolescent / Adult / Child / Humans / Male / Middle aged Idioma: En Revista: J Infect Dis Año: 1997 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos