An acutely lethal simian immunodeficiency virus stimulates expansion of V beta 7- and V beta 14-expressing T lymphocytes.
AUTOR(ES)
Chen, Z W
RESUMO
SIVsmmPBj14, a variant simian immunodeficiency virus isolated from a pig-tailed macaque, stimulates the proliferation of macaque T lymphocytes in vitro and induces an acutely lethal disease in macaques characterized, in part, by lymphadenopathy and splenomegaly. To determine whether SIVsmmPBj14 exhibits superantigen-like activity, in vitro and in vivo studies of T-cell receptor V beta repertoire were undertaken using PCR-based quantitative methods. Whereas in vitro phytohemagglutinin stimulation of macaque peripheral blood lymphocytes did not cause a perturbation of T-cell receptor V beta repertoire, SIVsmmPBj14 stimulated the expansion of both CD4+ and CD8+ T-lymphocyte subpopulations expressing the V beta 7 and V beta 14 gene families. Such V beta 7 and V beta 14 expansions could be confirmed by a multiple RNase protection assay. Furthermore, the expansion of the same lymphocyte subpopulations was also detected in peripheral blood lymphocytes and lymph node cells of virus-infected macaques. These observations suggest that SIVsmmPBj14-mediated V beta expansion may contribute to the induction of an acutely lethal disease in macaques.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=44429Documentos Relacionados
- Replication of an acutely lethal simian immunodeficiency virus activates and induces proliferation of lymphocytes.
- Divergent viral superantigens delete V beta 5+ T lymphocytes.
- Three epitopic peptides of the simian immunodeficiency virus Nef protein recognized by macaque cytolytic T lymphocytes.
- Selective expansion of T cells expressing T-cell receptor variable regions V beta 2 and V beta 8 in Kawasaki disease.
- Predominant use of a T-cell receptor V beta gene family in simian immunodeficiency virus Gag-specific cytotoxic T lymphocytes in a rhesus monkey.