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Science 7 March 1997:
Vol. 275. no. 5305, pp. 1393 - 0
DOI: 10.1126/science.275.5305.1393h
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A consequence of infection with human immunodeficiency virus-type 1 (HIV-1) is chronic hyperactivation of the immune system, a state that maintains infection because HIV-1 cannot infect resting T cells. Ott et al. (p. 1481) show that infection of peripheral human blood leukocytes in vitro with HIV-1-stimulated production of interleukin-2 (IL-2) when the cells were activated by T cells through the CD3 and CD28 receptors. Secreted IL-2 could cause noninfected cells to be more responsive toward activation in confined environments such as the lymph nodes. The same IL-2 response occurred in cells costimulated by CD3 and CD28 that expressed the HIV-1 transcriptional activator Tat; the second exon of Tat interacts with the CD28 pathway to stimulate IL-2 transcription.




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Science. ISSN 0036-8075 (print), 1095-9203 (online)