Ondoa Pascale, Vereecken Chris, Fransen Katrien, Colebunders Robert, van der Groen Guido, Heeney Jonathan L, Kestens Luc
Department of Microbiology, Institute of Tropical Medicine, Antwerp, Belgium.
J Med Virol. 2003 Mar;69(3):297-305. doi: 10.1002/jmv.10289.
This study was undertaken to explain why chimpanzees infected with HIV-1 (human immunodeficiency virus type 1) or SIV(cpz) (simian immunodeficiency virus of chimpanzee) are relatively resistant to AIDS (acquired immunodeficiency syndrome). The numbers of beta-chemokine-positive cells were compared between uninfected and infected humans and chimpanzees using three-color cytofluorometry. In humans, the percentage of beta-chemokine-positive cells was significantly higher in CD8(+) T and natural killer (NK) cells than in CD4(+) T cells in both uninfected and HIV-1-infected individuals. In the presence of HIV-1 infection, however, both CD8(+) and CD4(+) T cell subsets contained significantly more beta-chemokine-positive cells than in the absence of infection. Interestingly, in chimpanzees two important differences were noted. First, their percentage of beta-chemokine-positive CD8(+) T and NK cells was significantly higher than in uninfected humans. Second, in contrast to humans, infection with either HIV-1 or with SIV(cpz) was not associated with increased numbers of beta-chemokine-positive cells. These results indicate that: constitutive high levels of intracellular beta-chemokines in chimpanzees' CD8 lymphocytes and NK cells do not necessarily correspond to lower levels of virus replication during the chronic phase of infection; and increased percentages of beta-chemokine-positive cells in HIV-infection are not a correlate of disease resistance. The data suggest that neither pre-nor post-exposure levels of intracellular beta-chemokines are correlated with the subsequent control of disease progression.
本研究旨在解释感染1型人类免疫缺陷病毒（HIV-1）或黑猩猩猿猴免疫缺陷病毒（SIV(cpz)）的黑猩猩为何对获得性免疫缺陷综合征（AIDS）具有相对抗性。使用三色细胞荧光测定法比较了未感染和感染的人类及黑猩猩体内β趋化因子阳性细胞的数量。在人类中，无论是未感染个体还是感染HIV-1的个体，CD8(+) T细胞和自然杀伤（NK）细胞中β趋化因子阳性细胞的百分比均显著高于CD4(+) T细胞。然而，在感染HIV-1的情况下，CD8(+)和CD4(+) T细胞亚群中β趋化因子阳性细胞的数量均显著高于未感染时。有趣的是，在黑猩猩中发现了两个重要差异。第一，它们的β趋化因子阳性CD8(+) T细胞和NK细胞的百分比显著高于未感染的人类。第二，与人类不同，感染HIV-1或SIV(cpz)均未导致β趋化因子阳性细胞数量增加。这些结果表明：黑猩猩CD8淋巴细胞和NK细胞中细胞内β趋化因子的组成性高水平不一定对应于感染慢性期较低的病毒复制水平；HIV感染中β趋化因子阳性细胞百分比的增加与疾病抗性无关。数据表明，细胞内β趋化因子的暴露前和暴露后水平均与随后疾病进展的控制无关。
