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从20世纪80年代以来,科学家们一直在查明人类免疫缺陷病毒(human i mmunodeficiency virus,HI V)的致病机理。近年来人们发现:在原发HI V感染外周血CD4+T细胞的数量尚未出现改变时,肠道CD4+T细胞就已经开始丢失;即使进行高效抗逆转录病毒(highly active antiretroviral therapy,HAART)治疗,外周血CD4+T细胞开始恢复,病毒载量慢慢下降,这种情况依然存在。因此推测肠道是HI V的重要靶攻击部位。目前,研究发现,在原发HI V感染时,肠道归巢T细胞的自稳机制被首先打乱并持续存在,表现为特异性肠道归巢受体CCR9和整合素α4β7(Integrinα4β7)的显著性活化。随着T细胞的周转减少和HI V的高载量复制,导致机体的获得性免疫的完全崩溃,最终发展为艾滋病(acquiredi mmunodeficiency syndrome,AIDS)。
Since the 1980s, scientists have been investigating the pathogenesis of the human immunodeficiency virus (HI). In recent years, it has been found that intestinal CD4 + T cells have already begun to be lost when the number of CD4 + T cells in peripheral blood infected with primary HI V has not changed. Even with highly active antiretroviral therapy (HAART) Treatment, peripheral blood CD4 + T cells began to recover, the viral load decreased slowly, this situation still exists. Therefore speculated that the intestine is an important HI V target site of attack. At present, the study found that in the primary HIV infection, the self-stabilizing mechanism of intestinal homing T cells was first disrupted and persisted, manifested as specific intestinal homing receptors CCR9 and integrinα4β7 (Integrinα4β7) Significant activation. As T cell turnover decreases and HI V high-load replication leads to a complete collapse of the body’s adaptive immunity, eventually AIDS (Acquired M mmodeficiency syndrome, AIDS).