HIV/AIDS患者KIR3DS1基因与部分环境因素对其疾病进展的影响

目的:探讨KIR3DS1基因及部分环境因素与人类免疫缺陷病毒(human immunodeficiency virus,HIV)-1感染者疾病进程的关系?方法:收集86例通过自愿咨询检测确认为HIV+患者的抗凝全血标本,采用聚合酶链反应-限制性片段长度多态性方法,检测其KIR3DS1基因,并进行问卷调查(调查内容包括人口学基本信息?临床表现?高危行为?是否接受抗病毒治疗等)收集部分环境因素信息?结果:Cox回归分析显示,风险比(RR)值为0.217(95%CI:0.098~0.480)?结论:抗病毒治疗可以延缓HIV-1感染者疾病进程,携带KIR3DS1基因可能延缓HIV-1感染者疾病进程?     

Early impairment of gut mucosal immunity in HIV-1-infected children

This study was performed in 27 HtV-1⁺ children to characterize the IgA hyperglobulinaemia observed in the serum during the course of HIV-l infection. By contrast with serum IgG, which increased very early, IgA elevation was related to the decrease of CD4⁺ cell percentage. It was demonstrated that IgAl subclass increased selectively. Secretory IgA (SIgA) and IgA and IgG activity to gliadin, bovine serum albumin (BSA) and at a lower level to casein could be detected in the serum at the early stages of HIV infection, but SIgA levels and IgA activity to gliadin further increased during the course of immunodeficiency. By contrast, IgA and IgG activity to tetanus toxoid did not change. These data demonstrate that the hyper IgA, closely related to the degree of immunodeficiency, could be due in part to a disturbance of the gut mucosal immune system. Moreover, impaired intestinal immunity seems to appear very early, and to progress during the course of paediatric HIV-l infection.     

Apoptotic neurons in brains from paediatric patients with HIV-I encephalitis and progressive encephalopathy

The pathogenesis of human immunodeficiency virus type 1 (HIV-1) associated dementia in adults involves neuronal loss from discrete areas of the neocortex and subcortical regions, but the mechanism for neuronal death is poorly understood. Gene-directed cell death resulting in apoptosis is thought to be a normal feature of neuronal development, but little is known about neuronal apoptosis in disease states. We investigated whether HIV-1 infection of the central nervous system is spatially associated with apoptosis of neurons. Using an in situ technique to identify newly cleaved 3'-OH ends of DNA as a marker for apoptosis, we demonstrate the presence of apoptotic neurons in cerebral cortex and basal ganglia of children that had HIV-1 encephalitis with progressive encephalopathy. Furthermore, an association was observed between the localization of apoptotic neurons and perivascular inflammatory cell infiltrates containing HIV-1 infected macrophages and multinucleated giant cells. Apoptotic neurons and p24–positive macrophages were observed infrequently in cerebral cortex and basal ganglia in children with HIV-1 infection without encephalitis or clinical encephalopathy. In nine control (HIV-1 negative) brains, ranging from the first post-natal month of life to 16.5 years of age, infrequent neuronal apoptosis was observed in three cases. These findings suggest that neuronal apoptosis is unlikely to be associated with post-natal development except in early post-natal germinal matrix, and that it may instead represent the end result of specific pathological processes, such as HIV-1 encephalitis.