Zinkernagel Rolf M
Institute for Experimental Immunology, University Hospital, Schmelzbergstrasse 12, CH-8091 Zurich, Switzerland.
Vaccine. 2002 May 6;20(15):1913-7. doi: 10.1016/s0264-410x(02)00066-x.
Immunity and immunopathology of HIV infections leading to AIDS are reviewed from an evolutionary point of view. Accordingly infectious agents and host defences have co-evolved to reach balanced states where virus and host survive. While HIV has not quite yet reached an optimal balance, tuberculosis (TB), leprosy, HBV, HCV in humans or lymphocytic choriomeningitis virus (LCMV) in mice have successfully established persistence. These non- or poorly-cytopathic infections infect the next host usually before or at birth while hosts are immunoincompetent. They also infect immunocompetent hosts to persist at low levels concomitant with an ongoing T and B cell immune response that is repeatedly triggered by latent or persistent infection of extralymphatic or lymphatic host cells. This infectious or infection-immunity is the basis for cellular immunoprotection by antigen activated T cells. Because we cannot imitate this infection-immunity long-term and cannot build polyspecific vaccine combinations covering all possible neutralising variants yet, vaccines against TB, leprosy, HCV and HIV only protect transiently and incompletely.
从进化的角度对导致艾滋病的HIV感染的免疫和免疫病理学进行了综述。相应地，感染因子和宿主防御机制共同进化以达到病毒和宿主都能存活的平衡状态。虽然HIV尚未完全达到最佳平衡，但人类的结核病（TB）、麻风病、乙肝病毒（HBV）、丙肝病毒（HCV）或小鼠的淋巴细胞性脉络丛脑膜炎病毒（LCMV）已成功建立持续性感染。这些非细胞病变或低细胞病变感染通常在宿主免疫功能不全时，于出生前或出生时感染下一个宿主。它们也会感染免疫功能正常的宿主，并在低水平持续存在，同时伴随着由淋巴外或淋巴宿主细胞的潜伏或持续感染反复触发的T细胞和B细胞免疫反应。这种感染或感染免疫是抗原激活的T细胞进行细胞免疫保护的基础。由于我们无法长期模拟这种感染免疫，也无法构建涵盖所有可能中和变体的多特异性疫苗组合，因此针对结核病、麻风病、丙肝病毒和HIV的疫苗只能提供短暂且不完全的保护。
