研究显示基因变异令艾滋病病毒危害减弱
某些人携带的基因能够迫使艾滋病病毒发生变异，而变弱的病毒在传播给他人之后，其危害性会减弱。
发表在美国《公共科学图书馆病原卷》杂志上的研究报告说：“有些人所携带的ＨＬＡ基因能够迫使艾滋病病毒允许自身出现破坏复制能力的变异。”
艾滋病病毒会攻击人的免疫细胞。与其他病毒一样，它不能自我复制，而必须劫持一个细胞，把它变成一个病毒工厂。艾滋病病毒要完成这个任务时必须避开一些基因，比如一种叫做ＨＬＡ的免疫基因。
南非开普敦大学艾滋病专家卡罗琳·威廉森说，变弱了的病毒使得这些人的发病进程放慢了。而且这些弱化的病毒在传播给其他人之后也会有相同的表现，即使那些人并不具有保护性的ＨＬＡ基因。“这一研究表明，如果你感染的病毒带有与复制能力弱相关的基因特征，那么你的生存几率就会大一些”。
南非的科学家跟踪研究了２１名女性，她们都是在最近感染了弱化的艾滋病病毒，而自身又不具有保护作用的ＨＬＡ基因。研究发现，比起那些感染了未发生变异的艾滋病病毒的人，这些女性体内的艾滋病病毒水平要低得多。
威廉森说：“很可能这些不具有ＨＬＡ基因的人是从具有这种基因的人那里传染的病毒。”
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PLoS Pathogens online
Transmission of HIV-1 CTL Escape Variants Provides HLA-Mismatched Recipients with a Survival Advantage
1 Institute of Infectious Diseases and Molecular Medicine, Division of Medical Virology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa2 Centre for the AIDS Programme of Research in South Africa, University of Kwa-Zulu Natal, Durban, South Africa3 National Institute for Communicable Diseases, Johannesburg, South Africa4 South African National Bioinformatics Institute, University of the Western Cape, Cape Town, South Africa
Abstract
One of the most important genetic factors known to affect the rate of disease progression in HIV-infected individuals is the genotype at the Class I Human Leukocyte Antigen (HLA) locus, which determines the HIV peptides targeted by cytotoxic T-lymphocytes (CTLs). Individuals with HLA-B*57 or B*5801 alleles, for example, target functionally important parts of the Gag protein. Mutants that escape these CTL responses may have lower fitness than the wild-type and can be associated with slower disease progression. Transmission of the escape variant to individuals without these HLA alleles is associated with rapid reversion to wild-type. However, the question of whether infection with an escape mutant offers an advantage to newly infected hosts has not been addressed. Here we investigate the relationship between the genotypes of transmitted viruses and prognostic markers of disease progression and show that infection with HLA-B*57/B*5801 escape mutants is associated with lower viral load and higher CD4+ counts.
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