Stewart G T
Emeritus Professor of Public Health, University of Glasgow, UK.
Genetica. 1995;95(1-3):173-93. doi: 10.1007/BF01435009.
Epidemiologically, the Acquired Immune Deficiency Syndrome, AIDS, is transmitted and distributed in the USA and Europe almost entirely in well-defined subsets of populations engaging in, or subjected to, the effects of behaviours which carry high risks of genital and systemic infections. The persons predominantly affected are those engaging in promiscuous homosexual and bisexual activity, regular use of addictive drugs, and their sexual and recreational partners. In such persons and in subsets of populations with corresponding life-styles, the risk of AIDS increases by orders of magnitude. Because of continuity of risk behaviour and of associated indicator infections, the incidence of AIDS over 3-5 year periods is predictable to within 10% of actual totals of registered cases in the USA and UK. Secondary transmission of AIDS beyond these groups is minimal or, in many locations, absent. There is no indication of appreciable spread by heterosexual transmission to the general population. The Human Immunodeficiency Virus, HIV, is transmissible to some extent in general populations, and more so among promiscuous persons. It may cause viraemia, lymphadenopathy and latent infection (HIV disease) in anyone. In persons engaging in risk behaviours which themselves alter or suppress immune responses, it can interact with MHC, antibodies to other organisms and to semen, and other allogenic antigens to initiate a programmed death of CD4 lymphocytes and other defensive cells, as in graft-host rejections. This occurs also in haemophiliacs receiving transfusions of blood products, and is more pronounced in persons with reactive HLA haplotypes. The susceptibility of particular subsets of populations to AIDS is thereby largely explained. But these changes occur in the absence of HIV, and so do Kaposi's sarcoma, lymphadenopathies and opportunistic infections which are regarded as main indicators of AIDS. The hypothesis that HIV-1 can do all this by itself and thereby cause AIDS is falsifiable on biological as well as epidemiological grounds. An alternative hypothesis is proposed, linking the incidence of AIDS to the evolution of contemporary risk behaviour in particular communities and locations in the USA, UK and probably in most of Europe. It does not pretend to explain the reported incidence of AIDS in Africa and other developing regions where data are insufficient to provide validation of the pattern of disease and contributory variables. The immediate, practical implication of this alternative hypothesis is that existing programmes for the control of AIDS are wrongly orientated, extremely wasteful of effort and expenditure, and in some respects harmful.
从流行病学角度看，获得性免疫缺陷综合征（艾滋病）在美国和欧洲的传播与分布几乎完全集中在从事或遭受具有高生殖器和全身感染风险行为影响的特定人群亚组中。主要受影响的人群是那些从事滥交的同性恋和双性恋活动、经常使用成瘾性药物的人及其性伴侣和娱乐伙伴。在这些人和具有相应生活方式的人群亚组中，感染艾滋病的风险会增加几个数量级。由于风险行为和相关指标感染的持续性，在美国和英国，3至5年期间艾滋病的发病率预计在登记病例实际总数的10%以内。艾滋病在这些群体之外的二次传播极少，或者在许多地区根本不存在。没有迹象表明艾滋病会通过异性传播大量扩散到普通人群中。人类免疫缺陷病毒（HIV）在普通人群中会有一定程度的传播，在滥交人群中传播得更厉害。它可能在任何人身上引起病毒血症、淋巴结病和潜伏感染（HIV病）。在从事会改变或抑制免疫反应的风险行为的人群中，它可以与主要组织相容性复合体（MHC）、针对其他生物体和精液的抗体以及其他同种异体抗原相互作用，引发CD4淋巴细胞和其他防御细胞的程序性死亡，就像在移植物抗宿主排斥反应中一样。这种情况也发生在接受血液制品输血的血友病患者身上，在具有反应性人类白细胞抗原（HLA）单倍型的人中更为明显。由此很大程度上解释了特定人群亚组对艾滋病的易感性。但这些变化在没有HIV的情况下也会发生，卡波西肉瘤、淋巴结病和机会性感染也是如此，而这些被视为艾滋病的主要指标。关于HIV - 1自身就能做到这一切并从而导致艾滋病的假说，在生物学和流行病学方面都可以被证伪。本文提出了另一种假说，将艾滋病的发病率与美国、英国以及可能欧洲大部分地区特定社区和地点当代风险行为的演变联系起来。它并不试图解释非洲和其他发展中地区报告的艾滋病发病率，因为在这些地区，数据不足以证实疾病模式和相关变量。这一替代假说的直接实际意义在于，现有的艾滋病控制项目方向错误，极度浪费精力和开支，并且在某些方面是有害的。
