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Disease emergence often involves the introduction of a familiar microbial agent into a novel ecologic niche or the evolution of a previously unrecognized microorganism in what had ostensibly been a stable environment. So accustomed are we to emergence brought on by changes in an agent or its environment that we overlook effects of the third force of causality—the host. The easy justification for our relative indifference to the contributions of the host has been that host characteristics , especially those under genetic regulation , have less potential for rapid, epidemiologically significant evolution; moreover, the genetic mechanisms of host response have been too poorly elucidated to permit rational manipulation. The emergence of human immunodeficiency virus (HIV), however, has been different. HIV has " emerged " so masterfully by exploiting fundamental vulnerabilities in the immune system of primates that contributions of host immunity cannot be ignored. The virus has apparently evolved from its simian cousins toward a form that is extraordinarily well adapted to humans in several ways: 1) it rapidly replicates, ensuring high mutation rates within an individual host; 2) it is readily transmissible from person to person in the absence of an animal vector; and 3) because it is not invariably lethal before the age span for most human reproduction, evolutionary pressure toward radical change, attenuation, or disappearance from the population is not strong. The enormous epidemiologic implications of these basic facts have become obvious during the decade and a half of our struggle against the virus. We cannot control it by manipulating its macroenvironment as we might a parasite carried by a vector or waterborne virus. Interrupting local transmission by setting up psychosocial or mechanical barriers has limited potential. Despite the recent highly encouraging advances in antiretroviral therapy, direct and complete phar-macologic or immunologic eradication of the virus worldwide is still an untenable prospect. So we have little choice but to search for biologic strategies that reliably interdict the host-virus relationship; to accomplish that will require insight into the fundamental mechanisms of that interaction—knowledge at the level of viral and host genetics. Indeed, modulating genetically determined features of the immune response to the virus may represent the best hope for its ultimate conquest. Recent breakthroughs have accelerated the accumulation of the knowledge necessary to accomplish that aim. In this issue of Emerging Infectious Diseases, the review of current information by McNicholl and colleagues about the genetics of virus-host interaction …

Host Genes and HIV Infection: Implications and Applications