02087nas a2200361   4500000000100000008004100001260001600042653001800058653003900076653001200115653002200127653003300149653001600182653000800198653001900206653001100225653001800236653002100254653002300275653002800298653003300326653003900359653000900398653002500407653001900432653001800451100001800469245005600487300001100543490000700554520115000561022001401711       2002                            d  c2002 May 0610aAIDS Vaccines10aAcquired Immunodeficiency Syndrome10aAnimals10aAntibodies, Viral10aCytopathogenic Effect, Viral10aDrug Design10aHIV10aHIV Infections10aHumans10aImmune System10aImmunocompetence10aImmunologic Memory10aImmunotherapy, Adoptive10aLymphocytic Choriomeningitis10aLymphocytic choriomeningitis virus10aMice10aT-Lymphocyte Subsets10aViral Vaccines10aVirus Latency1 aZinkernagel R00aImmunity, immunopathology and vaccines against HIV?  a1913-70 v203 a<p>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.</p>  a0264-410X