Keystone Symposium on HIV, March 28-April 3, Keystone, Colorado: more than one way to skin a virus: innate immune factors that suppress HIV replication
by Jo Ann Berg
Report from Keystone, March 2001
This year’s annual Keystone Symposium on HIV, held March 28 to April 3 in Keystone, Colorado, featured concurrent sessions on “AIDS Vaccines in the New Millennium” and “HIV Pathogenesis” (how the microbe causes disease).
Previous meetings on pathogenesis have emphasized the adaptive immune response: antibodies and CD8+ cytotoxic T lymphocytes (CTLs). The antibodies are specifically shaped to attach to and help eliminate free HIV particles in the body while the CTLs are specially selected and activated to kill HIV-infected cells. Antibodies to HIV have generally proven ineffective, and the CTL response wanes as HIV infection progresses. AIDS scientists are taking a renewed interest in the body’s first line of defence – the nonspecific, or innate, immune system. Fifteen years ago, Jay Levy’s laboratory at the University of California San Francisco observed that certain CD8+ T-cells active during HIV infection do not kill HIV-infected cells.1 They instead release a soluble factor or factors that render nearby CD4+ T-helper cells resistant to destruction by HIV.