In the early 1980s, homosexual men in the San Francisco area began contracting and dying from unusual infections in the setting of immunodeficiency characterized by specific depletion of a subset of white blood cells, known as helper T cells or CD4+ T cells. This was the initial presentation of the acquired immunodeficiency syndrome or AIDS. Within a few years, the human immunodeficiency virus (HIV) was discovered as the etiologic agent for AIDS: those who were infected with HIV would ultimately develop AIDS. Since that time, almost thirty years later, the number of individuals who are infected with HIV has skyrocketed.

According to the World Health Organization, in 2007 there were 33 million people infected with HIV worldwide (over 1 million in the United States and 22 million in Sub-Saharan Africa), with 2 million of these HIV-positive individuals losing their lives to AIDS (over 20,000 in the United States and 1.5 million in Sub-Saharan Africa).

Scientists have characterized HIV at the molecular level and have used this information to develop drugs to treat HIV infection, but the fundamental problem caused by HIV—that is, how HIV causes AlIDS—has not yet been solved. HIV infection depletes the body of a subset of white blood cell cells known as CD4+ or “helper” T cells. Since helper T cells play an important role in the immune system’s ability to ward off infection, gradual depletion of these cells eventually leaves the HIV+ individual susceptible to opportunistic infections that are normally harmless to people with healthy immune systems
(this is the definition of AIDS). It is possible that if the mechanism for the depletion of helper T cells during HIV infection were known, it could be therapeutically targeted, transforming HIV from a lethal infection to a harmless nuisance.


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