Hypothesis: absence of graft-versus-host disease in AIDS is a consequence of HIV-1 infection of CD4+ T cells.
We hypothesize that graft-versus-host disease (GVHD) does not occur in HIV-1-infected subjects because graft cells (or host cells recognizing antigenic differences in other host cells) mediating the graft-versus-host reaction are CD4+ T cells that become infected with HIV-1 and are rendered immunologically incompetent. GVHD has been documented in all forms of genetic or acquired severe T-cell deficiencies, except in patients with AIDS. Its striking absence in multiply transfused patients suggests that HIV-1 infection prevents its occurrence. We propose the following sequence of events. Transfusion of immunocompetent cells into HIV-1-infected subjects results in an in vivo allogeneic cell response. The activated CD4+ T cells become infected with HIV-1 and are rendered immunologically incompetent or are destroyed and cannot, therefore, initiate GVHD. Suggestions have been made by others that a GVHD-like mechanism results from HIV-1 infection and is a potentially important factor in the pathogenesis of AIDS and that, therefore, immunosuppressive therapy should be evaluated in HIV-infected patients. However, since most immunosuppressive therapy cannot be targeted to a specific functional immune cell, and since enhancement of immunity is more likely to prevent many of the complications of HIV-1 infection that ultimately cause death, treatment of HIV-1-infected patients should be directed toward improving immune function rather than immunosuppression.
Ammann
A J
AJ
Ariel Project for the Prevention of HIV Transmission from Mother to Infant, Novato, CA 94949.
D000163:Acquired Immunodeficiency Syndrome / Q000150:complications* / Q000209:etiology / Q000276:immunology; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000382:microbiology*; D006086:Graft vs Host Disease / Q000276:immunology*; D015497:HIV-1 / Q000502:physiology*; D006801:Humans