An Outbreak of Community-AcquiredPneumocystis cariniiPneumonia

Abstract

Eleven cases of community-acquired Pneumocystis carinii pneumonia occurred between 1979 and 1981 and prompted clinical and immunologic evaluation of the patients. Young men who were drug abusers (seven patients), homosexuals (six), or both (two) presented with pneumonia. Immunologic testing revealed that absolute lymphocyte counts, T-cell counts, and lymphocyte proliferation were depressed, and that humoral immunity was intact. Of the 11 patients, one was found to have Kaposi's sarcoma, and another had angioimmunoblastic lymphadenopathy. Eight patients died. In the remaining three, no diagnosis of an immunosuppressive disease was established, despite persistence of immune defects. These cases of pneumocystosis suggest the importance of cell-mediated immune function in the defense against P. carinii. The occurrence of this infection among drug abusers and homosexuals indicates that these groups may be at high risk for this infection.

Transforming growth factor beta and noncytopathic mechanisms of immunodeficiency in human immunodeficiency virus infection.

“…TGF(3 inhibits the response of T lymphocytes to "recall antigens" such as TT or PPD, a response that is predominantly a function of CD4+ T cells (25). PBMCs from HIV+ donors have impaired proliferation after TT and PPD stimulation (26). Thus these in vitro systems were used to investigate the role of TGFI3 in the cellular immune responses in HIV infection.…”

Immediate-early gene region of human cytomegalovirus trans-activates the promoter of human immunodeficiency virus.

“…Biologicallyj interactions between the causative agent of AIDS and HCMV have been suggested even before the discovery of HIV. In early publications describing AIDS, HCMV was postulated as a possible causative agent (3,18). Not only may HIV infection reactivate HCMV through immunosuppression, but HCMV might directly affect the course of HIV infection.…”

Mechanisms of B cell activation in patients with acquired immunodeficiency syndrome and related disorders. Contribution of antibody-producing B cells, of Epstein-Barr virus-infected B cells, and of immunoglobulin production induced by human T cell lymphotropic virus, type III/lymphadenopathy-associated virus.

“…characterized by opportunistic infections and the development of Kaposi's sarcoma (1)(2)(3). It has since been learned that this disorder is caused by infection with a newly discovered human retrovirus, human T cell lymphotropic virus, type III (HTLV-III), also known as lymphadenopathy-associated virus (LAV), which preferentially infects and destroys T cells bearing the OKT4 antigen (4)(5)(6).…”