The specific aims are to : 1. Determine the seroprevalence of HIV-1 and HTLV-I and HTLV-II co-infection in Hawaii. 2. Determine differences in clinical manifestation with co-infection as compared to single infections with HIV-1 or HTLV-I. 3. Determine differences in virologic and immunologic dynamics of each virus with co-infection. HTLV-I and HTLV-II are type C oncoviruses, members of the family Retroviridae. HTLV-I appears to be the etiologic agent of adult T-cell leukemia-lymphoma (ATLL). Virtually all cases of ATLL are seropositive for HTLV-1, and HTLV-I provirus is monoclonally integrated in leukemic cells. ATLL may present as a smoldering leukemia that is present for years or as a fulminant illness progressing to death within a few months. An AIDS wasting syndrome like disease has been reported in a patient with chronic ATL (3). Opportunistic infections are frequent in patients with ATLL. The spectrum of infectious agents is similar to that seen in AIDS, including Pneumocystitis carinii pneumonia, Cryptococcus neofonnans meningitis and candidal esophagitis. Immunity may also be impaired in HTLV-I infected persons in the absence of extensive malignant disease. The transmission pattern for HTLV-I mimics that of HIV- l. It is transmitted from mother to child by breast milk, by sexual contact from male to female and male to male, by blood transfusion, and by contaminated needles. In endemic areas, seropositives are clustered in families, probably reflecting the predominance of mother-child and male-female transmission. Limited evidence suggests similar routes of transmission for HTLV-II. The infection appears topersist for life and the virus is consistently isolated from seropositive persons regardless of their clinical status. HTLV-II has been detected in patients with hematologic malignancies, suchas atypical hairy cell leukemia, cutaneous CD8+ lymphoma and mycosis fungoides. However, definitive evidence that HTLV-IIl is the etiologic agent for these malignancies is lacking. Although uncommon, neurologic disease similar to the spastic myelopathy caused by HTLV-I has been reported in HTLV-II infected individuals (5). To what extent co-infection with HIV-1and HTLV-I/II contributes to significant alterations in the natural history of each infection is unclear. Several studies have suggested that co-infection with HTLV-I can accelerate progression of AIDS. Increased risk of chronic myelopathy has been suggested with HIV-1 and HTLV-I co-infection, as well as with HIV-1 and HTLV-II co-infection (6). Acquired ichthyosis has been reported as a possible manifestation of combined HIV-1 and HTLV-IIl infection (7), and lower total leucocyte and platelet counts and hematocrits have been found in patients co-infected with HIV-1 and HTLV-I/II (8). In general, studies of dual infection with HIV-1 and HTLV-I/II have been hampered by the lack of sufficient numbers of co-infected individuals. Detailed studies of these individaals, however, have direct relevance to ethnic groups in Hawaii and in several Pacific communities having high prevalences of HTLV-I infection. Furthermore, as mentioned earlier the immunosuppressive and T-cell activation properties of HTLV-I may place populations in which HTLV-I is endemic at added risk for HIV-1 infection. Thus, virologic and immunologic studies of dually infected individuals may contribute significantly to our understanding about both HIV-1 and HTLV-I/II pathogenesis.
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