No abstract

The isolation from macaques of retroviruses related to human immunodeficiency virus (HIV) led to the identification of a second group of human retroviruses (termed HIV-2), which are prevalent in West Africa and closely related to the simian immunodeficiency virus (SIV). We have cloned and determined the complete nucleotide sequence of the human West African retrovirus HIV-2NIH-Z and compared it to that of a previously described strain of HIV-2 (HIV-2ROD) as well as to SIV and HIV-1. We have reached the following conclusions: (i) The HIV-2 isolates are (slightly) more closely related to each other than to SIV, compatible with their isolation from different species. (ii) The variability between HIV-2 isolates is similar in degree and kind to that found among HIV-1 isolates. The equivalent degrees of intragroup divergence suggest that HIV-1 and HIV-2 have existed in their present ranges in Africa for approximately equal lengths of time. The fact that acquired immunodeficiency syndrome is widespread in regions where HIV-1 is prevalent but not in regions where HIV-2 is prevalent suggests a substantial difference in the morbidity rates associated with HIV-1 vs. HIV-2 infection. (iii) HIV-2 and SIV are related to each other more closely than they are to HIV-1.

We have investigated in utero human immunodeficiency virus type 1 (HIV-1) transmission by analyzing human fetal tissues for the presence of viral DNA by means of the polymerase chain reaction (PCR). Thirty three fetal samples: thymus, spleen, and peripheral mononuclear blood cells (PMBC) were obtained at abortion (16 to 24 weeks) from HIV-1-infected asymptomatic women. The results of HIV-1-DNA detection were considered only in 9 cases where contamination of fetal samples by infected mother cells could be definitely eliminated by using primers specific for a polymorphic cellular locus. PCR allowed the identification of HIV-1 DNA sequences in 6/8, 8/9, and 5/9 of specimens from thymus, spleen, and PMBC, respectively. Positive results were shown in fetuses as early as 16 weeks. Viral cultures as well as assays for serum p24 HIV-1 antigen were negative in 9.9 and 33/33 tested, respectively. Therefore, our results indicate early and frequent in utero HIV-1 infection. Different patterns of viral activation after birth might then lead to either rapid or delayed onset of acquired immunodeficiency syndrome.

New human retroviruses antigenically related to HIV and even more closely to STLV-III have been recently isolated from individuals from some West African countries. One of these viruses, HTLV-IVP, was reportedly isolated from lymphocytes of a healthy female prostitute. Another isolate, LAV-2FG, was obtained from an AIDS patient and third, SBL-6669, from an individual with lymphadenopathy. Current epidemiological studies indicate that some of these virus isolates cause immune deficiency whereas others may not or may be less efficient at inducing immune deficiency. Similarly, STLV-III apparently does not cause immune deficiency in its natural host, African green monkey. A novel feature of HIV is the possession of a gene termed tat, which is implicated in its pathobiology. We report here that, like HIV, HTLV-IVP, LAV-2FG (HIV-2) and SBL-6669, as well as STLV-IIIAGM possess the putative tat gene, irrespective of their pathogenic potential in vivo. Interestingly, HTLV-IVP/LAV-2FG long terminal repeat (LTR) is equally well transactivated by the HTLV-IVP/LAV-2FG and HTLV-IIIB tat function, HTLV-IIIB LTR responds better to its own tat function.

A lymphotropic virus HTLV-III/LAV was recently identified as the etiologic agent of the acquired immune deficiency syndrome (AIDS). In a study of concomitant hepatitis B infections in patients with AIDS or the AIDS-related complex, DNA sequences of hepatitis B virus (HBV) were found in fresh and cultured lymphocytes from patients with AIDS even in the absence of conventional HBV serological markers. Furthermore, the restriction DNA pattern was consistent with the integration of the viral DNA. These results should prompt additional studies to reevaluate a possible role of HBV as a cofactor in AIDS in addition to the HTLV-III/LAV causal agent.