The nucleotide sequences of the envelope genes of an African and a North American acquired immunodeficiency syndrome (AIDS) viral isolate have been determined. When their deduced amino acid sequences were aligned with the-envelopes of the lymphoadenopathy and AIDS-associated retrovirus isolates, conserved and divergent regions were readily identified. (4,10,11). For example, sequence analysis of the env region of the lymphoadenopathy virus (LAV) and AIDSassociated retrovirus (ARV) isolates revealed the presence of numerous nucleotide substitutions and several reciprocal insertions and-deletions resulting in 9% polynucleotide sequence heterology and a 15% difference in the deduced amino acid sequence (10).The AIDS retrovirus interacts with the immune system in a puzzling way. Virtually everyone infected with the virus synthesizes an antibody directed against a portion of the viral envelope (11-14). However, unlike antibodies reactive with other viral envelopes, the one detected in the sera of individuals exposed to the AIDS retrovirus has little if any protective value (15). Since several therapeutic and preventative strategies of viral intervention currently focus on envelope proteins, a definitive evaluation of the structurally diverse env gene and its polypeptide products is urgently needed. In this report we present the nucleotide and deduced amino acid sequences ofthe env genes of one African and one North American AIDS retrovirus isolate. Their alignment with the analogous segment of the LAV and ARV isolates indicates the location of highly conserved and profoundly divergent domains of the env gene. MATERIALS AND METHODSVirus holates and Molecular Cloning. The African (Z3) and North American (NY5) AIDS retroviruses used in this study were isolated in 1983 and 1984, respectively, and have been previously described (5). Molecular clones of proviral DNAs were obtained from cellular DNA preparations isolated from infected, phytohemagglutinin-stimulated, normal peripheral blood lymphocytes (16). On the basis of previous restriction mapping (5), integrated proviral DNA of NY5 was cloned as two separate EcoRI restriction fragments. Infected cellular DNA was prepared as previously described (17), digested with EcoRI, ligated to EcoRI-digested X Charon 4A (18) arms with T4 DNA ligase, packaged in vitro, and plated on Escherichia coli DP50 supF as previously described (19). The Z3 clone was obtained from a library prepared from a size-selected partial Mbo I digest of infected cellular DNA, inserted into BamHI-cleaved EMBEL-3 (20) phage DNA, packaged in vitro, and plated on E. coli NM539 cells (Promega Biotec, Madison, WI). Approximately 2 x 106 phage plaques from each library were screened (21), using the 2P-labeled pBENN-6 (16) DNA clone of the LAV provirus.Restriction maps of the proviral DNA clones were constructed by using Southern blot hybridization (22) and several contiguous 32P-labeled LAV probes as previously outlined (5). Presumptive full-length proviral DNAs were inserted into pBR322 (NY5 as two s...
To assess the risk of nosocomial transmission of human T-cell lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV), we prospectively evaluated a cohort of 531 health care workers. One hundred fifty of these employees reported percutaneous or mucous membrane exposures to blood or body fluids from a patient with the acquired immunodeficiency syndrome (AIDS) during the treatment of 238 such patients since 1981. None of these 150 employees had serologic evidence of HTLV-III/LAV infection on follow-up from 6 to 46 months after exposure. Of the 150, 46 were studied immunologically and 29 had lymphocytes cultured for HTLV-III/LAV. Results of all studies were normal. Of the 531 employees, 3 (0.56%) had serologic evidence of HTLV-III/LAV infection. All were seropositive at the time of study entry; none reported adverse nosocomial exposures. All acknowledged membership in one or more established risk groups for AIDS. This study provides strong evidence that the risk of nosocomial transmission of HTLV-III/LAV is extremely low.
Injection of rabbits with a human T cell line infected with HIV-1 caused seroconversion within 6 wk, and HIV-1 could be isolated from PBL cultures of infected rabbits. Identity of the isolated virus with HIV-1 was shown by analysis of products amplified by the polymerase chain reaction. HIV-1 infection was seen in rabbits injected with HIV-1-infected cells alone as well as in those that were first infected with HTLV-1 and subsequently with HIV-1. There were no consistent signs of disease in the rabbits infected with HIV-1 alone but HTLV-1/HIV-1-infected rabbits showed signs of illness including diarrhea and weight loss, transient neurologic impairment and, in one animal, a rapidly progressing mammary adenocarcinoma. Examination of organs taken at necropsy from both HIV-1- and HTLV-1/HIV-1-infected animals showed splenic hyperplasia and lymphocyte infiltration of the lungs, as well as moderate damage to liver and kidney in some cases.
Normal human peripheral blood lymphocytes were tested for their susceptibility to infection with retroviruses isolated from patients with the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex. Of 10 normal individuals tested, lymphocytes from all subjects became infected and produced virus as detected by assay for Mg+2-dependent reverse transcriptase. Lymphocytes from different individuals were demonstrated to be either high or low producers of reverse transcriptase after infection. The kinetics of virus production were similar in cells from both high- and low-producing individuals. A significant correlation was observed between high and low viral-producing lymphocytes and expression of the Leu-3/T4 (CD4) surface molecule. Mitogen-stimulated peripheral blood lymphocytes exposed to HTLV-III/LAV manifested productive viral infection, as reflected by the appearance of early syncytia, followed by reverse transcriptase. Unstimulated peripheral blood lymphocyte cultures displayed late syncytia but no detectable reverse transcriptase upon exposure to virus. The addition of anti-human interferon-alpha did not appear to have an appreciable effect on viral production in normal peripheral blood lymphocytes exposed to the virus.
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