PubMed · 7674750
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J Decosas, F Kane, J K Anarfi, K D Sodji, H U Wagner. 1995-09-23. Migration and AIDS.. https://doi.org/10.1016/s0140-6736(95)91631-8
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Cardiomyopathy associated with HIV-1 infection is a well-recognized complication. However, it is unknown whether direct cardiomyocyte infection is involved in the pathogenesis of the cardiomyopathy. An HIV-1-based lentiviral vector and wild-type HIV-1 were used to infect human fetal cardiac myocytes in a primary culture. Quantitative polymerase chain reaction, viral p24 antigen determination, and immunofluorescence were used to detect the synthesis of HIV-1 DNA and proteins after the infection. High-efficiency infection occurred using the HIV-1-based lentiviral vector, although no infection occurred with the wild-type HIV-1 strain. Dual-labeling immunofluorescence for HIV-1 proteins and myosin confirmed that cardiomyocytes were infected. This in vitro analysis suggests that direct myocyte infection with wild-type HIV-1 may not be involved in the pathogenesis of HIV-1 cardiomyopathy. However, HIV-1-based vectors may prove useful for ex vivo cardiovascular gene therapy.
A large collection of natural HIV-1 integrase (IN) sequences has not previously been described. We reasoned that analysis of such sequences would address whether natural variation of HIV-1 IN contributes to the pathogenesis of AIDS and might also identify amino acid residues important for IN function. Sequences encoding HIV-1 IN were amplified from cryopreserved lymphocytes or plasma obtained at different times from 10 hemophilia patients who had been observed for up to 17 years. The region of the HIV-1 genome that encodes the 288-amino acid IN protein was sequenced from a total of 102 clones; information was obtained for 99.97% of 29,478 amino acid positions. Phylogenetic analysis indicated that patient samples were unique. Interpatient nucleic acid distances ranged from 0.8% to 4.9%, highlighting the tight conservation of this genomic region. No major differences were found between DNA and RNA or between early and late time points from the same patient. Significantly, no amino acid changes that might account for the variable rate of disease progression between patients were evident. Only one amino acid substitution involved a highly conserved residue known to be important for enzymatic activity. However, several interesting amino acid substitutions were noted, including residues within the C-terminal region of the protein for which sequence comparisons between animal retroviruses have not been very informative. These results should encourage the pursuit of anti-integrase therapies, especially inasmuch as the apparent biologic constraints on the IN sequence may deter the development of drug resistance.
We used data from a national serosurvey to describe national and regional trends in the prevalence of HIV among women giving birth in the United States from 1989 through 1994, and to estimate the number of women between 15 and 44 years old with HIV infection who had not yet developed opportunistic infections defining AIDS. We compared these estimates with AIDS prevalence and mortality estimates from the national AIDS case surveillance system. HIV seroprevalence among childbearing women remained stable nationwide from 1989 through 1994, ranging from 1.5 to 1.7/1000 women. In the Northeast, seroprevalence declined significantly after 1989. Seroprevalence increased significantly in the South through 1991 and then stabilized, although seroprevalence among black women continued to increase through 1994 in some southern states. Although AIDS prevalence and mortality increased nationwide each year from 1989 through 1994, the number of women infected with HIV who had not yet developed AIDS changed little and was approximately 86,000 in 1994. Our data suggest that new HIV infections among women of reproductive age are occurring at a rate that offsets losses from this population due to aging, disease progression, and death.