Mutations were introduced into the regulatory sequences in the long terminal repeat of an infectious molecular clone of the human immunodeficiency virus. Viruses in which the NF-KB binding sites were deleted or ones in which one or two Spl binding sites were mutated still replicated efficiently in human T lymphocytes. A deletion of the two NF-KcB sites plus the three Spl sites or a mutation of the tat-responsive region rendered the virus replication incompetent. Thus, the NF-KcB sequences are not required for human immunodeficiency virus infectivity; however, a tat-responsive region is essential.

Microbial coinfections variably influence HIV-1 infection through immune activation or direct interaction of microorganisms with HIV-1 or its target cells. In this study, we investigated whether exposure of macrophages to bacterial products impacts the susceptibility of these cells to HIV-1 of different cellular tropisms.We demonstrate that (1) macrophages exposed to bacterial cell wall components such as lipopolysaccharide (

BackgroundPhysiological regulation of cellular iron involves iron export by the membrane protein, ferroportin, the expression of which is induced by iron and negatively modulated by hepcidin. We previously showed that iron chelation is associated with decreased HIV-1 transcription. We hypothesized that increased iron export by ferroportin might be associated with decreased HIV-1 transcription, and degradation of ferroportin by hepcidin might in turn induce HIV-1 transcription and replication. Here, we analyzed the effect of ferroportin and hepcidin on HIV-1 transcription.ResultsExpression of ferroportin was associated with reduced HIV-1 transcription in 293T cells and addition of hepcidin to ferroportin-expressing cells counteracted this effect. Furthermore, exposure of promonocytic THP-1 cells to hepcidin was associated with decreased ferroportin expression, increased intracellular iron and induction of reporter luciferase gene expression. Finally, exposure of human primary macrophages and CD4+ T cells to hepcidin and iron was also associated with induction of viral production.ConclusionOur results suggest that the interplay between ferroportin-mediated iron export and hepcidin-mediated degradation of ferroportin might play a role in the regulation of HIV-1 transcription and may be important for understanding of HIV-1 pathogenesis.

Sera of rabbits immunized with pili or formalized cultures of Neisseria gonorrhoeae contained pili antibodies. The reaction between pili and specific gamma globulin was followed by direct visual observation with an electron microscope. Using pili from 31 strains and antisera against three strains, only a few crossreactions between pili were observed. From this it is concluded that gonococcal pili are antigenically heterogeneous. However, serum raised with a T3 culture (with no detectable pili) contained antibodies against pili of the homologous T2 strain. It is proposed that the pilus antigen may exist in a form different from the typical pilus in gonococci.

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