Bacterial vaginosis-associated microflora isolated from the female genital tract activates HIV-1 expression.
Alteration of cervicovaginal microbial flora can lead to vaginosis, which is associated with an increased risk of HIV-1 transmission. We recently characterized a soluble HIV-inducing factor (HIF) from the cervicovaginal lavage (CVL) samples of women. The goals of this study were to determine the effect of cervicovaginal microflora on HIV-1 expression and to elucidate the relationship between HIF activity and microflora. Physiologically relevant microorganisms, Mycoplasma, diphtheroid-like bacteria, Gardnerella vaginalis, Streptococcus agalactiae, and Streptococcus constellatus, cultured from the CVL of a representative woman with a clinical condition of bacterial vaginosis and possessing HIF activity, induced HIV-1 expression. The magnitude of virus induction varied widely with the greatest stimulation induced by diphtheroid-like bacteria and Mycoplasma. The transcriptional induction by Mycoplasma was mediated by activation of the KB enhancer, an activation mechanism shared with HIF. Also as with HIF, Mycoplasma induced AP-1 dependent transcription. Polymerase chain reaction (PCR)-based speciation showed that the isolate was M. hominis. Our data indicate that bacterial vaginosis-associated microflora can enhance HIV-1 transcription and replication and identify M. hominis as a potential source for HIF activity. The virus-enhancing activities associated with the microflora and HIF may increase genital tract viral load, potentially contributing to HIV transmission.
Department of Immunology/Microbiology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois 60612, USA. lalharth@rush.edu
L
L
Al-Harthi
K A
KA
Roebuck
G G
GG
Olinger
A
A
Landay
B E
BE
Sha
F B
FB
Hashemi
G T
GT
Spear
D005591:Chemical Fractionation; D004742:Enhancer Elements, Genetic; D005260:Female; D015967:Gene Expression Regulation, Viral; D005836:Genitalia, Female / Q000382:microbiology*; D016325:HIV Long Terminal Repeat; D015497:HIV-1 / Q000235:genetics*; D006801:Humans; D019169:Jurkat Cells; D009174:Mycoplasma / Q000378:metabolism / Q000502:physiology; D016328:NF-kappa B / Q000378:metabolism; D012995:Solubility; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014158:Transcription, Genetic; D016585:Vaginosis, Bacterial / Q000382:microbiology
D016328:NF-kappa B; D018808:Transcription Factor AP-1