Bacterial vaginosis-associated microflora isolated from the female genitaltract activates HIV-1 expression

Citation
L. Al-harthi et al., Bacterial vaginosis-associated microflora isolated from the female genitaltract activates HIV-1 expression, J ACQ IMM D, 21(3), 1999, pp. 194-202
Citations number
35
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY
ISSN journal
15254135 → ACNP
Volume
21
Issue
3
Year of publication
1999
Pages
194 - 202
Database
ISI
SICI code
1525-4135(19990701)21:3<194:BVMIFT>2.0.ZU;2-M
Abstract
Alteration of cervicovaginal microbial flora can lead to vaginosis, which i s associated with an increased risk of HIV-1 transmission. We recently char acterized a soluble HIV-inducing factor (HIF) from the cervicovaginal lavag e (CVL) samples of women. The goals of this study were to determine the eff ect of cervicovaginal microflora on HIV-1 expression and to elucidate the r elationship between HIF activity and microflora. Physiologically relevant m icroorganisms, Mycoplasma, diphtheroid-like bacteria, Gardnerella vaginalis , Streptococcus agalactiae, and Streptococcus constellatus, cultured from t he CVL of a representative woman with a clinical condition of bacterial vag inosis 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 mec hanism shared with HIF. Also as with HIF, Mycoplasma induced AP-1 dependent transcription. Polymerase chain reaction (PCR)-based speciation showed tha t the isolate was M. hominis. Our data indicate that bacterial vaginosis-as sociated microflora can enhance HIV-1 transcription and replication and ide ntify M. hominis as a potential source for NIF activity. The virus-enhancin g activities associated with the microflora and HIF may increase genital tr act viral load, potentially contributing to HIV transmission.