Target intelligence / Profile preview

Bacterial vaginosis-associated microbiota (BVAB) (BVAB)

Target
BVAB
Molecular classification
Microbiome, Bacterial population, Other
01

Overview

Bacterial vaginosis-associated microbiota represents a dysbiotic state characterized by the depletion of lactic acid-producing Lactobacillus species and an overgrowth of diverse anaerobic bacteria (Fredricks et al., 2005, New England Journal of Medicine). This polymicrobial population includes Gardnerella vaginalis, Atopobium vaginae, and various Clostridiales-like organisms termed BV-associated bacteria 1, 2, and 3 (BVAB1-3) (Fredricks et al., 2005). These organisms often organize into resilient biofilms on the vaginal epithelium, which are implicated in high rates of treatment failure and recurrence (Swidsinski et al., 2005, Obstetrics & Gynecology). The metabolic activity of these bacteria produces malodorous amines and degradative enzymes like sialidases, which compromise the vaginal mucosal barrier (Lewis et al., 2013, Journal of Biological Chemistry). Clinically, this target is addressed using antibiotics such as metronidazole and clindamycin, which aim to reduce the anaerobic burden, though they often fail to eradicate the underlying biofilm (Muzny et al., 2019, The Journal of Infectious Diseases). Emerging therapeutic approaches also target these populations through the use of probiotics or vaginal microbiota transplantation to restore a healthy microbial balance (Borges et al., 2014, Archives of Gynecology and Obstetrics).

Other names
BV-associated bacterial populationsVaginal dysbiosisBacterial vaginosis-associated bacteriaAnaerobic vaginal microbiotaBV-associated microbiota
02

Mechanism of action

Antibiotics like metronidazole and tinidazole act by disrupting DNA synthesis in anaerobic bacteria, while clindamycin inhibits protein synthesis by binding to the 50S ribosomal subunit (Workowski et al., 2021, MMWR Recommendations and Reports). Probiotic interventions aim to restore the dominance of Lactobacillus species through competitive exclusion and production of lactic acid and hydrogen peroxide (Borges et al., 2014, Archives of Gynecology and Obstetrics).

03

Biological functions

Biofilm formationMetabolic competitionPathogenesisImmune modulationOther
04

Disease associations

InfectionInflammationOther
05

Safety considerations

Antibiotic resistanceHigh recurrence ratesDisruption of commensal Lactobacillus speciesGastrointestinal side effectsVulvovaginal candidiasis following treatment
06

Interacting drugs

Metronidazole

4 more in the full profile.

07

Biomarkers

Nugent scoreAmsel criteriaGardnerella vaginalis DNAAtopobium vaginae DNASialidase activity

Beyond the preview

Go deeper on Bacterial vaginosis-associated microbiota (BVAB) (BVAB).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Bacterial vaginosis-associated microbiota (BVAB) (BVAB).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call