Differential sexual network connectivity offers a parsimonious explanation for population-level variations in the prevalence of bacterial vaginosis: a data-driven, model-supported hypothesis

Abstract

Background: The prevalence of bacterial vaginosis (BV) and vaginal microbiota types varies dramatically between different populations around the world. Understanding what underpins these differences is important, as high-diversity microbiotas associated with BV are implicated in adverse pregnancy outcomes and enhanced susceptibility to and transmission of sexually transmitted infections.

Main text: We hypothesize that these variations in the vaginal microbiota can, in part, be explained by variations in the connectivity of sexual networks. We argue: 1) Couple-level data suggest that BV-associated bacteria can be sexually transmitted and hence high sexual network connectivity would be expected to promote the spread of BV-associated bacteria. Epidemiological studies have found positive associations between indicators of network connectivity and the prevalence of BV; 2) The relationship between BV prevalence and STI incidence/prevalence can be parsimoniously explained by differential network connectivity; 3) Studies from other mammals are generally supportive of the association between network connectivity and high-diversity vaginal microbiota.

Conclusion: To test this hypothesis, we propose a combination of empirical and simulation-based study designs.

Keywords: Bacterial vaginosis; Concurrency; HIV; Microbiome; STI; Sexual network connectivity.

Fig. 1

Schematic illustration of interactions between sexual network connectivity, frequency distribution of vaginal community state types (CSTs) and the prevalence of STIs using the example of non-Hispanic blacks and non-Hispanic whites in the USA. Non-Hispanic blacks have been noted to have higher network connectivity - largely due to a high prevalence of sexual partner concurrency [67]. This enhanced network connectivity facilitates the spread of STIs as well as the bacteria responsible for bacterial vaginosis (BV) and possibly less resilient L. iners vaginal community state types. BV and the STIs then further facilitate the spread of one another. (The distribution of vaginal CSTs is taken from a study by Ravel et al. [4], the prevalence ratios of STIs are taken from [67, 77]. The community state types are described by the presence of BV or the predominant Lactobacillus species present e.g. ‘L. iners’ refers to a Lactobacillus iners dominant type. The numbers around the pie-charts denote the percent each CST comprises)

Fig. 2

Schematic illustration of how high sexual network connectivity can enhance transmission of bacterial vaginosis associated bacteria (BVAB - depicted in red). In the low connectivity network (right), the BVAB are trapped in the A-B relationship until this breaks up when woman A can transmit the BVAB to her new partner (C). Man B may then also transmit BVAB to his new partner (D) but if the gap between his old and new partner exceeds the duration of penile colonization for BVAB (time between T₂ and T₃) then he will not transmit to his new partner. In the high connectivity network (left), the BVAB does not need to wait for the A-B partnership to end and can, without impediment, spread to other individuals connected via sexual partnerships (Squares-men, Circles-women, Red/Gray nodes-BVAB−/non-BVAB -containing genital microbiome, Gray lines-sexual partnership active on first day of the month; see text for further details)