Welcome to the part of this topic most everyone will want to read – how do the bacteria in the vagina relate to HPV and cervical health? Because why else would you want to read about vaginal bacteria…
We often hear that about 80% of women will have HPV at some point in their life, but the vast majority of those cases are transient, and the virus clears up between 6 -18 months. Why is it that some women get the virus, but never get dysplasia, while others advance to CIN 2/3 between one Pap smear and the next? It may be due to a woman’s vaginal microbiota (VBM) – the community of bacteria and viruses found in the vagina.
To recap the information from last week in Part 1, there are basically 5 different types of vaginal environments (classified by the predominating type of lactobacilli bacteria) which can be affected by such factors as ethnicity, hormones, smoking, recent sex, and vaginal douching. The vaginal environment is dynamic, changing throughout the month as estrogen/progesterone levels ebb and flow – when the hormone levels increase or decrease, the levels of lactobacilli do, too.
For the sake of limiting jargon, let’s just say there are ‘5 Types of Vaginal Environments’; it’s easier to follow than explaining “Community State Types” again, don’t you think?
*Type 4 is the odd man out here - it has a high diversity of bacterial species, several of which are associated with bacteria vaginosis. Instead of lactobacillia, it is predominantly populated instead by strict anaerobic bacteria (Gardnerella, Megasphera, Sneathia and Prevotella). Of the five types, this could be considered the unhealthy environment comparitively.
Between lactobacilli and other species, there is an inverse relationship: if the lactobacilli are high, everything else is really low; if the anaerobic bacteria are high, the lactobacilli are low. It’s important to keep this in mind. Any time “high species diversity” is mentioned, it indicates the lactobacilli levels are low.
So how does this relate to HPV, cervical intraepithelial neoplasia (CIN), cervical cancer, and overall cervical health? It appears that increased species diversity is associated with increased probability of having a persistent a HPV infection and subsequent lesions which may become cervical cancer. Let’s look at a few studies mentioned:
- A Korean twin study found that between HPV+ and HPV- twins, the twin who was positive for HPV had significantly lower amounts of lactobacilli and increased species diversity. (We may be able to guess by this description that the HPV+ twins were Type 4)
- An American study found HPV+ women were most likely have Type 3 or Type 4 environments and found that Type 2 might have the fastest rate of HPV clearance.
- A study from the UK looked at women with cervical lesions versus those without and found a positive correlation between the severity of the lesions and the species diversity. Also, as the severity increased, so did the likelihood of being Type 4 – low-grade CIN, high-grade CIN, and invasive cervical cancer were 2x, 3x, 4x as likely than controls to be Type 4, respectively.
- They found significantly higher levels of other anaerobic bacteria: Snethia sanguinegens, Anaerococcus tetradius, and Peptostreptococcus anaerobis
- A small Mexican study also found increased levels of anaerobic bacteria (Sneathia spp. and Fusobacterium spp.) in women with lesions or cervical cancer compared to unaffected women.
- The Fusobacterium genus may help hide the HPV virus from the immune system by immunosuppression (decreasing the immune systems functionality).
- Another Korean study found women with CIN had increased vaginal bacterial diversity, and found the combination of Anaerococcus vaginae, Gardarella vaginalis (major player is bacterial vaginosis), and L. iners (the Type 3 bacteria!) in the absence of L. crispatus was the most high-risk environment for “high-risk HPV” strains to progress to CIN. Just having A. vaginae alone had an odds ratio of 29.9. Even having L. iners had an odds ratio of 10.9 (likely because the transition from Type 3 to Type 4 is so much easer than it is for the other vaginal environment types).
So to translate this a bit, overall having decreased levels of lactobacilli (or you could say having increased levels of anaerobic bacteria) was correlated with having HPV, CIN, or cervical cancer. The type of vaginal environment you have may either help or hurt your chances of having a persistent HPV infection.
This review, however, makes a very important point: “All four studies in patients with CIN are observational studies, and with lack of longitudinal data, it is only possible to demonstrate association with disease states rather than causality.” The studies show these outcomes happen concurrently, but it’s not fully known if the VBM causes the virus to persist or if the effects of the virus influence the microbiota.
This cause-and-effect relationship is still being pieced together, but next time we will look into some of the microbial interactions.
Coming Up in Part III: How healthy bacteria prevent anaerobic bacteria colonization and how degradation of the vaginal epithelial barrier may help the HPV virus.
Read the full review, if you would like to find out more.
Mitra, A., Macintyre, D. A., Marchesi, J. R., Lee, Y. S., Bennett, P. R., & Kyrgiou, M. (2016). The vaginal microbiota, human papillomavirus infection and cervical intraepithelial neoplasia: What do we know and where are we going next? Microbiome,4(1). doi:10.1186/s40168-016-0203-0
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