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LB1.2 What is the strength of evidence for hiv and hpv interactions? results from systematic reviews and meta-analyses of longitudinal studies
  1. katharine j Looker1,
  2. Minttu M Rönn2,
  3. Patrick M Brock3,
  4. Marc Brisson4,
  5. Melanie Drolet4,
  6. Philippe Mayaud5,
  7. Marie-Claude Boily6
  1. 1University of Bristol, Bristol, UK
  2. 2Harvard T. H. Chan School of Public Health, Boston, USA
  3. 3University of Glasgow, Glasgow, UK
  4. 4Université Laval, Québec, Canada
  5. 5London School of Hygiene and Tropical Medicine, London, UK
  6. 6Imperial College London, London, UK

Abstract

Introduction We conducted two systematic reviews. Review 1 (R1) summarised evidence for the influence of HIV on HPV acquisition and clearance. Review 2 (R2) summarised the evidence for the influence of HPV on HIV acquisition. R1 is the first meta-analytic review to quantify the impact of HIV on HPV infection. R2 updates two earlier meta-analyses.

Methods Both reviews were conducted according to PRISMA and MOOSE guidelines. We searched PubMed and Embase up to January 2017 for longitudinal studies of HPV incidence and clearance rate by HIV status and of HIV incidence by HPV status. We derived pooled relative risk (RR) estimates using a random effect model and performed subgroup analyses to understand main sources of heterogeneity, examined dose-response relationship and produced funnel plots.

Results In R1, 37 publications comprising 25 independent study populations were included. The incidence of HPV (pooled crude RR [cRR]=1.55, 95% CI 1.29–1.88) and of high-risk (HR) HPV (pooled cRR=2.20, 95% CI 1.90–2.54) was doubled whereas HPV clearance rate (pooled cRR=0.53, 95% CI 0.42–0.67) and HR-HPV clearance (pooled cRR=0.69, 95% CI 0.57–0.83) was nearly halved among people living with HIV (PLHIV). HPV incidence when CD4 count ≤200 cells/µL among PLHIV was higher, but not statistically significant, than for CD4 >200 cells/µL (pooled cRR=6.65, 95% CI 2.98–14.85 vs 3.20, 95% CI 2.48–4.13). In R2, 14 publications comprising 11 independent study populations were included. HIV incidence was almost doubled in the presence of prevalent HPV infection (pooled cRR=1.91, 95% CI 1.38–2.65) and for HR-HPV (pooled cRR=1.63, 95% CI 1.26–2·09). Risk of HIV acquisition increased with the number of HPV types. Crude and adjusted pooled estimates were similar in both reviews. There was more evidence of publication bias in R2 than R1.

Conclusions The findings met most Bradford-Hill criteria for causation. Our results have clinical and public health relevance: HPV vaccination may benefit PLHIV and indirectly help to reduce HIV transmission. HIV prevention may also reduce HPV transmission.

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