Lack of regression of anal squamous intraepithelial lesions and anal HPV infection despite immune restoration under cART
Presented by Christophe Piketty (France).
C. Piketty1, A. Si-Mohamed1, E. Lanoy2, B. Cochand-Priollet3, S. Trabelsi2, P.-M. Girard4, R. Tubiana5, L. Abramowitz6, E. Tartour1, L. Weiss1, D. Costagliola2,5, and the Valparaiso Study Group
1Hopital Européen Georges Pompidou, Paris, France, 2INSERM U943 - UPMC UMR S943, Paris, France, 3Hopital Lariboisiere, Paris, France, 4Hopital Saint Antoine, Paris, France, 5Hopital de La Pitie-Salpetriere, Paris, France, 6Hopital Bichat-Claude Bernard, Paris, France
Background: A high prevalence of anal squamous intraepithelial lesions (ASIL) and HPV infection have been observed in HIV-infected MSM in the pre-cART era. To date, the impact of cART on the natural history of HPV infection and ASIL is poorly documented.
Methods: 94 HIV-infected MSM naïve of cART were enrolled in a longitudinal study before starting a first line regimen of cART. Each patient provided anal samples for cytology, histology and HPV DNA testing at baseline, and months 12 and 24 of cART. HPV DNA was detected by real time PCR and the Roche Linear Array assay. Anal cytology was processed by the Thin Prep method (Hologic). CD4+ and CD8+ T cells responses to HPV-16 E6 and E7 proteins were measured in a subgroup of individuals exhibiting HPV-16 anal infection at inclusion.
Results: The median age of the patients was 39.7 years (33.2 - 43.5).Baseline and month 12 results are presented in the Table 1:
| ||CD4 cells /mm3
median (Q1-Q3)||Plasma HIV RNA Log copies/mL||VL < 50||Anal SIL||Low grade SIL;
High grade SIL||High risk HPV;
HPV-16||Number of HPV
(242 - 342)||4.8
(4.17 - 5.26)||1%||51 (54%)||30 (32%);
8 (9%)||83 (90%);
49 (53%)||5 (2 - 7)|
(411 - 575)||1.6
(1.6 - 1.6)||93%||41 (58%)||24 (34%);
10 (14%)||59 (87%);
28 (41%)||5 (2 - 6)|
Prevalence of HPV infection, low and high grade SIL, were similar at baseline and M12. Among patients with normal cytology and/or histology at baseline, 44% progressed to ASIL at M12 whereas 31% of patients with ASIL at baseline exhibited a regression at M12. Specific anti-HPV CD4 T cell responses were mostly undetectable both at baseline and M12.
Conclusion: Our results demonstrate a high prevalence and incidence of ASIL and anal HPV infection in HIV-infected MSM despite CD4 reconstitution under cART. These data suggest that all HIV-positive MSM remain at risk of anal SIL despite immune restoration.
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