HIV-positive men who have sex with men (MSM) have an increased risk for anal human papillomavirus (HPV)
infection, anal high-grade intraepithelial lesions (HSIL), and
anal cancer. Smoking is associated with abnormal anal cytology and with an increased risk for
anal cancer. We collected 3736 intraanal swabs from 803 HIV-positive MSM who participated in an
anal cancer screening program between October 2003 and August 2014. HPV prevalence, anal cytology and HPV
DNA load of high-risk (HR) HPV-types 16, 18, 31 and 33 of non-smokers and smokers were compared. HPV-typing was performed by alpha-HPV genus-specific PCR and hybridization with 38 type-specific probes using a multiplex genotyping assay. In samples positive for HPV16, 18, 31, or 33, HPV
DNA loads were determined by type-specific real-time PCRs and expressed as HPV
DNA copies per betaglobin gene copy. At baseline, HR-HPV
DNA (80.5 vs. 89.0%, p=0.001), HPV16
DNA (41.6 vs. 52.3%, p=0.003), HPV18
DNA (15.5 vs. 26.0%, p<0.001), anal dysplasia (LSIL+HSIL; 51.5 vs. 58.4%, p=0.045) and HSIL (17.2 vs. 22.7%, p=0.048) were detected more frequently in smokers compared to non-smokers. Throughout the study period 32.7% of non-smokers and 39.9% of smokers developed HSIL (p=0.011), and three smokers developed
anal cancer. Considering swabs from the entire study period (median HPV load value per patient per cytology grade), smokers with normal anal cytology had significantly higher HPV16 loads (median 0.29 vs. 0.87, n=201, p=0.007) and cumulative high-risk-HPV loads (median 0.53 vs. 1.08, n=297, p=0.004) than non-smokers. Since elevated HR-HPV
DNA loads are associated with an increased risk for HPV-induced anogenital
cancers, HPV-infected HIV-positive MSM should be counseled to refrain from smoking. Additionally, for smokers, shorter
anal cancer screening intervals than for non-smokers may be appropriate.