Increased anal HPV levels in HV-positive smokers
Simon Collins, HIV i-Base
The impact of smoking status on levels of HPV-16 viral load was reported in a poster by Norbert Brockmeyer and colleagues from University of Bochum, Germany in a prospective study of samples from 267 HIV-positive MSM participants in an HPV screening programme, half of whom were smokers.
1806 intraanal and perianal swabs (mean 3.5 per patient) were analysed for HPV genotype and HPV viral load, using real-time PCR (expressed as HPV16 DNA copies per beta-globin gene copy). High risk HPV genotyes were detected in 316 samples (for HPV-16) and 154 (for HPV-18), and at a statistically higher rate in smokers vs non-smokers.
Normal cytology, low-grade squamous intraepithelial lesions (LSIL), and high-grade squamous intraepithelial lesions (HSIL) were found in 60, 13, and 7% of perianal and in 49, 16, and 9% of intraanal swabs.
Smokers were at higher risk of HPV DNA, high-risk HPV DNA, and HPV16 DNA compared to non-smokers and had significanty higher levels of perianal and intraanal levels of HPV-16 (see Table 1) and HPV-18 viral load (data not shown). These differences were greater in patients with normal cytology results. The p-value for the effect of smoking remained significant after adjusting for age, CD4, viral load, AIDS and ARV use in a multivariate analysis.
As an elevated HPV viral load is a risk factor for progression to CIN/cancer in women with normal cytology, the authors concluded with the importance of emphasising smoking cessation for HIV-positive patients.
Table 1: Levels of HPV-16 viral load in non-smokers vs current smokers
|LSIL or HSIL||27% (46 LSIL + 9 HSIL)||36% (41 LSIL + 40 HSIL)||p=0.041|
|Mean intraanal HPV16 VL||21||318||p=0.023|
|Median intraanal HPV16 VL||0.3||3.7||p=0.023|
|Mean perianal HPV16 VL||013||186||p=0.017|
|Median perianal HPV16 VL||0.2||3.6||p=0.017|
|Mean intraanal HPV16 VL (normal cytology)||1.8||709||p=0.004|
|Mean intraanal HPV16 VL (all grades)||4.5||81.5||p=0.094|
Several other posters reported immunological impact of smoking on HIV-positive patients.
Apart from the expected links reported in studies looking at risk of cardiovascular disease (see D:A:D reports in this issue of HTB), these included reduced responses from hepatitis A vaccinations (smoking was an independent predictor of non-response to vaccine; 0R = 2.78, 95%CI 1.03 to 7.69, p = 0.02) , higher levels of oxidative stress , higher risk of fatal AIDS-defining malignancies (2.42; p <0.0001; not significant if lung cancers were excluded) , and reduced responses to prime-boost pneumococcal vaccine strategies. 
The report from D:A:D highlighted particularly low reports of smoking cessation even in patients diagnosed with a CVD event.
- Norbert Brockmeyer N, Kreuter A, Pfister H et al. Elevated Anal HPV16 DNA Loads in HIV+ Men Who Smoke. Poster 872.
- Launay O, Grabar S, Gordien E et al. Randomized Trial Comparing a 3-Dose Regimen to a Standard 2- Dose Regimen of Hepatitis A Vaccine in HIV-infected Adult Patients with CD4+ T Cells between 200 and 500 per mm3 (HEPAVAC Study). Poster 885.
- Dageforde LA, Shintani A, Haas D et al. NNRTI Use May Be Associated with Decreased Oxidant Stress during HIV Therapy. Poster 798.
- DArminio Monforte A, Abrams D, Pradier C et al. HIV-induced Immunodeficiency and Risk of Fatal AIDS-defining and Non-AIDS-defining Malignancies: Results from the D:A:D Study. Oral abstract 84.
- Lévy G, Tsch I, Lesprit P el at. Long-term Immunologenicity of a Prime-boost Strategy Combining a 7-Valent Pneumococcal Conjugate Vaccine followed by a 23-Valent Pneumococcal Polysaccharide Vaccine vs PPV Alone: ANRS 114 Pneumovac Study. Poster 866.