HIV
and Hepatitis.com Coverage of the 14th
Annual Conference on Retroviruses and Opportunistic Infections (14th CROI) February
25 - 28, 2007, Los Angeles, CA
HIV
Positive Smokers Have Higher Levels of Cancer-Causing HPV
HIV positive men who have sex
with men (MSM) have high rates of anal
human papilloma virus (HPV) infection and anal
dsyplasia (abnormal cells that may progress to anal cancer). Prior studies
have shown that tobacco smoking is associated with anal and cervical cell abnormalities
(squamous intraepithelial lesions, or neoplasia) and an elevated risk of anal
and cervical cancer.
As reported at the 14th Conference
on Retroviruses and Opportunistic Infections last month in Los Angeles, German
researchers conducted a prospective study in which intra-anal and perianal specimen
swabs were collected from 267 HIV positive MSM participating in an anal dysplasia
screening program; about half were current smokers. HPV typing was performed,
and levels of HPV types 16 and 18 (HPV-16, HPV-18), which are known to cause cancer,
were measured using PCR assays.
Results
•
Overall, 60% of perianal specimen swabs showed normal cells, 13% showed low-grade
squamous intraepithelial lesions (LSIL), and 7% showed high-grade squamous intraepithelial
lesions (HSIL).
•
For
intra-anal specimen swabs, the corresponding percentages were 49%, 16%, and 9%.
•
Among
perianal specimen swabs, any type of HPV DNA was detected in 87%, high-risk (types
16 and 18) HPV DNA in 74%, and HPV-16 DNA in 46%.
•
For
intra-anal specimen swabs, the corresponding percentages were 87%, 77%, and 55%.
•
Anogenital
HPV, high-risk HPV, and HPV-16 were detected significantly more often among smokers
compared with non-smokers (90%, 82%, and 53%, respectively, of swabs from smokers
vs 82%, 69%, and 48% of swabs from non-smokers).
•
Intra-anal HPV-16 viral loads were significantly higher among smokers compared
with non-smokers (median 4 vs 0.5 copies).
•
HPV-16 viral load differences between smokers and non-smokers were greatest among
individuals with normal cytology, but slight among subjects with HSIL, suggesting
that smoking may accelerate HPV disease progression.
•
Smokers
also had higher levels of HPV-18.
•
HSIL
was significantly more common among smokers compared with non-smokers (18% vs
4%).
Conclusion
"Smoking is associated with elevated anal HPV-16 DNA loads in HIV+
MSM, especially in those with normal cytology," the researchers concluded.
"Since high HPV-16 loads were previously shown to be associated with an increased
risk for anogenital cancers, HIV+/HPV+ MSM should be encouraged to refrain from
smoking."
Reference N
Brockmeyer, A Kreuter, H Pfister, and others. Elevated Anal HPV16 DNA Loads in
HIV+ Men Who Smoke. 14th Conference on Retroviruses and Opportunistic Infections.
Los Angeles, February 25-28, 2007. Abstract 872 (poster).
