WOMEN SMOKERS AND HPV
Women cervical cancer results from human papillomavirus (HPV) infection particularly the high-risk strains HPV-16 and HPV-18. However, smoking cigarette makes more possible that women HPV infection is leading to invasive cervical cancer. In fact, this hypothesis has been validated in late 2009 in a study conducted by ALTS on women smokers infected by HPV strains 16 and/or 18.
The plan is:
-Firstly, Measuring the viral genome/ng of cellular DNA using real-time polymerase chain method
-Secondly, Analysis using logistic and linear regression graph models. The x-axis represents cigarette smoking and the y-axis represents baseline viral load.
In general, the total number of participants were 1050 women:
752 women with HPV-16
258 women with HPV-18
40 women with HPV-16 and HPV-18
Also, 452 were current smokers where:
39.8% started smoking before turning 16
55.8% are smokers for 6 or more years
38.1% smokes 20 or more cigarettes daily
48.5% smokes 4 or more packs yearly
101 were former smokers
The viral HPV-16 and HPV-18 load was studied according to never smokers, smoking status and current smokers.
NEVER SMOKERS WOMEN:
The mean value of log10 HPV-16 E7 copies/ng of cellular DNA was 2.65. Whereas, the mean value of log 10 HPV-18 E7 copies/ng of cellular DNA was 3.73. Moreover, we classify the factors controlling the baseline HPV-16 load as race, parity and referral pap smear. Meanwhile, the baseline HPV-18 load is slightly correlated with other HPV strains infection.
Conclusion: Only referral pap and coinfection with other HPV strains were involved in baseline HPV load for both HPV-16 and HPV-18.
SMOKING STATUS:
Changes were made categorizing women (age, race, parity, referral pap, using oral contraceptives, and having another HPV strain coinfection)
Conclusion: for both HPV-16 and HPV-18, the baseline viral load p-value is way greater for women currently smoking than non smokers. On the other hand, for women who were smokers in the past, there isn’t much difference in HPV load p-value from non smokers.
Additional note regarding having 2 or more male partners, it didn’t interfere with the statistics of current smokers relative to HPV load knowing that mostly smokers have more than one partner.
CURRENT SMOKERS:
Is there a smoking dose relationship with baseline HPV load? The answer is no even for former smokers. Indeed, this relationship was studied according to a criteria including the age at beginning of smoking, number of smoking years, average number of cigarettes in a day, number of packs per year, and finally years of smoking plus cigarettes each day smoked.
Conclusion: The change in baseline HPV load for each HPV-16 and HPV-18 wasn’t important for both current smokers and women who stopped smoking.
SUMMARY
Smoking and HPV viral load are connected according to many studies. Aside from the information mentioned before taken from ALTS, other studies showed that HPV spreads in correlation with smoking. In addition, the rate and tenacity of the virus are connected to smoking. In fact, cigarette chemicals were detected in cervical mucus revealing their interference with cervical cells, which results in increasing cell proliferation and turnover. Actually, this only makes sense knowing that human papillomavirus replicates using the host replication machinery (Replisome). To clarify, if smoking increase proliferation of the cell, it also increase HPV replication and thus the viral load.
MEN SMOKERS AND HPV
For men, the infection by HPV might target the scrotum, penis glans and shaft, and the coronal sulcus. Whether you have a normal HPV infection, or one leading to cancer, a relationship with smoking study has been made. Hence, samples from the mentioned areas analysis showed that smoking increase the risk of acquiring HPV let alone oncogenic HPV. Besides, in 2014 another study was proposed for the purpose of knowing whether the infection spread due to acquisition or persistence of the virus in the genital area. When no remarkable relationship between smoking and persistence of HPV was detected, we can rule out that smoking increase the incidence of having genital HPV infection but not persistence.
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