Impact of smoking on the quantity and quality of antibodies induced by human papillomavirus type 16 and 18 AS04-adjuvanted virus-like-particle vaccine - a pilot study
Namujju, Proscovia; Pajunen, Emma; Simen-Kapeu, Aline; Hedman, Lea; Merikukka, Marko; Surcei, Heljä-Marja; Kirnbauer, Reinhard; Apter, Dan; Paavonen, Jorma; Hedman, Klaus; Lehtinen, Matti (2014)
Namujju, Proscovia
Pajunen, Emma
Simen-Kapeu, Aline
Hedman, Lea
Merikukka, Marko
Surcei, Heljä-Marja
Kirnbauer, Reinhard
Apter, Dan
Paavonen, Jorma
Hedman, Klaus
Lehtinen, Matti
2014
BMC Research Notes 7
445
Terveystieteiden yksikkö - School of Health Sciences
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Julkaisun pysyvä osoite on
https://urn.fi/URN:NBN:fi:uta-201408202044
https://urn.fi/URN:NBN:fi:uta-201408202044
Kuvaus
BioMed Central open access
Tiivistelmä
Background
The AS04-adjuvanted bivalent L1 virus-like-particle (VLP) vaccine (Cervarix™) against infection with human papillomavirus (HPV) types 16/18 holds great promise to prevent HPV16/18 infections and associated neoplasias, but it is important to rule out significant co-factors of the neoplasias like smoking.
Methods
We conducted a pilot study to compare the quantity and quality of HPV16/18 antibody response at baseline and 7 months post vaccination in 104 non-smoking and 112 smoking female participants vaccinated at 0, 1 and 6 months with Cervarix™ (55 and 48 study participants) or with Hepatitis A vaccine (HAVRIX™) (48 and 64 participants, respectively). These 216 women were a sub-sample of 4808 baseline 16- to 17-year old Finnish women initially enrolled in the double-blind, randomized controlled phase III PATRICIA trial. Following end-of-study unblinding in 2009 they were randomly chosen out of all the participants of the three major Finnish PATRICIA study sites in the Helsinki metropolitan area (University of Helsinki, N = 535, and Family Federation Finland, N = 432) and Tampere (University of Tampere, N = 428). Following enrolment, serum samples were collected at month 0 and month 7 post 1st vaccination shot, and were analysed for levels and avidity of IgG antibodies to HPV16 and HPV18 using standard and modified (4 M urea elution) VLP ELISAs.
Results
We found that at month 7 post vaccination women who smoked (cotinine level > 20 ng/ml) had levels of anti-HPV16/18 antibodies comparable to those of non-smoking women. Low-avidity HPV16/18 IgG antibodies were observed in 16% of the vaccinated women, and active smoking conferred a three-fold increased risk (95% CI 1.0-9.3) of having the low-avidity antibodies.
Conclusion
Our data suggest that while smoking does not interfere with the quantity of vaccine-induced peak IgG levels, it may affect the avidity of IgG induced by HPV16/18 vaccination.
The AS04-adjuvanted bivalent L1 virus-like-particle (VLP) vaccine (Cervarix™) against infection with human papillomavirus (HPV) types 16/18 holds great promise to prevent HPV16/18 infections and associated neoplasias, but it is important to rule out significant co-factors of the neoplasias like smoking.
Methods
We conducted a pilot study to compare the quantity and quality of HPV16/18 antibody response at baseline and 7 months post vaccination in 104 non-smoking and 112 smoking female participants vaccinated at 0, 1 and 6 months with Cervarix™ (55 and 48 study participants) or with Hepatitis A vaccine (HAVRIX™) (48 and 64 participants, respectively). These 216 women were a sub-sample of 4808 baseline 16- to 17-year old Finnish women initially enrolled in the double-blind, randomized controlled phase III PATRICIA trial. Following end-of-study unblinding in 2009 they were randomly chosen out of all the participants of the three major Finnish PATRICIA study sites in the Helsinki metropolitan area (University of Helsinki, N = 535, and Family Federation Finland, N = 432) and Tampere (University of Tampere, N = 428). Following enrolment, serum samples were collected at month 0 and month 7 post 1st vaccination shot, and were analysed for levels and avidity of IgG antibodies to HPV16 and HPV18 using standard and modified (4 M urea elution) VLP ELISAs.
Results
We found that at month 7 post vaccination women who smoked (cotinine level > 20 ng/ml) had levels of anti-HPV16/18 antibodies comparable to those of non-smoking women. Low-avidity HPV16/18 IgG antibodies were observed in 16% of the vaccinated women, and active smoking conferred a three-fold increased risk (95% CI 1.0-9.3) of having the low-avidity antibodies.
Conclusion
Our data suggest that while smoking does not interfere with the quantity of vaccine-induced peak IgG levels, it may affect the avidity of IgG induced by HPV16/18 vaccination.
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