Human papillomavirus serology and tobacco smoking in a community control group

Background HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-f...
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Autor*in:	Kelsey, Karl T [verfasserIn] Nelson, Heather H Kim, Stephanie Pawlita, Michael Langevin, Scott M Eliot, Melissa Michaud, Dominique S McClean, Michael

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	HPV Smoking Serology

Anmerkung:	© Kelsey et al.; licensee BioMed Central. 2015

Übergeordnetes Werk:	Enthalten in: BMC infectious diseases - London : BioMed Central, 2001, 15(2015), 1 vom: 09. Jan.
Übergeordnetes Werk:	volume:15 ; year:2015 ; number:1 ; day:09 ; month:01

Links:	Volltext

DOI / URN:	10.1186/s12879-014-0737-3

Katalog-ID:	SPR028072510

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100	1		\|a Kelsey, Karl T \|e verfasserin \|4 aut
245	1	0	\|a Human papillomavirus serology and tobacco smoking in a community control group
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520			\|a Background HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals. Methods Subjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression. Results We found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked ($ p_{interaction} $ < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7). Conclusions Exposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers.
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700	1		\|a Langevin, Scott M \|4 aut
700	1		\|a Eliot, Melissa \|4 aut
700	1		\|a Michaud, Dominique S \|4 aut
700	1		\|a McClean, Michael \|4 aut
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allfields	10.1186/s12879-014-0737-3 doi (DE-627)SPR028072510 (SPR)s12879-014-0737-3-e DE-627 ger DE-627 rakwb eng Kelsey, Karl T verfasserin aut Human papillomavirus serology and tobacco smoking in a community control group 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Kelsey et al.; licensee BioMed Central. 2015 Background HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals. Methods Subjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression. Results We found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked ($ p_{interaction} $ < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7). Conclusions Exposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers. HPV (dpeaa)DE-He213 Smoking (dpeaa)DE-He213 Serology (dpeaa)DE-He213 Nelson, Heather H aut Kim, Stephanie aut Pawlita, Michael aut Langevin, Scott M aut Eliot, Melissa aut Michaud, Dominique S aut McClean, Michael aut Enthalten in BMC infectious diseases London : BioMed Central, 2001 15(2015), 1 vom: 09. Jan. (DE-627)326645381 (DE-600)2041550-3 1471-2334 nnns volume:15 year:2015 number:1 day:09 month:01 https://dx.doi.org/10.1186/s12879-014-0737-3 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2015 1 09 01
spelling	10.1186/s12879-014-0737-3 doi (DE-627)SPR028072510 (SPR)s12879-014-0737-3-e DE-627 ger DE-627 rakwb eng Kelsey, Karl T verfasserin aut Human papillomavirus serology and tobacco smoking in a community control group 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Kelsey et al.; licensee BioMed Central. 2015 Background HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals. Methods Subjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression. Results We found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked ($ p_{interaction} $ < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7). Conclusions Exposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers. HPV (dpeaa)DE-He213 Smoking (dpeaa)DE-He213 Serology (dpeaa)DE-He213 Nelson, Heather H aut Kim, Stephanie aut Pawlita, Michael aut Langevin, Scott M aut Eliot, Melissa aut Michaud, Dominique S aut McClean, Michael aut Enthalten in BMC infectious diseases London : BioMed Central, 2001 15(2015), 1 vom: 09. Jan. (DE-627)326645381 (DE-600)2041550-3 1471-2334 nnns volume:15 year:2015 number:1 day:09 month:01 https://dx.doi.org/10.1186/s12879-014-0737-3 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2015 1 09 01
allfields_unstemmed	10.1186/s12879-014-0737-3 doi (DE-627)SPR028072510 (SPR)s12879-014-0737-3-e DE-627 ger DE-627 rakwb eng Kelsey, Karl T verfasserin aut Human papillomavirus serology and tobacco smoking in a community control group 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Kelsey et al.; licensee BioMed Central. 2015 Background HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals. Methods Subjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression. Results We found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked ($ p_{interaction} $ < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7). Conclusions Exposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers. HPV (dpeaa)DE-He213 Smoking (dpeaa)DE-He213 Serology (dpeaa)DE-He213 Nelson, Heather H aut Kim, Stephanie aut Pawlita, Michael aut Langevin, Scott M aut Eliot, Melissa aut Michaud, Dominique S aut McClean, Michael aut Enthalten in BMC infectious diseases London : BioMed Central, 2001 15(2015), 1 vom: 09. Jan. (DE-627)326645381 (DE-600)2041550-3 1471-2334 nnns volume:15 year:2015 number:1 day:09 month:01 https://dx.doi.org/10.1186/s12879-014-0737-3 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2015 1 09 01
allfieldsGer	10.1186/s12879-014-0737-3 doi (DE-627)SPR028072510 (SPR)s12879-014-0737-3-e DE-627 ger DE-627 rakwb eng Kelsey, Karl T verfasserin aut Human papillomavirus serology and tobacco smoking in a community control group 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Kelsey et al.; licensee BioMed Central. 2015 Background HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals. Methods Subjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression. Results We found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked ($ p_{interaction} $ < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7). Conclusions Exposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers. HPV (dpeaa)DE-He213 Smoking (dpeaa)DE-He213 Serology (dpeaa)DE-He213 Nelson, Heather H aut Kim, Stephanie aut Pawlita, Michael aut Langevin, Scott M aut Eliot, Melissa aut Michaud, Dominique S aut McClean, Michael aut Enthalten in BMC infectious diseases London : BioMed Central, 2001 15(2015), 1 vom: 09. Jan. (DE-627)326645381 (DE-600)2041550-3 1471-2334 nnns volume:15 year:2015 number:1 day:09 month:01 https://dx.doi.org/10.1186/s12879-014-0737-3 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2015 1 09 01
allfieldsSound	10.1186/s12879-014-0737-3 doi (DE-627)SPR028072510 (SPR)s12879-014-0737-3-e DE-627 ger DE-627 rakwb eng Kelsey, Karl T verfasserin aut Human papillomavirus serology and tobacco smoking in a community control group 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Kelsey et al.; licensee BioMed Central. 2015 Background HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals. Methods Subjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression. Results We found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked ($ p_{interaction} $ < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7). Conclusions Exposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers. HPV (dpeaa)DE-He213 Smoking (dpeaa)DE-He213 Serology (dpeaa)DE-He213 Nelson, Heather H aut Kim, Stephanie aut Pawlita, Michael aut Langevin, Scott M aut Eliot, Melissa aut Michaud, Dominique S aut McClean, Michael aut Enthalten in BMC infectious diseases London : BioMed Central, 2001 15(2015), 1 vom: 09. Jan. (DE-627)326645381 (DE-600)2041550-3 1471-2334 nnns volume:15 year:2015 number:1 day:09 month:01 https://dx.doi.org/10.1186/s12879-014-0737-3 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2015 1 09 01
language	English
source	Enthalten in BMC infectious diseases 15(2015), 1 vom: 09. Jan. volume:15 year:2015 number:1 day:09 month:01
sourceStr	Enthalten in BMC infectious diseases 15(2015), 1 vom: 09. Jan. volume:15 year:2015 number:1 day:09 month:01
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	HPV Smoking Serology
isfreeaccess_bool	true
container_title	BMC infectious diseases
authorswithroles_txt_mv	Kelsey, Karl T @@aut@@ Nelson, Heather H @@aut@@ Kim, Stephanie @@aut@@ Pawlita, Michael @@aut@@ Langevin, Scott M @@aut@@ Eliot, Melissa @@aut@@ Michaud, Dominique S @@aut@@ McClean, Michael @@aut@@
publishDateDaySort_date	2015-01-09T00:00:00Z
hierarchy_top_id	326645381
id	SPR028072510
language_de	englisch
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We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals. Methods Subjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression. Results We found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked ($ p_{interaction} $ < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7). Conclusions Exposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">HPV</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Smoking</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Serology</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Nelson, Heather H</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kim, Stephanie</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pawlita, Michael</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Langevin, Scott M</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Eliot, Melissa</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Michaud, Dominique S</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">McClean, Michael</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">BMC infectious diseases</subfield><subfield code="d">London : BioMed Central, 2001</subfield><subfield code="g">15(2015), 1 vom: 09. 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author	Kelsey, Karl T
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topic_title	Human papillomavirus serology and tobacco smoking in a community control group HPV (dpeaa)DE-He213 Smoking (dpeaa)DE-He213 Serology (dpeaa)DE-He213
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title	Human papillomavirus serology and tobacco smoking in a community control group
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title_full	Human papillomavirus serology and tobacco smoking in a community control group
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author_browse	Kelsey, Karl T Nelson, Heather H Kim, Stephanie Pawlita, Michael Langevin, Scott M Eliot, Melissa Michaud, Dominique S McClean, Michael
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author-letter	Kelsey, Karl T
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title_sort	human papillomavirus serology and tobacco smoking in a community control group
title_auth	Human papillomavirus serology and tobacco smoking in a community control group
abstract	Background HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals. Methods Subjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression. Results We found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked ($ p_{interaction} $ < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7). Conclusions Exposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers. © Kelsey et al.; licensee BioMed Central. 2015
abstractGer	Background HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals. Methods Subjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression. Results We found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked ($ p_{interaction} $ < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7). Conclusions Exposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers. © Kelsey et al.; licensee BioMed Central. 2015
abstract_unstemmed	Background HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals. Methods Subjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression. Results We found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked ($ p_{interaction} $ < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7). Conclusions Exposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers. © Kelsey et al.; licensee BioMed Central. 2015
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title_short	Human papillomavirus serology and tobacco smoking in a community control group
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