ライフサイエンスコーパス: HPV infection

1 estimate the population prevalence of penile HPV infection.

2 al to eradicate most cancers attributable to HPV infection.

3 V) antibodies may protect against subsequent HPV infection.

4 nvestigated the link between bereavement and HPV infection.

5 icantly less likely than women to clear oral HPV infection.

6 nteracting protein and endocytosis factor in HPV infection.

7 ding efforts to study this important step of HPV infection.

8 y inform the design of therapeutics to limit HPV infection.

9 ll dynamics in the time it takes to clear an HPV infection.

10 al history and transmission dynamics of oral HPV infection.

11 viral load that is related to the course of HPV infection.

12 ar whether hA3 proteins can directly inhibit HPV infection.

13 in tumor types not typically associated with HPV infection.

14 HLA class II alleles in antibody response to HPV infection.

15 sion of p16 is used as a surrogate marker of HPV infection.

16 x partners was significantly associated with HPV infection.

17 50 healthy individuals were tested for oral HPV infection.

18 n might also protect MSM from HSV and penile HPV infection.

19 >6 sex partners showed a higher risk of oral HPV infection.

20 stive mucosa, and the presence or absence of HPV infection.

21 regression was used to estimate the odds of HPV infection.

22 en and to examine potential risk factors for HPV infection.

23 p16 is used as a surrogate marker for HPV infection.

24 les aged 14-59 years have detectable genital HPV infections.

25 despite the younger age and higher number of HPV infections.

26 nd Aptima, frequently do not detect the same HPV infections.

27 ay be attributed to stress-induced oncogenic HPV infections.

28 ignificantly associated with persistent 7 HR-HPV infections.

29 1.8-13.0) were associated with incident 7 HR-HPV infections.

30 ignificantly associated with persistent 7 HR-HPV infections.

31 of Gal-9 on T cells in hepatitis B virus and HPV infections.

32 1.8-13.0) were associated with incident 7 HR-HPV infections.

33 observed association between penile and oral HPV infections.

34 Cs) is attributable to human papillomavirus (HPV) infection.

35 h an increased risk of human papillomavirus (HPV) infection.

36 or alcohol use and/or human papillomavirus (HPV) infection.

37 es resembling those of human papillomavirus (HPV) infection.

38 er (CC) with high-risk human papillomavirus (HPV) infections.

39 ween vaccinated women with and those without HPV infections 1 year before infection (204 incident and

40 ical lesions (2.6; 1.0-4.3), and cervical HR-HPV infection (1.8; 1.0-3.2).

41 g those with than among those without penile HPV infection (19.3% vs 4.4%; prevalence ratio, 4.37 [95

42 edictive signature for the identification of HPV infection; (2) HPV infection could disrupt some regu

43 articles in 14 high-income countries: 23 for HPV infection, 29 for anogenital warts, and 13 for CIN2+

44 women with than among those without cervical HPV infection (7.0% vs 1.4%; prevalence ratio, 4.9 [95%

45 Human papillomavirus (HPV) infection, a primary cause of genital cancer, is al

46 determinants of current multiple anogenital HPV infections, abnormal cytology, and seropositivity fo

47 associated with current multiple anogenital HPV infections, abnormal cytology, and seropositivity to

48 HPV infection abrogated gene expression associated with

49 ned by differences in the prevalence of oral HPV infection across healthy populations.

50 Cutaneous beta human papillomavirus (HPV) infection across cutaneous and mucosal tissues with

51 icacy against one-time detection of incident HPV infections after three, two, and one dose(s).

52 In a cohort study of oral HPV infection among 409 individuals aged 18-25 years, th

53 we aim to evaluate the prevalence of genital HPV infection among adolescents and young adults in Braz

54 are needed to better understand the risk for HPV infection among male virgins.

55 Concordance of oral and genital HPV infection among men is unknown.

56 cing approach yielded a comprehensive map of HPV infections among different body sites of healthy hum

57 for vaccine effectiveness (VE) against anal HPV infections among women is limited.

58 ce of external genital human papillomavirus (HPV) infection among heterosexual males aged 16-24 years

59 5; I(2)=0%) and penile human papillomavirus (HPV) infection among HIV-infected MSM (0.71, 0.51-0.99;

60 data are available on human papillomavirus (HPV) infection among human immunodeficiency virus (HIV)-

61 well as the concordance of oral and genital HPV infection, among U.S. men and women.

62 of ART and other HIV-related factors on anal HPV infection, anal intraepithelial neoplasia (AIN), and

63 y of keratinocytes to control cutaneous beta-HPV infection and a high risk for non-melanoma skin canc

64 nadir CD4 counts might reduce anal high-risk HPV infection and anal cancer risk.

65 ries have shown the effect of vaccination on HPV infection and associated disease, and provided evide

66 n-1 interacting protein ALIX as critical for HPV infection and CD63-syntenin-1-ALIX complex formation

67 ly among minority females at higher risk for HPV infection and cervical cancer.

68 effective strategy to improve prevention of HPV infection and cervical cancer.

69 n for TZ tissue being the primary target for HPV infection and cervical carcinogenesis.

70 t of quadrivalent HPV (4vHPV) vaccination on HPV infection and disease.

71 the significance of the association between HPV infection and focal cortical dysplasia type IIb, and

72 elopment of prophylactic vaccines to prevent HPV infection and HPV assays that detect nucleic acids o

73 rimary and secondary prevention programs for HPV infection and HPV-related diseases should be priorit

74 oproteins, but the molecular architecture of HPV infection and its interaction with the host genome i

75 only vaccination programs in preventing oral HPV infection and potential herd immunity in unvaccinate

76 have potential as a therapeutic strategy for HPV infection and related cervical malignancy.

77 The prevalence of genital HPV infection and the HPV vaccination coverage rate amon

78 To estimate the prevalence of genital HPV infection and the HPV vaccination rate in the United

79 tial impact of HPV vaccination programmes on HPV infections and CIN2+ among girls and women, and on a

80 est that the higher burden of oral oncogenic HPV infections and HPV-positive oropharyngeal cancers am

81 the hypothesized causal association between HPV infections and lung cancer.

82 Although new HPV infections and precancers can occur throughout a wom

83 recently to evaluate the association between HPV infections and the risk of prostate cancer, the resu

84 al for both persistent human papillomavirus (HPV) infection and associated cancer progression.

85 crosimulation model of human papillomavirus (HPV) infection and cervical cancer to reflect 1) a shift

86 nce risk of persistent Human Papillomavirus (HPV) infection and cervical carcinogenesis.

87 sults-namely high-risk human papillomavirus (HPV) infection and cytohistopathology-predict anal HPV16

88 tions between cervical human papillomavirus (HPV) infection and human immunodeficiency virus (HIV) ac

89 s associated with oral human papillomavirus (HPV) infection and oral lesions in 161 human immunodefic

90 fic prevalence of anal human papillomavirus (HPV) infection and risk factors for anal high-risk (HR)

91 lations among the p53 Arg72Pro polymorphism, HPV infection, and the risk of developing oral cancer.

92 sed the role of specific ESCRT components in HPV infection, and we find an essential role for VPS4.

93 ota (VMB) composition, human papillomavirus (HPV) infection, and cervical intraepithelial neoplasia (

94 Human papillomavirus (HPV) infection, and its sequelae of precancerous cervica

95 alence of at least one HPV-related endpoint: HPV infection, anogenital warts, and high-grade cervical

96 ls and women against human papillomavirus on HPV infections, anogenital wart diagnoses, and cervical

97 f at least one HPV-related endpoint (genital HPV infections, anogenital wart diagnoses, or histologic

98 risk factors for and natural history of oral HPV infection are largely unknown.

99 rtant function in HPV replication.IMPORTANCE HPV infections are an important driver of many epithelia

100 atural history of anal human papillomavirus (HPV) infection are scarce in human immunodeficiency viru

101 Identification of HPV infection as the etiologic agent of virtually all ca

102 To determine the prevalence of oral HPV infection, as well as the concordance of oral and ge

103 incident high-risk human papillomavirus (HR-HPV) infection associated with recent sexual behaviors i

104 We report here that HPV infection associates with a 2.5-fold increase in HIV

105 These data suggest that HPV infections at these 2 sites are not independent, alt

106 compared the epidemiology of oral oncogenic HPV infection between men and women ages 14 to 69 years

107 garding the difference in prevalence of oral HPV infection between men and women is limited.

108 4.8%) specimens, with a different pattern of HPV infection between sexes.

109 arance of high-risk human papillomavirus (HR-HPV) infection between ethnicities.

110 nt in association with human papillomavirus (HPV) infection, both HPV16 and other HPV types.

111 ers have shown protection against subsequent HPV infection, but previous studies were restricted to f

112 at hA3A acts as a restriction factor against HPV infection, but the induction of this restriction mec

113 , 50% and 75% of women acquired their causal HPV infection by ages 20.6 (range: 20.1-21.1) and 30.6 (

114 we estimated the cumulative number of causal HPV infections by age, stratified by HPV genotype (HPV16

115 smitted infections worldwide, and persistent HPV infection can cause warts and even cancer.

116 Although new human papillomavirus (HPV) infections can occur at all ages, the age at which

117 Oncogenic human papillomavirus (HPV) infections cause most cases of cervical cancer.

118 t high-risk genus human Alphapapillomavirus (HPV) infections cause nearly every cervical carcinoma an

119 nvolves three independent, dynamic models of HPV infection, cervical carcinogenesis, screening, and p

120 The majority of anal HPV infections cleared within 3 years.

121 th HPV-OPC do not seem to have elevated oral HPV infection compared with the general population.

122 ype-specific test result), or newly acquired HPV infection, compared with HPV-negative women.

123 nfections were slower to clear than other HR-HPV infections, consistent with its role in anal cancer.

124 Human papillomavirus (HPV) infection correlates with higher rates of HIV acqui

125 mportance of nononcogenic viruses in a mixed HPV infection could be for stimulating or inhibiting a c

126 for the identification of HPV infection; (2) HPV infection could disrupt some regulatory miRNA-mRNA c

127 7) or between HIV acquisition and persistent HPV infection (defined as 2 positive HPV genotype-specif

128 st results at least 6 months apart), cleared HPV infection (defined as a positive HPV test result fol

129 , and was also more strongly associated with HPV infections designated as high-risk compared with low

130 Seventy percent of YMSM had any HPV infection detected during the study, and HPV-16 and/

131 Human papillomavirus (HPV) infection distinctly alters methylation patterns in

132 If beta-HPV infections do promote cSCCs, they are hypothesized t

133 us and categorical forms) and cervicovaginal HPV infection (due to high-risk HPV or vaccine-type HPV)

134 persistent anogenital human papillomavirus (HPV) infection, due to prolonged immunodeficiency.

135 persistent anogenital human papillomavirus (HPV) infection, due to prolonged immunodeficiency.

136 al acquisition of anal human papillomavirus (HPV) infection following a type-specific genital HPV inf

137 ence conferred protection against subsequent HPV infection for HPV16 and indicated possible protectio

138 infection following a type-specific genital HPV infection for the 9-valent vaccine HPV types and inv

139 women are at risk for human papillomavirus (HPV) infection from female and male sexual partners.

140 nce from the trials and present knowledge of HPV infection, future efficacy trials for new vaccines c

141 MSW with prior genital HPV infections had a higher risk of a subsequent type-sp

142 Human Papillomavirus (HPV) infection has been recognized as the main etiologic

143 Human papillomavirus (HPV) infection has been shown as a risk factor for certa

144 cy (VE) against vulvar human papillomavirus (HPV) infection has not been reported and data regarding

145 on with cervicovaginal human papillomavirus (HPV) infection has not been studied.

146 Many approaches that diagnose HPV infections have been developed, while most of them h

147 Persistent HPV infections have limited VL fluctuations.

148 l douching and genital human papillomavirus (HPV) infection have found contrary results.

149 Human papillomavirus (HPV) infections have been implicated in lung carcinogene

150 HPV type, and 25 men developed incident oral HPV infection (HPV-6 was detected in 7, HPV-11 in 0, HPV

151 on was used to study whether persistent anal HPV infections, HPV viral loads, and seropositivity for

152 at similar risk of clearing existing alpha-9 HPV infections (HR, 0.9; 95% CI, .7-1.3).

153 ntibodies protect against subsequent genital HPV infection (ie, natural immunity).

154 emale-only vaccination against oropharyngeal HPV infection in contemporaneously aged males.

155 ity against subsequent genital type-specific HPV infection in female and male subjects.

156 odest protection against subsequent cervical HPV infection in female subjects.

157 ults raise questions about the prevalence of HPV infection in focal cortical dysplasias and about its

158 ion and risk factors for anal high-risk (HR) HPV infection in human immunodeficiency virus (HIV)-infe

159 HPV Infection in Men (HIM) study participants who contri

160 HPV Infection in Men (HIM) Study participants who had HP

161 bcohort of men (n = 87) participating in the HPV Infection in Men (HIM) study provided eyebrow hairs,

162 Data from the HPV Infection in Men (HIM) study which followed particip

163 Among 1618 men participating in the HPV Infection in Men (HIM) Study, we evaluated oral rins

164 cohort of 209 men initially enrolled in the HPV Infection in Men (HIM) study.

165 ved between these factors and prevalent oral HPV infection in previous cross-sectional studies.

166 n at which individuals acquired their causal HPV infection in the absence of HPV vaccination or scree

167 These data confirm persistent oral HPV infection in the majority of patients with RRP.

168 ve was to determine the prevalence of penile HPV infection in the United States.

169 ated disease, prospective studies of genital HPV infection in this population are scarce.

170 The establishment and maintenance of HPV infection in undifferentiated basal cells of the squ

171 combinatorial vaccine(s) was able to reduce HPV infection in vivo and induce anti-VAR2CSA IgG antibo

172 We studied concurrent HPV infections in 17-year-old girls from two birth cohor

173 y, in addition to supporting a role for beta-HPV infections in certain skin cancers, we present studi

174 HR HPV infections in HIV infected females may consist of mo

175 HPV 45 accounted for a greater proportion of HPV infections in ICCs compared with normal cytological

176 We evaluated a potential causal role for HPV infections in lung cancer through an analysis involv

177 ong males, and vaccine efficacy against oral HPV infections in men has not been previously evaluated.

178 t (OR, 6.7 [95% CI, 1.5-30.7]) type-specific HPV infections in their partner.

179 e excess in detectable human papillomavirus (HPV) infection in Latin America, via a global T-helper t

180 The clustering of human papillomavirus (HPV) infections in some individuals is often interpreted

181 nce of penile and oral human papillomavirus (HPV) infections in the United States.

182 Prevalence of penile HPV infection increases with increasing age.

183 In the development of cancer, persistent HPV infections induce E6 and E7 oncoproteins, which prom

184 Whether type-specific human papillomavirus (HPV) infection influences the risk of acquiring infectio

185 Human Papillomavirus (HPV) infection involves multiple steps, from cell attach

186 However, HPV infection is believed to occur many years before can

187 Oral HPV infection is common among U.S. men.

188 x, collectively referred as non-OPSCC, where HPV infection is less common than in the oropharynx.

189 ausally associated with cervical cancer, but HPV infection is not sufficient for carcinogenesis.

190 population prevalence data for male genital HPV infection is not well known, while the HPV vaccinati

191 Persistent HPV infection is recognized as the main etiologic factor

192 HPV infection is strongly associated with the developmen

193 correlation between these proteins and beta-HPV infection is unclear.

194 Clearance of anogenital and oropharyngeal HPV infections is attributed primarily to a successful a

195 al correlation between times-at-risk for all HPV infections is not generally considered in the analys

196 ciated with high-risk human papilloma virus (HPV) infection is a growing clinical problem.

197 Although the risk of human papillomavirus (HPV) infection is greatest in young women, women older t

198 epidemiology of penile human papillomavirus (HPV) infection is not well understood.

199 High-risk human papillomavirus (HPV) infection is one of the first events in the process

200 High-risk anal human papillomavirus (HPV) infection is prevalent among men living with human

201 Oncogenic human papillomavirus (HPV) infection is the cause of nearly all cervical cance

202 wledge that persistent human papillomavirus (HPV) infection is the main cause of cervical cancer has

203 Persistent human papillomavirus (HPV) infection is the vital factor driving cervical carc

204 rsistence of high-risk human papillomavirus (HPV) infections is the key risk factor for developing HP

205 te marker of oncogenic human papillomavirus (HPV) infection, is recognized as a prognostic marker in

206 ociated with beta human papillomavirus (beta-HPV) infection-is increased by more than 100-fold in imm

207 man papilloma viruses (HPVs), and persistent HPV infections lead to cervical cancer or other deadly c

208 Other than an association with HPV infection, little is known about the genetic alterat

209 Taken together, the data indicate that HPV infection manipulates the differentiating keratinocy

210 In conclusion, HPV infections may contribute to the risk of prostate ca

211 that p53 Arg72Pro polymorphism together with HPV infection might jointly alter an individual's suscep

212 We conclude that the HPV infection model provides a valuable tool to distingu

213 Anal human papillomavirus (HPV) infection, most notably HPV16, the central cause of

214 t incremental reductions in the incidence of HPV infection occurring when offering vaccination both a

215 th high VL had more type-specific persistent HPV infections (odds ratio [OR], 4.6 [95% confidence int

216 and can be used to elucidate early stages in HPV infection of primary keratinocytes.

217 ine kinase Pyk2 during human papillomavirus (HPV) infection of human skin cells.

218 To address direct effects of HPV infection on the host cell transcriptome, we have us

219 the harmful effect of human papillomavirus (HPV) infection on pregnancy, but observational studies a

220 to 15% in each age stratum had a history of HPV infection or disease.

221 in each age stratum could have a history of HPV infection or disease.

222 d HPV reactivation or in immune responses to HPV infection or persistence.

223 ondary prevention through screening for oral HPV infection or seroreactivity to viral antigens.

224 ytokines profiled, cytokines associated with HPV infection overlap substantially with cytokines assoc

225 History of HPV infection, particularly in black organ transplant re

226 10-30% of oral high-risk HPV infections persisted >24 months.

227 ogistic regression was performed to evaluate HPV infection, persistence, and clearance as predictors

228 The overall genital HPV infection prevalence appears to be widespread among

229 The overall genital HPV infection prevalence was 45.2% (95% CI, 41.3%-49.3%)

230 smoke and harbor oral human papillomavirus (HPV) infections, putting them at higher risk for head an

231 anisms that block the early establishment of HPV infections remain mysterious.

232 olymorphism and the risk of oral cancer with HPV infection remains inconclusive.

233 oduction of infectious virus and reveal that HPV infection remodels keratinocytes for completion of t

234 For example, HPV infection repressed expression of the differentiated

235 the natural history of human papillomavirus (HPV) infection require reproducible, type-specific testi

236 MSM with prevalent high-risk HPV infection should be considered at increased risk for

237 ntrast, HIV-infected MSM with normal aLBC/HR-HPV infection should be considered for HRA.

238 exually active women for whom cervicovaginal HPV infection status and serum 25-hydroxyvitamin D (25[O

239 There was no evidence of association between HPV infection status and subsequent HIV acquisition.

240 variant patterns were similar regardless of HPV infection status.

241 ater predicted probability of high-risk oral HPV infection than women.

242 he age at which women acquire their "causal" HPV infection that develops into cervical cancer is poor

243 ital mucosa, may influence susceptibility to HPV infections that lead to cervical cancer.

244 discordance identified a cluster of low-risk HPV infections that were hardly ever associated with hig

245 After HPV infection, the E7 protein suppresses ubiquitin ligas

246 lactic HPV vaccination on the burden of oral HPV infection, the principal cause of HPV-positive oroph

247 in immunocompetent adolescents with cervical HPV infections, the immune response may contribute less

248 In human papillomavirus (HPV) infection, the cellular protein complex known as re

249 ies in cancer risk; the epidemiology of oral HPV infection; the latency period between infection and

250 78% (130/167) of the women had HR HPV infections; the prevalence of abnormal cervical cyto

251 nal role in the persistence or regression of HPV infections, this has yet to be described in women wi

252 nt of approaches that make the conversion of HPV infection to cancer development even more rare.

253 quired to understand the progression of oral HPV infection to HPV-OPC.

254 udy on the effects of human papilloma virus (HPV) infection to the EC's response to CD40 ligation.

255 cidence and prevalence of type-specific anal HPV infection using clinician-collected anal swabs for H

256 In addition, it is possible to assess HPV infection using serology-based methods; however, the

257 ) are at high risk for human papillomavirus (HPV) infection; vaccination is recommended for US males,

258 tection in women with prior vaccine-targeted HPV infections, vaccine cost, coverage, and natural- and

259 The overall prevalence of oral HPV infection was 11.5% (95% CI, 9.8% to 13.1%) in men a

260 me-sex partners, the prevalence of high-risk HPV infection was 12.7% (CI, 7.0% to 18.4%) and 3.6% (CI

261 We found that the prevalence of HPV infection was 18.93% (95% CI = 17.84-20.05%) in pros

262 al sex partners, the prevalence of high-risk HPV infection was 22.2% (CI, 9.6% to 34.8%).

263 The prevalence of >/=1 genotype-concordant HPV infection was 3.2% and was associated with sexual be

264 ear cumulative incidence of any type of oral HPV infection was 34% in HIV-infected persons and 19% in

265 prevalence among men with concurrent genital HPV infection was 4-fold greater (19.3%) than among thos

266 ed States, the overall prevalence of genital HPV infection was 45.2% (95% CI, 41.3%-49.3%).

267 The overall prevalence of any HPV infection was 45.2% (95% confidence interval [CI], 4

268 The prevalence of oral HPV infection was 5-fold higher among women with than am

269 The prevalence of HPV infection was 6.7% in the oral cavity and 16.9% for

270 required for 50% of participants to clear HR-HPV infection was 601 days for African American women (n

271 The prevalence of any HPV infection was almost 80% among men who reported havi

272 Sequential risk of anal HPV infection was assessed using hazard ratios (HRs) amo

273 Having a high-risk HPV infection was associated with sexual risk behavior a

274 At enrollment, HPV infection was detected in 54% of HIV-negative women,

275 olymorphism and the risk of oral cancer with HPV infection was detected in the Arg/Arg vs. Arg/Pro +

276 Concordance of any beta-HPV infection was greater (31.0%) across the 3 keratiniz

277 The predicted probability of high-risk oral HPV infection was greatest among black participants, tho

278 The risk of oral HPV infection was higher among men with genital infectio

279 Risk of HPV infection was modelled using mixed-effect logistic r

280 High-risk oral HPV infection was more prevalent among men (7.3% [CI, 6.

281 A cross-sectional study of anal and cervical HPV infection was nested within a gynecological cohort o

282 found: (1) Co-occurrence of mutant TP53 and HPV infection was rare; (2) Regardless of HPV status, HN

283 participants, but the frequency of incident HPV infection was the same in African American and Europ

284 higher risk of sequential type-specific anal HPV infections was observed for any of the 9 types (adju

285 Six months persistence of oral high-risk HPV infections was positively associated with age and gi

286 Prevalence of human papillomavirus (HPV) infections was assessed among 1033 young men who ha

287 n order to identify host lncRNAs affected by HPV infection, we expressed the high-risk HPV-16 E6 onco

288 oncogenic pathways in HNSCC with and without HPV infection, we used targeted next-generation sequenci

289 s, factors associated with prevalent anal HR-HPV infection were CD4(+)count <350/muL (odds ratio, 2.9

290 Similarly, the odds of vaccine-type HPV infection were increased in women with vitamin D lev

291 y, and marital status, the odds of high-risk HPV infection were increased per each 10 ng/mL decrease

292 artnership, approximately 64% of incident HR-HPV infections were attributable to one of those partner

293 Overall, multiple HPV infections were detected in 26% of the women.

294 Prevalence of hrHPV and multiple HPV infections were higher among HIV-infected than among

295 Cervical and anal HPV infections were highly correlated.

296 Persistent HPV infections were strongly associated with anal HSIL,

297 partners increased the risk of incident oral HPV infection, whereas male sex, older age, and current

298 safely streamlined by the use of persistent HPV infection, which occurs more frequently than CIN2+,

299 Oral HPV infection with vaccine types 16, 18, 6, or 11 was co

300 Moreover, we tested the association of HPV infections with prostate cancer risks by a meta-anal