ライフサイエンスコーパス: HPV infection

1 nteracting protein and endocytosis factor in HPV infection.

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

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

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

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

6 al history and transmission dynamics of oral HPV infection.

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

8 ar whether hA3 proteins can directly inhibit HPV infection.

9 in tumor types not typically associated with HPV infection.

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

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

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

13 x partners was significantly associated with HPV infection.

14 from HNSCC tissue specimens with and without HPV infection.

15 estimate the population prevalence of penile HPV infection.

16 ed with a significantly decreased risk of HR-HPV infection.

17 h a decreased risk of persistent cervical HR-HPV infection.

18 in the tonsillar crypts, the site of initial HPV infection.

19 HPV-positive men but had no association with HPV infection.

20 er survivors may be directly attributable to HPV infection.

21 tial immune modulating effects of obesity on HPV infection.

22 Both vaccines prevent HPV infection.

23 al to eradicate most cancers attributable to HPV infection.

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

25 V) antibodies may protect against subsequent HPV infection.

26 nvestigated the link between bereavement and HPV infection.

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

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

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

30 observed association between penile and oral HPV infections.

31 ociations were found for clearance in all HR-HPV infections.

32 of nononcogenic HPV types on the outcome of HPV infections.

33 on the redetection of oncogenic or high-risk HPV infections.

34 taminants from a partner and not established HPV infections.

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

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

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

38 host's defense against human papillomavirus (HPV) infection.

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

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

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

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

43 infections) of men acquired an incident oral HPV infection, 1.7% (1.2-2.5; n=53 incident infections)

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

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

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

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

48 HPV infection abrogated gene expression associated with

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

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

51 nce interval [CI], 3.5-4.8) and anal vs oral HPV infections (aHR = 1.5; 95% CI, 1.2-1.9).

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

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

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

55 mined the determinants of initial anogenital HPV infection among teenage MSM.

56 A lower cumulative probability of HPV infection among women with a sexual debut before the

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

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

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

60 that the prevalence of human papillomavirus (HPV) infection among women was 42.7% in the cervix and 3

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

62 edispose to neoplastic transformations after HPV infection and (ii) predispose to HPV infection itsel

63 sex with men (MSM) are at increased risk of HPV infection and anal cancer compared with HIV-negative

64 Risk factors for HPV infection and anal precancer are similar to establis

65 We evaluated risk factors for HPV infection and anal precancer in a population of HIV-

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

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

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

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

70 zards regression, type-specific incidence of HPV infection and clearance were modeled for each risk g

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

72 In cervical cancer, HPV infection and disruption of mechanisms involving cel

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

74 iving longer, have a high prevalence of oral HPV infection and have many of the currently determined

75 escribes the risk factors and burden of oral HPV infection and HPV-associated head and neck cancer (H

76 ession of miR-218 was lower in PSCCs with HR-HPV infection and in p53(-) cancers.

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

78 ere moderately low levels of knowledge about HPV infection and prevention of cervical cancer, but a m

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

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

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

82 We analyzed data from the "HPV Infection and Transmission Among Couples Through Het

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

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

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

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

87 risk of newly detected human papillomavirus (HPV) infection and cervical abnormalities in relation to

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

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

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

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

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

93 he association between human papillomavirus (HPV) infection and the risk of human immunodeficiency vi

94 e patients had data on human papillomavirus (HPV) infection and were followed up for at least 24 mo o

95 n=53 incident infections) an oral oncogenic HPV infection, and 0.6% (0.3-1.1; n=18 incident infectio

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

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

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

99 is (AOR, 3.1; 95% CI, 1.5-6.7), and cervical HPV infection (AOR, 2.6; 95% CI, 1.4-4.6).

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

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

102 Given that persistent oncogenic HPV infections are associated with cancer-related outcom

103 Anal human papillomavirus (HPV) infections are common, and the incidence of anal ca

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

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

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

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

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

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

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

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

112 en without anal HPV infection; men with anal HPV infection, but no precancer; and men with anal preca

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

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

115 , 50% and 75% of women acquired their causal HPV infection by ages 20.6 (range: 20.1-21.1) and 30.6 (

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

117 the presence of oncogenic and non-oncogenic HPV infections by the linear array method.

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

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

120 Oral human papillomavirus (HPV) infection causes a subset of oropharyngeal cancers.

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

122 HPV infection clearly attenuated the magnitude of the re

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

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

125 The number of concurrent HPV infections conformed to an overdispersed Poisson dis

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

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

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

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

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

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

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

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

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

135 the relationship between HPV antibodies and HPV infection during 2 years of follow-up among women ne

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 f 59 PSCCs and 8 condylomata for presence of HPV infection, for p16(INK4a), Ki-67, and p53 immunohist

140 Human papillomavirus (HPV) infection frequently induces hyperproliferation of

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

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

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

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

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

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

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

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

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

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

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

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 es of anal exposure to human papillomavirus (HPV) infection, immunodeficiency, and combined antiretro

155 The initial events regulating HPV infection impact the establishment of viral persiste

156 study was conducted to investigate cutaneous HPV infection in BCC.

157 00 had 7 times increased odds of carrying HR HPV infection in comparison to women with CD4+>200.

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

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

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

161 ears, in part because of increasing rates of HPV infection in HNSCC; however, the underlying mechanis

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

163 of anogenital cancer were recruited into the HPV Infection in Men (HIM) cohort study.

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

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

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

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

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

169 rospective analysis was conducted within the HPV Infection in Men Study, a multinational HPV cohort s

170 combination with HPV vaccination to prevent HPV infection in men.

171 med to establish the natural history of oral HPV infection in men.

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

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

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

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

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

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

178 Newly acquired oral oncogenic HPV infections in healthy men were rare and most were cl

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

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

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

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

183 st a large spectrum of mucosal and cutaneous HPV infections in vivo.

184 ated with high-risk human papillomavirus (HR-HPV) infection in 30% to 60% of cases.

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

186 acy of condoms against human papillomavirus (HPV) infection in males are limited.

187 oncurrence of multiple human papillomavirus (HPV) infections in 47,617 women who underwent cervical s

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

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

190 Prevalence of penile HPV infection increases with increasing age.

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

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

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

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

195 Oral HPV infection is commonly detected in HIV-infected indiv

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

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

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

199 Persistent HPV infection is recognized as the main etiologic factor

200 HPV infection is strongly associated with the developmen

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

202 The prevalence of anal vs oral HPV infections is higher in this population, but whether

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

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

205 Human papillomavirus (HPV) infection is necessary but not sufficient for cervi

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

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

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

209 s after HPV infection and (ii) predispose to HPV infection itself.

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

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

212 rovides support for the hypothesis that beta-HPV infections may contribute to nonmelanoma skin cancer

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

214 These data support the hypothesis that beta-HPV infections may promote tumorigenesis via genome dest

215 To estimate incidence and clearance of HPV infections, men residing in Brazil, Mexico, and the

216 s of risk factors comparing men without anal HPV infection; men with anal HPV infection, but no preca

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

218 survivors of PAYA cancers to assess whether HPV infections might be a reasonable area of future etio

219 boys as a strategy to avert the morbidity of HPV infection, most YMSM appear to remain naive to eithe

220 d that cervical cancer is directly linked to HPV infection, nearly 32% failed to identify it as a sex

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

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

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

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

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

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

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

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

229 The number of concurrent HPV infections per woman was studied by Poisson regressi

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

231 Oncogenic HPV infection predicted progression of cervical dysplasi

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

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

234 shed estimates of anal human papillomavirus (HPV) infection rates among young men who have sex with m

235 These HPVs likely represent true HPV infections rather than transitory exposure because o

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

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

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

239 For example, HPV infection repressed expression of the differentiated

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

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

242 ct on sexual behavior, low perceived risk of HPV infection, social influences, irregular preventive c

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

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

245 variant patterns were similar regardless of HPV infection status.

246 en and women, but a higher incidence of oral HPV infection (test of interaction P < 0.001).

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

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

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

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

251 After HPV infection, the E7 protein suppresses ubiquitin ligas

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

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

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

255 78% (130/167) of the women had HR HPV infections; the prevalence of abnormal cervical cyto

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

257 roteins are involved in the progression from HPV infection to cell transformation to cancer.

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

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

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

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

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

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

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

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

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

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

268 The probability of clearing an oncogenic HPV infection was 30% higher among nonmonogamous men who

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

270 The incidence rate for any new HPV infection was 38.5 per 1000 person-months and 15.3 p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

288 The prevalence of any and multiple HR-HPV infections was 83.4% and 60.5%, respectively.

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

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

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

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

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

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

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

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

297 ong the six male partners, no oncogenic oral HPV infections were detected.

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

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

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

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