ライフサイエンスコーパス: HPV-16

1 rs induced by type 16 human papilloma virus (HPV-16).

2 0-not estimable; n=5 cleared infections) for HPV 16.

3 or any HPV and 12.19 months (7.16-18.17) for HPV 16.

4 red with tumors showing negative results for HPV-16.

5 or HPV-52 to 0.96 (95% CI, 0.93 to 0.99) for HPV-16.

6 d in the regulation of the LCR of HPV-18 and HPV-16.

7 lated phylogenetically to the most prevalent HPV-16.

8 f different molecular variants of HPV-18 and HPV-16.

9 n with human papillomavirus (HPV), primarily HPV-16.

10 The highest risk of HSIL was observed for HPV-16 (0.036), followed by HPV-33 (0.028), HPV-58 (0.02

11 While PeIN lesions primarily contained HPV 16, 1 PeIN III lesion was positive for HPV 6 only.

12 18 (0.70; .43-.98) but not in male subjects (HPV-16: 1.22; .67-1.77 [P= .05 (test for heterogeneity)]

13 t common hrHPV types were HPV-35 (15.0%) and HPV-16 (13.0%).

14 o the Aptima HPV assay (AHPV) and the Aptima HPV 16 18/45 genotype assay (AHPV GT) for high-risk huma

15 n-level effectiveness of vaccination against HPV 16, 18, 6, and 11 infection in women and men, to exa

16 Elimination of HPV 16, 18, 6, and 11 is possible if 80% coverage in gir

17 For efficiency, incident infections due to HPV-16, -18, -31, -33, -35, -45, and -51 resulting in pe

18 quisition among men without vaccine-relevant HPV-16, -18, -31, -45, -6, or -11 infections at baseline

19 inst persistent or transient infections with HPV-16, -18, -33, -35, -45, and -51 did not differ signi

20 vaccine for the prevention of infection with HPV 16/18 and associated precancerous lesions at the cer

21 l abnormalities, and lesions associated with HPV 16/18 and CIN1+ irrespective of HPV type, and infect

22 e present data from the VIVIANE study of the HPV 16/18 AS04-adjuvanted vaccine in adult women after 7

23 efficacy, safety, and immunogenicity of the HPV 16/18 AS04-adjuvanted vaccine in adult women.

24 s were randomly assigned (1:1) to receive an HPV 16/18 AS04-adjuvanted vaccine or control hepatitis A

25 l neoplasia grade 3 or worse associated with HPV 16/18 cervical infection detected at colposcopy refe

26 for vaccine efficacy included women who were HPV 16/18 DNA-negative at vaccination.

27 The pooled sensitivity of HPV 16/18 genotyping for CIN3+ was about 70% for women w

28 assessment of vaccine efficacy against anal HPV 16/18 infection.

29 sider an indication that type replacement of HPV 16/18 is unlikely to be an issue in the general popu

30 egion, age stratum, baseline HPV DNA status, HPV 16/18 serostatus, and cytology.

31 L) who were triaged with tests for hrHPV and HPV 16/18 to find cervical intraepithelial neoplasia (gr

32 L) who were triaged with tests for hrHPV and HPV 16/18 to find cervical intraepithelial neoplasia (gr

33 Conclusion: Testing for HPV 16/18 to triage women with minor abnormal cytology i

34 Testing for HPV 16/18 to triage women with minor abnormal cytology i

35 unexpected, moderately protective effect of HPV 16/18 vaccination against GW.

36 In women older than 25 years, the HPV 16/18 vaccine continues to protect against infection

37 In women older than 25 years, the HPV 16/18 vaccine is efficacious against infections and

38 omen were randomly assigned (1:1) to receive HPV 16/18 vaccine or aluminium hydroxide control, with a

39 ned healthy women older than 25 years to the HPV 16/18 vaccine or control (1:1), via an internet-base

40 ined significance or greater associated with HPV 16/18 was also significant.

41 Proportion of CIN2+ cases associated with HPV 16/18 was highest (56.3%) in 25- to 29-year-old wome

42 ersistent infection or CIN1+ associated with HPV 16/18 was significant in all age groups combined (90

43 compared with continuing vaccination against HPV 16/18 will reduce rates by a further 36% (from 9.5 t

44 Vaccination against HPV types 16 and 18 (HPV 16/18) could see cervical cancer rates in women aged

45 cording to proposed vaccine efficacy against HPV 16/18, vaccine coverage, cervical cancer incidence a

46 y of the bivalent HPV vaccine for preventing HPV 16/18-associated cervical intraepithelial neoplasia

47 Cumulative vaccine efficacy against HPV 16/18-associated CIN2+ over the 11-year period was 9

48 t year 11, vaccine efficacy against incident HPV 16/18-associated CIN2+ was 100% (95% CI 89.2-100.0);

49 Similar protection was observed against HPV 16/18-associated CIN3-specifically at year 11, vacci

50 HPV 16/18-associated lesions were less common in non-His

51 valent HPV vaccine has high efficacy against HPV 16/18-associated precancer for more than a decade af

52 esting is recommended for hrHPV-positive but HPV 16/18-negative women depends on local decision thres

53 spectively, and was 5% in hrHPV-positive but HPV 16/18-negative women with either ASC-US or LSIL.

54 he average risk for CIN3+ was 17% and 19% in HPV 16/18-positive women with ASC-US and LSIL, respectiv

55 Vaccine efficacy against HPV 16/18-related 6-month persistent infection or CIN1+

56 Vaccine efficacy against HPV 16/18-related cytological abnormalities (atypical sq

57 a grade 1 or greater (CIN1+) associated with HPV 16/18.

58 direct referral if the woman is positive for HPV 16/18.

59 ia grade 1 or higher (CIN1+) associated with HPV 16/18.

60 direct referral if the woman is positive for HPV 16/18.

61 for women whose lesions tested positive for HPV-16/18 (vaccine-type cases) with all other CIN2+ (con

62 for women whose lesions tested positive for HPV-16/18 (vaccine-type cases) with that for women who h

63 End points included noninferiority of HPV-16/18 antibodies by enzyme-linked immunosorbent assa

64 Endpoints included noninferiority of HPV-16/18 antibodies for 2D_M0,6 versus 3D_M0,1,6; 2D_M0

65 Neutralizing anti-HPV-16/18 antibodies were measured by pseudovirion-based

66 The primary objective was to evaluate HPV-16/18 antibody responses at month 7.

67 ng Cervarix vaccinees, women had higher anti-HPV-16/18 antibody titers compared to men.

68 of the bivalent vaccine, whose target types HPV-16/18 are associated with approximately 90% of HPV-r

69 ears) and randomized (2:1) to receive either HPV-16/18 AS04-adjuvanted vaccine (n = 450) or placebo (

70 ted the efficacy of the human papillomavirus HPV-16/18 AS04-adjuvanted vaccine against non-vaccine on

71 The HPV-16/18 AS04-adjuvanted vaccine appears to have modera

72 The 2D regimens for the HPV-16/18 AS04-adjuvanted vaccine in girls aged 9-14 yea

73 randomised controlled clinical trials of the HPV-16/18 AS04-adjuvanted vaccine in young women, were c

74 The HPV-16/18 AS04-adjuvanted vaccine was highly immunogenic

75 n and cervical abnormalities associated with HPV-16/18 between seronegative vs seropositive women (15

76 sistent infection and CIN2+ (with or without HPV-16/18 co-infection) was seen across cohorts for HPV-

77 52, 56, 58, 59, 66, and 68), with or without HPV-16/18 co-infection, was 46.8% (95% CI 30.7-59.4) in

78 han 12 months of follow-up or those who were HPV-16/18 DNA-positive at enrolment (for the HPV-16/18 e

79 HPV-16/18 DNA-positive at enrolment (for the HPV-16/18 endpoint), we calculated vaccine efficacy agai

80 rls aged 9-14 years (M0,6 or M0,12) elicited HPV-16/18 immune responses that were noninferior to 3D i

81 Vaccine efficacy against incident HPV-16/18 infection for two-dose women who received thei

82 e assessed vaccine efficacy against incident HPV-16/18 infection in the modified total vaccinated coh

83 son-months for HPV-16/18; 19% had persistent HPV-16/18 infection.

84 int was one-time detection of first incident HPV-16/18 infections accumulated during the follow-up ph

85 Vaccine efficacy against incident HPV-16/18 infections for three doses was 77.0% (95% CI 7

86 /18 vaccine seem to protect against cervical HPV-16/18 infections, similar to the protection provided

87 VLP was formulated with the L1 VLPs from the HPV-16/18 L1 vaccine.

88 -2, -4, or -9, including the AS04-adjuvanted HPV-16/18 L1 vaccine.

89 vaccine history available, 1,561 (47%) were HPV-16/18 positive, 136 received (4%) 1 dose, 108 (3%) 2

90 .76), suggesting comparable effectiveness of HPV-16/18 vaccination against genital and anal infection

91 The AS04-HPV-16/18 vaccine administered as a 2-dose schedule was

92 he efficacy of fewer than three doses of the HPV-16/18 vaccine after 4 years of follow-up.

93 TRICIA show cross-protective efficacy of the HPV-16/18 vaccine against four oncogenic non-vaccine HPV

94 The main aim of the study was to ascertain HPV-16/18 vaccine efficacy in both full and naive cohort

95 after vaccination suggests that the bivalent HPV-16/18 vaccine has protective efficacy in men.

96 years after vaccination with AS04-adjuvanted HPV-16/18 vaccine in 2007-2009.

97 and 45 following 2 doses of AS04-adjuvanted HPV-16/18 vaccine in girls aged 9-14 years or following

98 Women were randomly assigned (1:1) to HPV-16/18 vaccine or a control hepatitis A vaccine, via

99 domly assigned to receive three doses of the HPV-16/18 vaccine or to a control vaccine; yet, some rec

100 n aged 15-25 years, one and two doses of the HPV-16/18 vaccine seem to protect against cervical HPV-1

101 xually active women in the control arm of an HPV-16/18 vaccine trial had a single anal specimen colle

102 22-29 in the control and vaccine arms of an HPV-16/18 vaccine trial in Costa Rica had oral, cervical

103 irect assessment of one-dose efficacy of the HPV-16/18 vaccine.

104 The prevalence of HPV-16/18 was 6% among YMSM with a history of 1 receptiv

105 repeated cross-sectional survey, VE against HPV-16/18 was 89.9% (95% confidence interval, 63.0%-97.2

106 GMCs for HPV-16/18 were not noninferior for 2 versus 3 doses, exc

107 inst CIN2+, where all cases co-infected with HPV-16/18 were removed, vaccine efficacy was noted for H

108 n papillomavirus 16/18 AS04-adjuvanted (AS04-HPV-16/18) vaccine schedules at months 0 and 6 (2D_M0,6)

109 sults, and vaccine history, 1,561 (47%) were HPV-16/18-positive, 136 (4%) received 1 dose of HPV vacc

110 valence was also significantly reduced among HPV-16/18-vaccinated (4.1%) compared with unvaccinated s

111 human papillomavirus (HPV) prevalence among HPV-16/18-vaccinated and unvaccinated Finnish male adole

112 or vaccine types and cross-protective types (HPV-16/18/31/33/45), the avidity index was noninferior f

113 antibody concentrations and avidity against HPV-16/18/31/33/45/52/58 were assessed.

114 n-months and 15.3 per 1000 person-months for HPV-16/18; 19% had persistent HPV-16/18 infection.

115 A total of 4% of women had HPV-16, 22% had oncogenic HPV, and 31% had any HPV detec

116 s not taking ART vs the comparison group for HPV-16 (2393 vs 3892 milli-Merck units per milliliter [m

117 58 (5.3%), HPV-52 (4.3%), HPV-18 (4.3%), and HPV-16 (3.9%) were most prevalent.

118 tion site in BPV-1 (tyrosine 102) and one in HPV-16/31 (tyrosine 138) site have been characterized.

119 en was 24.78%, the most prevalent types were HPV 16 (4.13%), HPV 31 (4.12%) and HPV 51 (3.39%), while

120 The most common types were HPV-16 (42%), HPV-51 (24%), HPV-39 (23.7%), and HPV-59 (

121 HPV 6 (43.8%), HPV 11 (10.7%), and HPV 16 (9.8%) were the genotypes most commonly detected

122 ion of HPV type 18 (HPV-18) and HPV type 16 (HPV-16), a high-throughput transfection array was used.

123 In Africa, HPV 16 accounted for 13% of HPV-positive WHIV with norma

124 and MSWM and was a median of 6.9 months for HPV-16 after combining men from the 2 groups.

125 tes of incident infections were observed for HPV 16 among baseline-seropositive men [adjusted HR, 1.3

126 in addition to girls increased the RRprev of HPV 16 among women and men by 0.18 (0.13-0.32) and 0.35

127 ge and girls-only vaccination, the RRprev of HPV 16 among women and men was 0.53 (80% UI 0.46-0.68) a

128 rls-only vaccination coverage, the RRprev of HPV 16 among women and men was 0.93 (0.90-1.00) and 0.83

129 A bivalent vaccine containing HPV 16 and 18 and a quadrivalent vaccine containing HPV

130 5-8 years of vaccination, the prevalence of HPV 16 and 18 decreased significantly by 83% (RR 0.17, 9

131 cervical infection and pre-cancer related to HPV 16 and 18 in women aged 15-26 years who were not inf

132 s were also efficacious at the prevention of HPV 16 and 18 infections at other anatomical sites in bo

133 fected females may consist of more than just HPV 16 and 18, but also HPV 52 and 58.

134 ing cervical cancer cell lines infected with HPV 16 and 18, in vivo tumor models, and ex vivo-treated

135 of women who were negative for both cervical HPV 16 and HPV 18 DNA and who were HPV 16 and HPV 18 ser

136 Findings for HPV 16 and HPV 18 in Europe/North America, Asia, and Lat

137 HPV 16 and HPV 18 in particular, but also HPV 45, at lea

138 cervical HPV 16 and HPV 18 DNA and who were HPV 16 and HPV 18 seronegative before enrolment (HPV nai

139 ons with the most carcinogenic types of HPV (HPV 16 and HPV 18) at the cervix and other anatomical si

140 A negative interaction was found between HPV 16 and several other HPV types for women with abnorm

141 h available genotype carried infections with HPV 16 and/or HPV 18; genotypes of unknown risk were als

142 Among these 14 high-risk types, HPV-16 and -18 account for approximately 70% of cervical

143 Post-2vHPV NAb titers against HPV-16 and -18 were not statistically different between

144 hylogenetic distance to vaccine target types HPV-16 and -18.

145 irls (3 doses): 0.95 (95% CI, 0.73-1.23) for HPV-16 and 0.68 (95% CI, 0.54-0.85) for HPV-18.

146 omen (3 doses): 2.07 (95% CI, 1.62-2.65) for HPV-16 and 1.76 (95% CI, 1.41-2.19) for HPV-18.

147 nths were 5808.0 (95% CI, 4961.4-6799.0) for HPV-16 and 1729.9 (95% CI, 1504.0-1989.7) for HPV-18; 53

148 re-substantial incidence reductions: 63% for HPV-16 and 84% for HPV-18.

149 accine group were seropositive for both anti-HPV-16 and anti-HPV-18 antibodies (n = 130 and n = 128 f

150 participants developed detectable serum anti-HPV-16 and anti-HPV-18 antibodies, and most had detectab

151 Anti-HPV-16 and anti-HPV-18 antibody levels remained stable a

152 Specimens were tested for anti-HPV-16 and anti-HPV-18 immunoglobulin G (IgG) levels by

153 tes and 3D/2D geometric mean titers for anti-HPV-16 and anti-HPV-18.

154 ighly conserved phospho-acceptor site on the HPV-16 and bovine papillomavirus 1 (BPV-1) L2 proteins.

155 tation of the phospho-acceptor sites of both HPV-16 and BPV-1 L2 resulted in the production of infect

156 e repository for potential substrates of the HPV-16 and HPV-11 E6 proteins in complex with E6AP.

157 ociated with both carcinogenic vaccine types HPV-16 and HPV-18 (2-sided P value <.05).

158 of HPV DNA, selective discrimination between HPV-16 and HPV-18 and good reproducibility.

159 omising candidate for the local treatment of HPV-16 and HPV-18 and other high-risk types, an importan

160 llomavirus (HPV) high-risk genotypes such as HPV-16 and HPV-18 cause the majority of anogenital tract

161 ether VGX-3100, synthetic plasmids targeting HPV-16 and HPV-18 E6 and E7 proteins, delivered by elect

162 .5) of geometric mean titer (GMT) ratios for HPV-16 and HPV-18 for girls (2 doses) compared with youn

163 We analyzed incidence and clearance of HPV-16 and HPV-18 in a French cohort of HIV-infected MSM

164 2 chimeric VLP (alone or in combination with HPV-16 and HPV-18 L1 VLPs) formulated with AS04 has the

165 HPV-16 and HPV-18 loads were measured with a LightCycler

166 of HPV vaccine 6 months apart, responses to HPV-16 and HPV-18 one month after the last dose were non

167 rval (CI) of the type-specific GMT ratio for HPV-16 and HPV-18 was greater than 0.5 (primary outcome)

168 Genotyping for HPV-16 and HPV-18 was simultaneously performed by the co

169 etric mean antibody titer ratios (3D/2D) for HPV-16 and HPV-18 were 1.09 (95% confidence interval, .9

170 GMTs for HPV-16 and HPV-18 were higher in 10-14-year-olds (18 423

171 ons (about 20% lower after 50 years for both HPV-16 and HPV-18).

172 papillomavirus (HPV) vaccine, which targets HPV-16 and HPV-18, against HPV-31, -33, and -45 infectio

173 isk human papillomaviruses (HPVs), including HPV-16 and HPV-18, are the causative agents of cervical

174 3100 were assessed in CIN2/3 associated with HPV-16 and HPV-18, in a randomised, double-blind, placeb

175 quences from these high-risk strains, mostly HPV-16 and HPV-18, represents promising strategy for ear

176 show efficacy against CIN2/3 associated with HPV-16 and HPV-18.

177 Anal HPV-16 and HPV-51 were more frequent in women born in Ca

178 k of HSIL was similar in women infected with HPV-16 and other types, compared with women infected wit

179 HPV infection detected during the study, and HPV-16 and/or -18 were detected in 37%.

180 When considering only positive HPV-16 and/or HPV-18 genotype results, the cobas test sh

181 eatest specificity (86.6%) observed when the HPV-16 and/or HPV-18 genotypes were detected.

182 Human papillomavirus virus type 16 (HPV-16) and HPV-18 cause a large proportion of oropharyn

183 ic acids, including human papillomavirus 16 (HPV-16) and parvovirus B19 (PB-19), with a picomolar sen

184 ne, thioacetamide), oncogenic viruses (SV40, HPV-16), and genetic manipulation.

185 Naturally acquired antibodies to HPV-16, and to a lesser extent HPV-18, are associated wi

186 HPV-16- and HPV-18-specific antibody levels, normalized

187 Both HPV-16- and HPV-18-transformed cells were found to be re

188 High titers of naturally acquired HPV-16 antibodies and/or linear trend for increasing ant

189 Naturally acquired HPV-16 antibody levels of 371 (95% confidence interval [

190 No significant differences in anti-HPV-16 antibody titers were found among vaccine groups.

191 h-risk human papillomaviruses (HPV), such as HPV-16, are etiologic agents of a variety of anogenital

192 Human papilloma virus-16 (HPV-16) associated oropharyngeal cancer (HPVOPC) is incr

193 Infection with human papillomavirus type 16 (HPV-16) can lead to low- or high-grade squamous intraepi

194 idated by MusPV1 or human papillomavirus 16 (HPV 16) capsids, efficiently induced the outgrowth of pa

195 Median times to HPV-16 clearance were also comparable, with point estima

196 and Relevance: This study demonstrates that HPV-16 detection precedes the incidence of oropharyngeal

197 Oral HPV-16 detection was associated with incident HNSCC (OR,

198 The risk of CIN3 increased with increasing HPV-16 DNA load at the follow-up visit (odds ratio, 1.63

199 ell lines containing integrated and episomal HPV-16 DNA.

200 Here, we demonstrate that HPV-16 E2 Y138E bound to full-length Brd4 but not to the

201 The human papillomavirus type 16 (HPV-16) E5 oncoprotein is embedded in membranes of the e

202 The high-risk human papillomavirus type 16 (HPV-16) E5 protein (16E5) induces tumors in a transgenic

203 al vaccines that express a fusion protein of HPV-16 E6 and E7 (Ad.E6E7) alone or fused with p16 (Ad.E

204 tion sensitivity was seen in cell expressing HPV-16 E6 despite the effect of E6 to degrade p53.

205 by HPV infection, we expressed the high-risk HPV-16 E6 oncoprotein in primary human keratinocytes and

206 V-16 E7 transgene onto a background in which HPV-16 E6 was constitutively expressed.

207 Systemic HPV-16 E6- and E7-specific T-cell responses were common

208 16 positive cervical cancer cell lines in an HPV-16 E6-dependent manner but independently of p53 regu

209 roteins for low-risk HPV-11 E6 and high-risk HPV-16 E6.

210 We discovered 15-19 amino acid peptides from HPV-16 E6/E7 for which induction of T-cell immunity corr

211 vector system, and human papillomavirus 16 (HPV 16) E6 and E7 gene-immortalized normal human epiderm

212 Human papillomavirus type 16 (HPV-16) E6 (16E6) binds the E3 ubiquitin ligase E6AP and

213 g full-length human papilloma virus type 16 (HPV-16) E6, the LxxLL motif of E6AP and the core domain

214 tional profiling of keratinocytes expressing HPV-16 E7 and identified more than 200 genes that were d

215 cers arising in transgenic mice that express HPV-16 E7 in an inducible manner require the continuous

216 ongly argue that the oncogenic properties of HPV-16 E7 in human cervical carcinogenesis may involve d

217 d are, therefore, highly relevant targets of HPV-16 E7 in its contribution to HPV-positive HNSCC.

218 We have recently found that HPV-16 E7 oncogene induces polyploidy in response to DNA

219 cytotoxic T cell responses by targeting the HPV-16 E7 oncoprotein.

220 We placed the inducible HPV-16 E7 transgene onto a background in which HPV-16 E6

221 ped head and neck cancer as frequently as do HPV-16 E7 transgenic mice.

222 roteins have been reported to associate with HPV-16 E7, which is thought to dysregulate the cell cycl

223 Upon DNA damage, HPV-16 E7-expressing cells arrest at the G(2) checkpoint

224 Here we present evidence demonstrating that HPV-16 E7-expressing cells have an intact G(2) checkpoin

225 profile of keratinocytes expressing HPV 16 (HPV-16) E7.

226 Enhanced expression of MUC16, SIRPA and HPV-16-E7 protein was detectable in the circulating exos

227 sive HPVOPC cells harboring MUC16, SIRPA and HPV-16-E7 proteins augmented invasion and induced epithe

228 be replicated in raft cultures of early-pass HPV-16 episomal cell lines, at both the level of patholo

229 were greater for HPV 6, 11, and 18 than for HPV 16 for all scenarios investigated.

230 story, alcohol consumption, and detection of HPV-16 for beta- and gamma-HPVs.

231 The cultured cells contained HPV-16, formed colonies in soft agar and rapidly produce

232 In individual analyses, men with prior HPV 16 genital infections had a significantly higher ris

233 The HPV-16 genome was integrated adjacent to the Myc gene, b

234 Anal cytology and HPV-16 genotyping had the best screening performance.

235 that received doses at 0, 12, and 24 months (HPV-16 GMT ratio: 0.64 [95% CI, 0.48-0.84]; HPV-18 GMT r

236 sion arm, compared with the control arm, for HPV-16 (hazard ratio [HR], 0.32 [95% confidence interval

237 iptional profile of keratinocytes expressing HPV 16 (HPV-16) E7.

238 Only HPV 16, HPV 18, and HPV 45 accounted for a greater propo

239 y conserved between E6 proteins derived from HPV-16, HPV-18, and HPV-58 while being somewhat weaker o

240 The HPV genotypes identified included HPV-16 in 10 tumors (48%), HPV-31 in 5 tumors, HPV-33 in

241 ction (HPV-6 was detected in 7, HPV-11 in 0, HPV-16 in 17, and HPV-18 in 1).

242 Here we sought evidence for HPV-16 in an independent cohort of surgical specimens.

243 eported evidence of human papillomavirus 16 (HPV-16) in a very high proportion of pathological specim

244 e high prevalence of HR-HPV types, including HPV-16, in the anal canal of HIV-positive women is conce

245 (0.3-1.1; n=18 incident infections) an oral HPV 16 infection.

246 confidence interval [CI], 1.1-16.4) and anal HPV-16 infection (OR, 16.1; 95% CI, 5.4-48.3) was associ

247 Abnormal anal cytology and HPV-16 infection performed best as a screening strategy

248 to persistent human papillomavirus type 16 (HPV-16) infection.

249 significantly higher risk of subsequent anal HPV 16 infections (HR, 4.63; 95% confidence interval [CI

250 Eight of the 18 incident oral HPV 16 infections persisted for two or more study visits

251 PV, 82.6% of low-risk (LR) HPV, and 76.2% of HPV-16 infections had cleared.

252 HPV-16 infections were slower to clear than other HR-HPV

253 with significant reductions in oropharyngeal HPV-16 infections.

254 type replacement in women vaccinated against HPV 16 is unlikely to be an issue for the general popula

255 In conclusion, anal HPV-16 is more persistent than HPV-18, and its incidence

256 Human papillomavirus-16 (HPV-16) is associated etiologically with many human cerv

257 ospho-specific modification of the BPV-1 and HPV-16 L2 capsid proteins.

258 For those with prevalent HPV-16 (n = 27), 29.6% were persistent for at least 24 m

259 at baseline for the corresponding HPV type [HPV-16: n = 8193; HPV-18: n = 8463]).

260 to obtain estimates for HPV-16-positive and HPV-16-negative lesions.

261 r within 10 years, as compared with 0.6% for HPV-16-negative lesions.

262 responses 1 month after last vaccination for HPV-16 of 7736 milli-Merck units per mL (mMU/mL) (95% CI

263 esolution anoscopy, we measured responses to HPV-16 oncogenic proteins E6 and E7, using the CD25/CD13

264 her types, compared with women infected with HPV-16 only.

265 , most YMSM appear to remain naive to either HPV-16 or -18 well into their sexual lives and would ben

266 pes with close phylogenetic relationships to HPV-16 or -18.

267 ere we show that immortalization of HFK with HPV-16 or 18 causes down-regulation of the ASncmtRNAs an

268 clearance of oncogenic HPV types other than HPV-16 or HPV-18 (HR, 2.2; P = .01).

269 respective of their baseline HPV DNA status, HPV-16 or HPV-18 serostatus, or cytology.

270 onfirmed recurrent or advanced HPV-positive (HPV-16 or HPV-18) cervical cancer, and who had progresse

271 9 years after vaccination for vaccine types HPV-16 or HPV-18.

272 the multivariable model, concurrent cervical HPV-16 (P < .001), weekly alcohol use (P = .015), anal t

273 ring anal sex (P = .04) were associated with HPV-16 persistence.

274 subsequent infection in female subjects with HPV-16 (pooled RR, 0.65; 95% confidence interval, .50-.8

275 inhibit the proliferation of a conventional HPV-16 positive cervical cancer cell line.

276 ingly, FAM83H-AS1 was found overexpressed in HPV-16 positive cervical cancer cell lines in an HPV-16

277 nd cancer incidences to obtain estimates for HPV-16-positive and HPV-16-negative lesions.

278 ble to downregulate E6 and E7 transcripts in HPV-16-positive CC CaSki cells.

279 62) were women diagnosed with CIN3 following HPV-16-positive detection at a follow-up visit.

280 ositive lesions was similar, but 2.4% of the HPV-16-positive lesions progressed to cancer within 10 y

281 The median duration for HPV-16-positive lesions was similar, but 2.4% of the HPV

282 viral DNA has been documented in a subset of HPV-16-positive malignant lesions.

283 Oropharyngeal HPV-16 prevalence in unvaccinated males was similar to v

284 Overall, oropharyngeal HPV-16 prevalence was significantly lower in vaccinated

285 the proteolysis of both L1 and L2 in mutated HPV-16 PsVs.

286 Tumors with positive HPV-16 results were larger (68 vs. 34 mm2; P=0.08, Mann-

287 nificantly correlated with serum levels (for HPV-16, rho was 0.90 for mouthwash specimens and 0.92 fo

288 sion arm, compared with the control arm, for HPV-16 (risk ratio [RR], 0.36 [95% CI, .18-.72]) and HPV

289 In multivariable analyses, HPV-16 seropositivity was significantly more common in W

290 ted, 1.3% had carcinogenic HPV, and 0.4% had HPV-16; similar patterns for non-16/18 HPV types were ob

291 HPV-16-specific CD8(+) T cell responses were significant

292 we have conducted proteome-wide profiling of HPV-16-specific T cell responses in a cohort of 66 patie

293 RERI for HPV 16 was 1.79 (95% CI, -2.57 to 6.16) and 2.78 for bet

294 HPV 16 was most common (49.1%), followed by HPV 31 (10.4

295 dies in both oral specimen types at month 7 (HPV-16 was detected in 93.2% of mouthwash specimens and

296 When HPV-16 was present at both enrollment and follow-up, vir

297 the association was not affected by whether HPV-16 was present at enrollment.

298 HPV-16 was the most prevalent type in both the anal cana

299 Females infected with HPV-16 were at higher risk of acquiring other alpha-9 HP

300 h-risk human papillomaviruses (HPVs) such as HPV-16, which have been causally associated with maligna