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

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

11 18 (0.70; .43-.98) but not in male subjects (HPV-16: 1.22; .67-1.77 [P= .05 (test for heterogeneity)]

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

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

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

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

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

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

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

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

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

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

22 similar to vaccine efficacy against cervical HPV 16/18 infection (87.9%, 77.4-94.0).

23 Vaccine efficacy against cervical HPV 16/18 infection in the same women at the 4-year visi

24 l cohort, vaccine efficacy against prevalent HPV 16/18 infection measured one-time, 4 years post vacc

25 ricted cohort, vaccine efficacy against anal HPV 16/18 infection was 83.6% (66.7-92.8), which was sim

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

27 vaccine efficacy against persistent cervical HPV 16/18 infections and associated precancerous lesions

28 Prevalence of anal HPV 16/18 infections, reported as vaccine efficacy, was

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

34 Conclusion: 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 anal infection with HPV 16, HPV 18, or both (HPV 16/18).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 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

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

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

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

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

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

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

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

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

79 /18 vaccine seem to protect against cervical HPV-16/18 infections, similar to the protection provided

80 -2, -4, or -9, including the AS04-adjuvanted HPV-16/18 L1 vaccine.

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

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

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

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

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

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

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

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

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

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

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

92 22-29 in the control and vaccine arms of an HPV-16/18 vaccine trial in Costa Rica had oral, cervical

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

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

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

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

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

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

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

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

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

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

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

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

105 versity students who had an alpha9 HPV type (HPV-16, -31, -33, -35, -52, -58, or -67) detected in the

106 in 6.5% of subjects), followed by HPV 53 and HPV 16 (4.7%), both of which are oncogenic types.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 HPV vaccines prevent infection with HPV 16 and 18, which account for 70% of cases of cervica

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

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

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

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

126 We assessed efficacy of an AS04-adjuvanted HPV 16 and HPV 18 vaccine against anal infection with HP

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

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

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

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

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

132 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.

133 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.

134 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

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

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

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

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

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

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

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

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

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

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

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

146 2 chimeric VLP (alone or in combination with HPV-16 and HPV-18 L1 VLPs) formulated with AS04 has the

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

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

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

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

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

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

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

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

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

156 3100 were assessed in CIN2/3 associated with HPV-16 and HPV-18, in a randomised, double-blind, placeb

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 vels of E6, E7, and L1 genes in flash-frozen HPV-16 cervical carcinomas.

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

178 o had evidence of intervening negativity for HPV-16, compared with 1 of 49 who consistently tested po

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

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

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

182 -time polymerase chain reaction was used for HPV-16 DNA quantification.

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

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

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

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

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

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

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

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

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

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

193 lls expressing human papillomavirus type 16 (HPV-16) E6 and E7 proteins exhibit deregulation of G2/M

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

195 line-inducible transgene that expresses both HPV-16 E7 and firefly luciferase.

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

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

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

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

200 We show that this activity of HPV-16 E7 involves attenuation of DNA damage checkpoint

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 Among women with HPV-16 found initially during follow-up, viral load in t

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

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

218 nd epithelial clones containing unintegrated HPV-16 genomes expressed mRNAs spliced from HPV-16 SD880

219 llar or foreskin epithelia immortalized with HPV-16 genomes.

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

221 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

222 s that received doses at 0, 3, and 9 months (HPV-16 GMT ratio: 0.92 [95% CI, 0.71-1.20]; HPV-18 GMT r

223 CI, 0.68-1.11]) and at 0, 6, and 12 months (HPV-16 GMT ratio: 0.98 [95% CI, 0.75-1.29]; HPV-18 GMT r

224 Human Papillomavirus 16 (HPV-16) has been identified as the causative agent of 50

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

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

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

228 d HPV 18 vaccine against anal infection with HPV 16, HPV 18, or both (HPV 16/18).

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

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

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

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

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

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

235 (0.3-1.1; n=18 incident infections) an oral HPV 16 infection.

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

237 5.1% of MSM and 0.0% of MSW had a persistent HPV-16 infection at the 6-month visit.

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

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

240 the course of human papillomavirus type 16 (HPV-16) infection.

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

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

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

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

245 load predict persistence and progression of HPV-16 infections.

246 HPV 16 is a prognostic marker for enhanced overall and d

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

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

249 Vaccination with a monovalent HPV-16 L1 VLP vaccine was associated with modulation of

250 gulation of immune/defense response genes by HPV-16 L1 VLP, in particular, IFN-induced genes, was obs

251 nd a set of 31 keratinocyte clones expressed HPV-16 major early promoter (MEP)-initiated mRNAs splice

252 ng MSW, and the prevalence of infection with HPV-16 may differ substantially by geography.

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

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

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

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

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

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

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

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

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

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

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

264 keratinocytes >4-fold more effectively than HPV-16 or HPV-31 and >20-fold more efficiently than HPV-

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

266 igher viral load at enrollment (P< .001, for HPV-16; P=.01, for HPV-18).

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

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

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

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

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

272 HPV-16-positive controls (n = 152) without CIN2 or CIN3

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

274 viral DNA status and E6-E7 mRNA sequences in HPV-16-positive HNC tumors to those in independent human

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

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

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

278 ly during follow-up, viral load in the first HPV-16-positive sample was associated with short-term pe

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

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

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

282 HPV-16 genomes expressed mRNAs spliced from HPV-16 SD880 to SA3358 and terminating at the viral earl

283 HPV-16 seroconversion at 24 months was 13% (95% confiden

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

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

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

287 This report demonstrates matching HPV-16 strains in 2 couples with concurrent development

288 e epitope (E7(11-19)) highly conserved among HPV-16 strains was detected.

289 er prevalence of infection with HPV type 16 (HPV-16) than that among men in Sao Paulo or Cuernavaca (

290 physical presence among peptides eluted from HPV-16-transformed epithelial tumor HLA-A*0201 immunopre

291 factor Brn-3a, whereas the URR of a low-risk HPV-16 variant is not.

292 egions (URRs) of high- and intermediate-risk HPV-16 variants are activated by the cellular transcript

293 ls of Brn-3a infected with low- or high-risk HPV-16 variants have augmented E6 levels, and were more

294 We sequenced HPV-16 variants in longitudinal pairs of specimens from

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

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

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

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

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

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