ライフサイエンスコーパス: HPV-18

1 coinfection, P=.002 for HPV-16 and P=.34 for HPV-18).

2 20% lower after 50 years for both HPV-16 and HPV-18).

3 o contain reads for human papillomavirus 18 (HPV-18).

4 enrollment (P< .001, for HPV-16; P=.01, for HPV-18).

5 rols and tested for antibodies to HPV-16 and HPV-18.

6 r HPV, 3 for HPV type 16 (HPV-16), and 4 for HPV-18.

7 to other HPV types, including the oncogenic HPV-18.

8 fter vaccination for vaccine types HPV-16 or HPV-18.

9 dence reductions: 63% for HPV-16 and 84% for HPV-18.

10 cy against CIN2/3 associated with HPV-16 and HPV-18.

11 for HPV-16 and 0.68 (95% CI, 0.54-0.85) for HPV-18.

12 for HPV-16 and 1.76 (95% CI, 1.41-2.19) for HPV-18.

13 ometric mean titers for anti-HPV-16 and anti-HPV-18.

14 lowed by HPV-33 (0.028), HPV-58 (0.024), and HPV-18 (0.022).

15 0.65; 95% confidence interval, .50-.80) and HPV-18 (0.70; .43-.98) but not in male subjects (HPV-16:

16 %), HPV 31 (4.12%) and HPV 51 (3.39%), while HPV 18 (1.70%) was less prevalent among infected women.

17 .67-1.77 [P= .05 (test for heterogeneity)]; HPV-18: 1.50; .46-2.55; [P= .15]).

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

19 mavirus-16 cleared significantly slower than HPV-18 (32% versus 54% by 24 months).

20 Here, we report that in cervical tumors, HPV-18, -39, and -45 transcribe E6/E7 mRNAs with extreme

21 HPV-51 (7.6%), HPV-58 (5.3%), HPV-52 (4.3%), HPV-18 (4.3%), and HPV-16 (3.9%) were most prevalent.

22 cted in adenocarcinoma were HPV 16 (50%) and HPV 18 (40%), followed by HPV 45 (10%), HPV52 (2%), and

23 units per milliliter [mMU/mL], P = .012) and HPV-18 (463 vs 801 mMU/mL, P = .003).

24 PV-16 and 1729.9 (95% CI, 1504.0-1989.7) for HPV-18; 5368.5 (95% CI, 4632.4-6221.5) and 1502.3 (95% C

25 irus (HPV) vaccine, which targets HPV-16 and HPV-18, against HPV-31, -33, and -45 infection and an in

26 For HPV-18, although seropositivity was associated with lowe

27 6 E2 DBD is structurally more similar to the HPV 18 and bovine papillomavirus type 1 (BPV1) E2 protei

28 ent and persistent infection with HPV 16 and HPV 18 and their associated cytological and histological

29 selective discrimination between HPV-16 and HPV-18 and good reproducibility.

30 ce of cytological abnormality after incident HPV-18 and HPV-16 infections.

31 s implicated in the regulation of the LCR of HPV-18 and HPV-16.

32 e vectors of different molecular variants of HPV-18 and HPV-16.

33 hly homologous types (HPV-6b and HPV-11, and HPV-18 and HPV-45) exhibited detectable serological cros

34 didate for the local treatment of HPV-16 and HPV-18 and other high-risk types, an important unmet med

35 d influence early expression of HPV type 18 (HPV-18) and HPV type 16 (HPV-16), a high-throughput tran

36 nt vaccine types (HPV-6, HPV-11, HPV-16, and HPV-18) and related types (HPV-31, and HPV-45) decreased

37 Only HPV 16, HPV 18, and HPV 45 accounted for a greater proportion of

38 rsistent cervical infections with HPV-16 and HPV-18, and associated cytological abnormalities and les

39 ved between E6 proteins derived from HPV-16, HPV-18, and HPV-58 while being somewhat weaker or absent

40 clusion, anal HPV-16 is more persistent than HPV-18, and its incidence correlates with a prior detect

41 ugh more than 98% of girls in all groups had HPV 18 antibodies.

42 e seropositive for both anti-HPV-16 and anti-HPV-18 antibodies (n = 130 and n = 128 for 10-14-year-ol

43 Anti-HPV-18 antibodies were associated with cancers at all si

44 eloped detectable serum anti-HPV-16 and anti-HPV-18 antibodies, and most had detectable antibodies in

45 Anti-HPV-16 and anti-HPV-18 antibody levels remained stable and above natural

46 Anti-HPV-18 antibody titers were higher in the Cervarix group

47 6, 31, 33, 52 and alpha-7 phylogenetic group HPV 18 are the most frequently detected in normal-to-hig

48 sk human papillomavirus type 16 (HPV-16) and HPV-18 are associated with the majority of human cervica

49 irus (HPV) type 16 (HPV 16) and HPV type 18 (HPV 18) are implicated in the induction and progression

50 s (human papillomavirus type 16 [HPV-16] and HPV-18) are much more active than are the E2 proteins fr

51 ups: high-risk HPV types, such as HPV 16 and HPV 18, are associated with cancer, low-risk HPV types,

52 antibodies to HPV-16, and to a lesser extent HPV-18, are associated with some reduced risk of subsequ

53 apillomaviruses (HPVs), including HPV-16 and HPV-18, are the causative agents of cervical carcinomas

54 ning programmes in reducing the frequency of HPV-18-associated cancers.

55 me of diagnosis of high-grade CIN is because HPV-18-associated disease rapidly progresses through the

56 iated viral types (16, 31, 33, 35, or 58) or HPV-18-associated types (18 or 45) (P<0.001), which are

57 noninferior for 2 versus 3 doses, except for HPV-18 (at 2-3 years after first dose).

58 re only noninferior for 2 versus 3 doses for HPV-18 (at 2-3 years after the first dose; GMC ratio, 0.

59 e most carcinogenic types of HPV (HPV 16 and HPV 18) at the cervix and other anatomical sites at whic

60 ued growth of individual keratinocytes, with HPV-18 being the most aggressive mucosal HR HPV type tes

61 4 vaccine genotypes at month 7, but not for HPV-18 by month 24 or HPV-6 by month 36.

62 ed, 28 activated and 36 inhibited the LCR of HPV-18 by more than 2-fold.

63 man papillomavirus (HPV), such as HPV-16 and HPV-18, can lead to malignant progression and tumorigene

64 an papillomavirus virus type 16 (HPV-16) and HPV-18 cause a large proportion of oropharyngeal cancers

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

66 es of human papillomavirus, such as type 18 (HPV-18), cause cervical carcinoma, one of the most frequ

67 ecurrent or advanced HPV-positive (HPV-16 or HPV-18) cervical cancer, and who had progressed after av

68 The numbers of HPV-16 and HPV-18 copies per nanogram of cellular DNA at baseline w

69 human papillomavirus (HPV) types, HPV-16 and HPV-18, could prevent development of up to 70% of cervic

70 o were negative for both cervical HPV 16 and HPV 18 DNA and who were HPV 16 and HPV 18 seronegative b

71 CK or TPCK during their immortalization with HPV 18 DNA demonstrated that either TLCK (5--10 microM)

72 We have previously shown that HPV-18 DNA amplification initiates in spinous cells in o

73 n 4/5 malignant and 2/5 benign tissues, with HPV-18 DNA being present in 1/5 malignant and 1/5 benign

74 ection, defined as the presence of HPV-16 or HPV-18 DNA in 2 consecutive vaginal samples self-collect

75 approximately 100 to 200 episomal copies of HPV-18 DNA per cell.

76 HPV-18 DNA was detected in 44.7% of adenocarcinomas of t

77 when analyses were restricted to HPV-16- or HPV-18 DNA-positive cases.

78 tion of primary keratinocytes by transfected HPV-18 DNA.

79 in viral load with persistence of HPV-16 or HPV-18 during the first 6 months of the study was statis

80 ation (ori)-containing DNA by using purified HPV-18 E1 and E2 gene products expressed as fusion prote

81 We also present evidence that the HPV-18 E1 DNA-binding domain does not share the same nuc

82 esent the crystal structure of the monomeric HPV-18 E1 DNA-binding domain refined to 1.8-A resolution

83 HeLa cell-derived HPV-18 E1 protein is truncated at the carboxyl terminus

84 o sequestration by the endogenous, defective HPV-18 E1 protein.

85 nd the low risk HPV-11 are also required for HPV-18 E1.

86 Our studies thus categorize HPV-18 E2 and BPV-1 E2 in the same protein family, a fin

87 Surprisingly, HPV-18 E2 behaves more similarly to BPV-1 E2 than HPV-16

88 that separate the closely related HPV-16 and HPV-18 E2 proteins but classify together the more diverg

89 assify together the more divergent BPV-1 and HPV-18 E2 proteins.

90 All of the resulting hybrids expressed HPV 18 E6 from the HeLa parent and some of the hybrids a

91 Recently, we developed a Drosophila 'HPV 18 E6' model that displayed loss of cellular morphol

92 -binding motifs of Ad9 E4-ORF1 and high-risk HPV-18 E6 also mediate binding to the widely expressed c

93 with retroviruses that express the wild-type HPV-18 E6 and E7 genes from the native differentiation-d

94 100, synthetic plasmids targeting HPV-16 and HPV-18 E6 and E7 proteins, delivered by electroporation,

95 iments with a series of peptides showed that HPV-18 E6 bound hDlg PDZ2 about 5-fold stronger than HPV

96 We show that the translation of HPV-18 E6 cistron is regulated by the motif ACCaugGCGCG(

97 We further show that the translation of HPV-18 E6 largely relies on the cap structure and eIF4E

98 An immortalization-defective HPV-18 E6 mutant genome was also characterized for the f

99 , we now report the characterization of four HPV-18 E6 mutations.

100 of interaction in which six residues of the HPV-18 E6 peptide are contacted by the PDZ2 domain, in c

101 tructure of the complex of PDZ2 bound to the HPV-18 E6 peptide.

102 MUPP1 within the cytoplasm of cells whereas HPV-18 E6 targets this cellular protein for degradation.

103 eraction of a peptide from the C-terminus of HPV-18 E6 to the second PDZ domain (PDZ2) from the human

104 t, hTapp1, mTapp2, TARP, NG2, claudin-1, and HPV-18 E6).

105 ational changes required for PDZ2 to bind to HPV-18 E6.

106 With this approach, HPV-18 E6/E7 expression significantly altered the expres

107 ption of transcript changes brought about by HPV-18 E6/E7 in a physiologically relevant model and sho

108 and activity were significantly elevated in HPV-18 E6/E7-immortalized human genital epithelial cells

109 The effects of human papillomavirus type 18 (HPV-18) E6 and E7 proteins on global patterns of host ge

110 Expression of the HPV 18 E7 oncoprotein, like Ad 12 E1A, resulted in repre

111 HKs) transduced with retroviruses expressing HPV-18 E7 oncogene from its native upstream regulatory r

112 HPV-18 E7 promotes S phase re-entry in post-mitotic diff

113 primary human keratinocytes transduced with HPV-18 E7 were pulse-chase-pulse-labeled with (3)H-thymi

114 rest in HeLa cells despite the expression of HPV-18 E7.

115 The human papillomavirus type 18 (HPV-18) E7 protein promotes S-phase reentry in postmitot

116 resence of the human papillomavirus type 18 (HPV-18) E7 protein.

117 nificant vaccine efficacy against HPV-16 and HPV-18 endpoints: incident infection, 96.9% (95% CI 81.3

118 etric mean titer (GMT) ratios for HPV-16 and HPV-18 for girls (2 doses) compared with young women (3

119 d the long control region (LCR) of HPV-16 or HPV-18 from three oral cancer cell lines and two lines o

120 of the proto-oncogene MYC by the integrated HPV-18 genome approximately 500 kilobases upstream, and

121 ration of the human papilloma virus type 18 (HPV-18) genome occurred and that is likely to be the eve

122 eproducible system that generates autonomous HPV-18 genomes in primary human keratinocytes (PHKs), th

123 HPV-18 genomes were purified from bacterial vector seque

124 When considering only positive HPV-16 and/or HPV-18 genotype results, the cobas test showed a sensiti

125 city (86.6%) observed when the HPV-16 and/or HPV-18 genotypes were detected.

126 notype carried infections with HPV 16 and/or HPV 18; genotypes of unknown risk were also frequently o

127 (HPV-16 GMT ratio: 0.64 [95% CI, 0.48-0.84]; HPV-18 GMT ratio: 0.77 [95% CI, 0.62-0.96]).

128 (HPV-16 GMT ratio: 0.92 [95% CI, 0.71-1.20]; HPV-18 GMT ratio: 0.87 [95% CI, 0.68-1.11]) and at 0, 6,

129 (HPV-16 GMT ratio: 0.98 [95% CI, 0.75-1.29]; HPV-18 GMT ratio: 0.91 [95% CI, 0.71-1.17]).

130 II, and with E2 proteins encoded by HPV-16, HPV-18, HPV-11, and bovine papillomavirus type 1 (BPV-1)

131 gainst HPV type 6b (HPV-6b), HPV-11, HPV-16, HPV-18, HPV-31, HPV-33, and HPV-45 was analyzed.

132 Twelve different HPV types including HPV-18, HPV-33, HPV-35, HPV-39, HPV-45, HPV-51, HPV-52,

133 neutralized pseudoviruses HPV5, HPV6, HPV16, HPV 18, HPV31, HPV 45, HPV 52, HPV 58, bovine papillomav

134 [95% confidence interval {CI}, .20-.49]) and HPV-18 (HR, 0.34 [95% CI, .21-.54]).

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

136 , paxillin, were also notably increased upon HPV-18 immortalization of genital epithelial cells and i

137 ntify PTKs that were abundantly expressed in HPV-18-immortalized epithelial cells and HPV-containing

138 ecimens were tested for anti-HPV-16 and anti-HPV-18 immunoglobulin G (IgG) levels by an L1 virus-like

139 Findings for HPV 16 and HPV 18 in Europe/North America, Asia, and Latin America

140 HPV 16 and HPV 18 in particular, but also HPV 45, at least in Afric

141 3%), HPV-16 in 1.5% (95% CI, 0.9%-2.6%), and HPV-18 in 0.8% (95% CI, 0.4%-1.5%) of female participant

142 etected in 7, HPV-11 in 0, HPV-16 in 17, and HPV-18 in 1).

143 alyzed incidence and clearance of HPV-16 and HPV-18 in a French cohort of HIV-infected MSM, aged >=35

144 ysis on a panel of NPC cell lines identified HPV-18 in CNE1 and HONE1 as well as three additional NPC

145 f the chromosomal integration arrangement of HPV-18 in NPCs revealed patterns identical to those obse

146 capitulated a highly productive infection of HPV-18 in organotypic epithelial cultures.

147 ssessed in CIN2/3 associated with HPV-16 and HPV-18, in a randomised, double-blind, placebo-controlle

148 Human papillomavirus-16 and HPV-18 incidence were similar (~10% incident infections

149 However, HPV-18 induced colony growth in all keratinocytes >4-fol

150 p of human papillomaviruses (e.g. HPV-16 and HPV-18) infect and induce tumors of mucosal epithelium.

151 Risk of persistent HPV 18 infection was significantly lower among seroposit

152 and the interval between incident HPV-16 or HPV-18 infection and biopsy-confirmed CIN grade 2-3 appe

153 ust protection against persistent HPV-16 and HPV-18 infection for up to 13 years, suggesting that a b

154 pport the long-held view that the reason why HPV-18 infection is under-represented at the time of dia

155 that the cytological changes detected after HPV-18 infection might understate the severity of underl

156 trial found that the incidence of HPV-16 and HPV-18 infection was low with both the 2-dose and 2 + 1-

157 he primary outcome was persistent HPV-16 and HPV-18 infection, defined as the presence of HPV-16 or H

158 Among women with incident HPV-16 or HPV-18 infection, the 36-month cumulative incidence of c

159 for the prevention of persistent HPV-16 and HPV-18 infection.

160 However, in cross-sectional studies, HPV-18 is rarely detected at the time of diagnosis of hi

161 man papillomavirus types 16 (HPV-16) and 18 (HPV-18) is an important consideration for guidelines for

162 Human papillomavirus type 18 (HPV-18) is the second most frequent of the HPV types det

163 weeks post-Ty21a vaccination, and HPV-16 and HPV-18 L1 protein-specific IgG concentration at 4 weeks

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

165 The chimeric VLP consisted of HPV-18 L1 with insertions of HPV-33 L2 (amino acid resid

166 Therefore, the novel HPV-18 L1/L2 chimeric VLP (alone or in combination with

167 HPV-16 and HPV-18 loads were measured with a LightCycler real-time

168 he corresponding HPV type [HPV-16: n = 8193; HPV-18: n = 8463]).

169 poson insertion, suggesting that these three HPV-18(+) NPC lines are likely products of a somatic hyb

170 ficiency for HPV 16 of 62.5% (15/24) and for HPV 18 of 73.9% (17/23).

171 nits per mL (mMU/mL) (95% CI, 6651-8999) and HPV-18 of 1730 mMU/mL (95% CI, 1512-1980).

172 nocytes that have been engineered to express HPV-18 oncoproteins stably.

173 cine 6 months apart, responses to HPV-16 and HPV-18 one month after the last dose were noninferior to

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

175 5% confidence interval {CI}, 1.29-1.82]; for HPV-18: OR, 1.35 [95% CI, 1.09-1.68]) but not among wome

176 ogenously added YY1 fusion protein inhibited HPV-18 ori replication.

177 the putative E1 protein binding site in the HPV-18 ori.

178 cation for the human papillomavirus type 18 (HPV-18) origin of replication (ori)-containing DNA by us

179 0% for HPV-11, 5.1% for HPV-16, and 1.5% for HPV-18 (P < .001 for all comparisons).

180 rget cells in three patients with HPV 16- or HPV 18-positive cervical cancer.

181 tein E1, whereas cervical carcinoma-derived, HPV-18-positive HeLa cells or cell extracts support HPV

182 HPV 18 prevalence was 5.5% overall.

183 nterval {CI}, .01-.04]) and a 99% decline in HPV-18 prevalence (OR, 0.01 [95% CI, .00-.04]) among the

184 s with HPV 16-related cancers, patients with HPV 18-related cancers were at increased risk for TM (HR

185 HPV 18-related cervical carcinomas, particularly those d

186 Eighty-six patients had HPV 18-related tumors and 210 patients had HPV 16-relate

187 Cumulative TM among patients with HPV 18-related tumors and among patients with HPV 16-rel

188 enefits of averting other HPV-16-related and HPV-18-related cancers, the prevention of HPV-6-related

189 m these high-risk strains, mostly HPV-16 and HPV-18, represents promising strategy for early screenin

190 ve for HPV type 16 (HPV-16) and HPV type 18 (HPV-18), respectively, at the time of enrollment into in

191 HPV-18 results were similar.

192 specimens and 0.92 for sponge specimens; for HPV-18, rho was 0.89 and 0.86, respectively).

193 risk ratio [RR], 0.36 [95% CI, .18-.72]) and HPV-18 (RR 0.34 [95% CI, .13-.86]).

194 PV 16 and HPV 18 DNA and who were HPV 16 and HPV 18 seronegative before enrolment (HPV naive), and al

195 Anti-HPV 18 seropositivity at 24 months did not meet non-infe

196 minant for human papillomavirus (HPV)-16 and HPV-18 seropositivity.

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

198 The primary outcome was HPV 16 specific or HPV 18 specific seropositivity following one dose compar

199 HPV-16- and HPV-18-specific antibody levels, normalized to total IgG

200 In the absence of vaccine types HPV 16 and HPV 18, the SLTR for ICC was reduced to 157 per 100,000

201 e E7 proteins of the high-risk mucosotrophic HPV-18, the benign cutaneous HPV-1, and, to a lesser ext

202 urth (HPV-45) is the most closely related to HPV-18; the second most prevalent type.

203 Effective vaccination against HPV 16 and HPV 18 to prevent cervical cancer will require a high le

204 Rates ranged from 92.3% (for HPV-18) to 100.0% (for HPV-6) among participants not tak

205 cultures in which the productive program of HPV-18 took place.

206 Both HPV-16- and HPV-18-transformed cells were found to be responsive to

207 demographic data using models of HPV-16 and HPV-18 transmission and cervical carcinogenesis to compa

208 The human papillomavirus type 18 (HPV-18) upstream regulatory region (URR) controls viral

209 the switch region which is critical for the HPV-18 URR activity in HeLa cells.

210 region and contributes to cell-type-specific HPV-18 URR activity.

211 The HPV-18 URR is active in HeLa cells but inactive in HepG2

212 this raft culture model system, we show that HPV-18 URR-E7 induces the universal cyclin-dependent kin

213 d by increased transcription directed by the HPV-18 URR.

214 ed efficacy of an AS04-adjuvanted HPV 16 and HPV 18 vaccine against anal infection with HPV 16, HPV 1

215 We show that HPV-16 and HPV-18 VLPs are immunogenic when administered orally and

216 oded by cancer-inducing high risk HPV-16 and HPV-18, wart-causing low risk HPV-11, and bovine papillo

217 p=0.58, HPV-16 was 0.72 (0.44-1.77), p=0.19, HPV-18 was 0.71 (0.47-1.09), p=0.11; tetanus toxoid was

218 o HPV-16 was 0.97 (0.69-1.35; p=0.85) and to HPV-18 was 1.03 (0.76-1.40; p=0.83); and toxoid-specific

219 erline nuclear abnormality after exposure to HPV-18 was 2.06 (95% CI 1.24-3.43) and that after exposu

220 ection with a higher viral load of HPV-16 or HPV-18 was associated with short- but not long-term pers

221 ash specimens and 95.7% of sponge specimens; HPV-18 was detected in 72.1% and 65.5%, respectively).

222 f the type-specific GMT ratio for HPV-16 and HPV-18 was greater than 0.5 (primary outcome).

223 Genotyping for HPV-16 and HPV-18 was simultaneously performed by the cobas HPV tes

224 antibody titer ratios (3D/2D) for HPV-16 and HPV-18 were 1.09 (95% confidence interval, .97-1.22) and

225 126 cases with HPV-16 and the 42 cases with HPV-18 were compared with 250 controls with no evidence

226 GMTs for HPV-16 and HPV-18 were higher in 10-14-year-olds (18 423 [95% confi

227 arison, the LCRs of the wild-type HPV-16 and HPV-18 were studied.