ライフサイエンスコーパス: HPV-18

1 20% lower after 50 years for both HPV-16 and HPV-18).

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

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

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

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

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

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

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

9 to other HPV types, including the oncogenic 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 lowed by HPV-33 (0.028), HPV-58 (0.024), and HPV-18 (0.022).

14 0.65; 95% confidence interval, .50-.80) and HPV-18 (0.70; .43-.98) but not in male subjects (HPV-16:

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

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

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

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

19 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

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

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

22 6 E2 DBD is structurally more similar to the HPV 18 and bovine papillomavirus type 1 (BPV1) E2 protei

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

51 4 vaccine genotypes at month 7, but not for HPV-18 by month 24 or HPV-6 by month 36.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 100, synthetic plasmids targeting HPV-16 and HPV-18 E6 and E7 proteins, delivered by electroporation,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 HPV-18 genomes were purified from bacterial vector seque

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

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

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

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

111 (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,

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

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

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

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

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

117 [95% confidence interval {CI}, .20-.49]) and HPV-18 (HR, 0.34 [95% CI, .21-.54]).

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

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

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

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

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

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

124 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 5% confidence interval {CI}, 1.29-1.82]; for HPV-18: OR, 1.35 [95% CI, 1.09-1.68]) but not among wome

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

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

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

155 0% for HPV-11, 5.1% for HPV-16, and 1.5% for HPV-18 (P < .001 for all comparisons).

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

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

158 HPV 18 prevalence was 5.5% overall.

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

160 HPV 18-related cervical carcinomas, particularly those d

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

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

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

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

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

166 HPV-18 results were similar.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 126 cases with HPV-16 and the 42 cases with HPV-18 were compared with 250 controls with no evidence

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

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