ライフサイエンスコーパス: HPV-11

1 HPV-11 E2 bound Fl-E2BS with an apparent Kd of 0.84 nM.

2 HPV-11 E7ER and, much less efficiently, HPV-6 E7ER also

3 HPV-11 genomes were found to be maintained in keratinocy

4 HPV-11 L1 VLPs could also be dissociated by treatment wi

5 HPV-11-transfected or control colonies failed to expand

6 our study, the human papillomavirus type 11 (HPV-11) E1 protein functioned with the HPV-16 E2 protein

7 Histone H1 was identified as an HPV type 11 (HPV-11) E1-binding protein by far-Western blotting and b

8 he full-length human papillomavirus type 11 (HPV-11) E2 protein and showed that the resultant fusion,

9 omavirus (BPV)/human papillomavirus type 11 (HPV-11) E2 proteins.

10 gonists of the human papillomavirus type 11 (HPV-11) E2-DNA association were identified using a filam

11 anscriptional regulation of the HPV type 11 (HPV-11) enhancer-promoter located in the upstream regula

12 e 7.9-kb human papillomavirus virus type 11 (HPV-11) genome, whereas the pulmonary tumor cells contai

13 stable maintenance of episomes, HPV type 11 (HPV-11) genomes that contained translation termination m

14 tralization of human papillomavirus type 11 (HPV-11) has been demonstrated using serum and cervical s

15 The human papillomavirus type 11 (HPV-11) L1 major capsid protein can be trypsinized to ge

16 ns between the human papillomavirus type 11 (HPV-11) origin recognition and initiator protein E1 and

17 ion, the oral immunogenicity of HPV type 11 (HPV-11) VLPs in mice was previously investigated; it was

18 sid protein of human papillomavirus type 11 (HPV-11) was expressed in Escherichia coli, and the solub

19 LP)-based vaccine at generating HPV type 11 (HPV-11)-specific cellular and humoral immune responses i

20 protein E2 of human papillomavirus types 11 (HPV-11), 16, and 18 colocalized with the mitotic spindle

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

22 HPV-6 was found in 130/195, HPV-11 in 63/195, and HPV-6/HPV-11 in 2/195 samples.

23 -6 was detected in 1.3% (95% CI, 0.8%-2.3%), HPV-11 in 0.1% (95% CI, 0.03%-0.3%), HPV-16 in 1.5% (95%

24 ound in 130/195, HPV-11 in 63/195, and HPV-6/HPV-11 in 2/195 samples.

25 ntisera raised against HPV type 6b (HPV-6b), HPV-11, HPV-16, HPV-18, HPV-31, HPV-33, and HPV-45 was a

26 oral HPV infection (HPV-6 was detected in 7, HPV-11 in 0, HPV-16 in 17, and HPV-18 in 1).

27 HPV 6 (43.8%), HPV 11 (10.7%), and HPV 16 (9.8%) were the genotypes mos

28 lly different in cell-free replication of an HPV-11 origin-containing plasmid.

29 neutralizing antibody response to HPV 6 and HPV 11 in her serum, and these antibodies transferred to

30 confidence interval [CI] = 16.9 to 48.0) and HPV-11 VLP-specific antibody titers following the first

31 154 x 108 copies/mg of tissue; P = .003) and HPV-11 (from 0.121 x 108 to 0.017 x 108 copies/mg of tis

32 ts for specific DNA recognition as BPV-1 and HPV-11 E1.

33 p of quadrivalent vaccine types, HPV-45, and HPV-11.

34 ce area of AGWs and viral load for HPV-6 and HPV-11.

35 Human papillomavirus type 6 (HPV-6) and HPV-11 are the etiological agents of approximately 90% o

36 uman papillomavirus (HPV) type 6 (HPV-6) and HPV-11, induce benign genital warts that rarely progress

37 e E2 proteins from low-risk HPVs (HPV-6b and HPV-11).

38 Only highly homologous types (HPV-6b and HPV-11, and HPV-18 and HPV-45) exhibited detectable sero

39 cancers, the prevention of HPV-6-related and HPV-11-related genital warts and juvenile-onset recurren

40 In this assay, HPV-11 capsomere polyclonal antisera exhibited neutraliz

41 d epitopes found on the surface of authentic HPV-11 virions.

42 have characterized the interactions between HPV-11 E1, HPV-11 E2, and DNA in solution at equilibrium

43 as identical results were observed for both HPV-11 URR-lacZ and LTR-lacZ in murine retrovirus produc

44 on of HPV-11 E1 with the E2 proteins of both HPV-11 and HPV-16 and inhibited in vitro replication wit

45 anges in cellular gene expression induced by HPV-11 were similar to those observed with high-risk HPV

46 31 was found to be activated or repressed by HPV-11.

47 experiments involving transfection of cloned HPV-11 DNA.

48 immunosuppressed types most often contained HPV 11.

49 In organotypic cultures, HPV-11-positive cells exhibited altered differentiation

50 The immunogenicity of a yeast-derived HPV-11 L1 VLP vaccine was tested in women.

51 ly characterized as recognizing two distinct HPV-11 capsid-neutralizing antigenic domains, were each

52 cterized the interactions between HPV-11 E1, HPV-11 E2, and DNA in solution at equilibrium.

53 Addition of excess HPV-11 E1 to Fl-E1E2BS lowered the dissociation constant

54 ex from human cells conditionally expressing HPV-11 E2.

55 type, with 6.3% observed for HPV-6, 2.0% for HPV-11, 5.1% for HPV-16, and 1.5% for HPV-18 (P < .001 f

56 o 53.7) for HPV-6, 30.3% (-45.0 to 67.5) for HPV-11, and 49.5% (21.0 to 68.3) for HPV-74.

57 Serum specimens were evaluated for HPV-11 titer by competitive radioimmunoassay (cRIA) and

58 The largest decrease was observed for HPV-11, with decreases of 8- and 9-fold for ages 20-29 a

59 the interpentamer linker arm responsible for HPV-11 capsid formation, much like the carboxy-terminal

60 phoproliferative responses were specific for HPV-11, since SIs generated against bovine papillomaviru

61 Bound H1 was displaced from HPV-11 DNA by the addition of E1, suggesting that E1 can

62 taining the spindle localization domain from HPV-11 E2C gained the ability to localize to the mitotic

63 etics of cell spreading, while E6 genes from HPV-11 or bovine papillomavirus type 1 did not.

64 This region is conserved in HPV-11, -16, and -18 and bovine papillomavirus type 4 (B

65 from 104 subjects showed a dose response in HPV-11 cRIA titers and neutralization.

66 embled VLPs similarly neutralized infectious HPV-11 virions.

67 g antiserum raised previously against intact HPV-11 VLPs.

68 The E7 proteins of LR HPV-11 and -6b uniquely possess lysine residues followin

69 n cell culture, and inhibited E1-E2-mediated HPV-11 DNA replication in vitro.

70 o a lesser extent, the low-risk mucosotropic HPV-11 destabilized p130.

71 ro infectivity assay and found to neutralize HPV-11 virions.

72 era from these immunized monkeys neutralized HPV-11 in the athymic mouse xenograft system.

73 h-risk HPV types, we examined the ability of HPV-11 to be stably maintained as episomes following tra

74 In addition, the amplification of HPV-11 DNA, as well as the induction of several viral me

75 trongly inhibited transient amplification of HPV-11, -16, and -18 origin-containing plasmid DNA in tr

76 ds described allow for a genetic analysis of HPV-11 in the context of its differentiation-dependent l

77 irions produced regionally separate areas of HPV-11 and -40 infection as determined by in situ hybrid

78 icroscopy was used to visualize complexes of HPV-11 DNA ori bound by purified E2 protein.

79 85 to 308 in the carboxyl-terminal domain of HPV-11 E2 (E2C) is necessary and sufficient to confer lo

80 DNA and E2, the carboxyl-terminal domain of HPV-11 E2 protein (E2C) was expressed in Escherichia col

81 -like particles purified after expression of HPV-11 L1 in insect cells.

82 : this peptide also inhibited interaction of HPV-11 E1 with the E2 proteins of both HPV-11 and HPV-16

83 Significant levels of HPV-11-neutralizing antibodies also were observed in cer

84 lotted in relation to a transcription map of HPV-11, it is apparent that the major RNA transcripts pr

85 and E2-independent cell-free replication of HPV-11, whereas p70 inhibits E2-dependent but stimulates

86 for the development of infectious stocks of HPV-11.

87 The trypsin susceptibility of HPV-11 L1 capsids suggests a possible mechanism for viri

88 ccinated with CRPV, HPV type 16 (HPV-16), or HPV-11 VLPs were challenged with both homologous (CRPV c

89 been demonstrated for the low-risk HPV-6 or HPV-11 E7 proteins.

90 that genital warts are common after HPV-6 or HPV-11 infection in young men.

91 tal warts among women with incident HPV-6 or HPV-11 infection was 64.2% (95% CI, 50.7%-77.4%).

92 g 46 men with incident detection of HPV-6 or HPV-11 infection, 2.0% (95% CI, 0.5%-7.9%) among 161 men

93 ed by human papillomavirus type 6 (HPV-6) or HPV-11.

94 All vaccine recipients had positive HPV-11 VLP-specific lymphoproliferative responses at mon

95 for the quantitative disassembly of purified HPV-11 L1 VLPs to the level of capsomeres, demonstrating

96 or E1 dimerization in BPV-1 and the low risk HPV-11 are also required for HPV-18 E1.

97 isk HPV-16 and HPV-18, wart-causing low risk HPV-11, and bovine papillomavirus type 1, in part throug

98 ngth mucosal HPV genomes, i.e., the low-risk HPV-11 and HR HPV-16, -18, and -31, to persist in and al

99 eins in the episomal maintenance of low-risk HPV-11 genomes and suggest that they may act in a manner

100 0, which we reported previously to stimulate HPV-11 E1 binding to the origin and promote dihexameric

101 In the present study, HPV-11 virion-neutralizing monoclonal antibodies H11.F1

102 alone are essential to maintaining long-term HPV-11 L1 VLP structure at physiological ionic strength.

103 reciprocal hybrids containing amino-terminal HPV-11 sequences exhibited a high activity with HPV-16 E

104 or HPV-31 and >20-fold more efficiently than HPV-11 or controls.

105 We recently showed that HPV-11 E1 interacts with cyclin/cyclin-dependent kinase

106 The HPV-11 cRIA titer appears to be a surrogate marker for n

107 sites in sequence derived directly from the HPV-11 origin of replication.

108 However, the HPV-11 E2 protein did not associate with Brd4 during mit

109 A significant decline in the HPV-11 viral load was achieved only with the Mw vaccine.

110 Interestingly, the HPV-11-positive cells exhibited an extended life span th

111 binding sites are located within or near the HPV-11 LCR.

112 for the diverse regulatory functions of the HPV-11 E2 protein during mRNA transcription and viral DN

113 this study, we show the localization of the HPV-11 E2 protein to be dynamic.

114 Furthermore, a region of the HPV-11 genome containing the origin of replication was i

115 ctures in the modeling and regulation of the HPV-11 ori is discussed.

116 as YY1 also inhibited the replication of the HPV-11 ori, which does not have a known or suspected YY1

117 This mutation no longer repressed the HPV-11 upstream regulatory region-controlled reporter ex

118 in exhibited no detectable activity with the HPV-11 E2 protein.

119 s from the seven E2-binding sites within the HPV-11 genome were titrated to establish a hierarchy of

120 d on aluminum adjuvant elicited high-titered HPV-11 VLP-specific serum antibody responses.

121 responses of 25 controls and 10 patients to HPV-11 L1 virus-like particles (VLP) were compared.

122 A range of T-cell proliferative responses to HPV-11 VLP were observed in DRB1*0301-positive healthy d

123 than in cells transfected with the wild-type HPV-11 genome.

124 ed reporter gene activity from the wild-type HPV-11 URR or the C/EBP mutation in PHKs grown in undiff

125 activity with HPV-16 E2 but no activity with HPV-11 E2.

126 s infection of human foreskin fragments with HPV-11, -40, and -LVX82/MM7 virions produced regionally

127 an green monkeys systemically immunized with HPV-11 VLPs expressed in Saccharomyces cerevisiae and fo

128 subunits of pol alpha/primase interact with HPV-11 E1.

129 ma) in response to in vitro stimulation with HPV-11 VLP.

130 ed more efficiently with HPV-16 E2 than with HPV-11 E2.

131 Examination of cells transfected with HPV-11 genomes in which E7 function was inhibited were f

132 s, we identified immunogenic peptides within HPV-11 early proteins.