ライフサイエンスコーパス: HPV-6

1 ist during follow-up than were antibodies to HPV-6.

2 cts were seropositive for HPV-16 and 62% for HPV-6.

3 their specificity for E7 and L1 proteins of HPV-6.

4 hieving clinical and virologic clearance for HPV-6.

5 In 2014, a nonavalent vaccine containing HPV 6, 11, 16, 18, 31, 33, 45, 52, and 58 antigens was l

6 the nine-valent human papillomavirus (9vHPV; HPV 6, 11, 16, 18, 31, 33, 45, 52, and 58) vaccine again

7 HPV 31, 33, 45, 52, and 58, and non-inferior HPV 6, 11, 16, and 18 antibody responses when compared w

8 and 18 and a quadrivalent vaccine containing HPV 6, 11, 16, and 18 antigens are in use in vaccination

9 Overall, 415 MSM (69.7%) were negative to HPV 6, 11, 16, and 18 at enrollment by both serology and

10 n time to clearance of persistently detected HPV 6, 11, 16, and 18 DNA was 6.7, 3.2, 9.2, and 4.7 mon

11 (excluding a decrease of 1.5 times) of anti-HPV 6, 11, 16, and 18 geometric mean titres (GMT).

12 HPV 6, 11, 16, and 18 GMTs were non-inferior in the 9vHP

13 termined by a reduction in the prevalence of HPV 6, 11, 16, and 18 infection among young women.

14 he population-level impact of vaccination on HPV 6, 11, 16, and 18 infections in high-income countrie

15 HPV 6, 11, 16, and 18 seroprevalence was 8.1%, 13.9%, 12

16 s when compared with quadrivalent HPV (qHPV; HPV 6, 11, 16, and 18) vaccine.

17 t girls and boys vaccination would eliminate HPV 6, 11, 16, and 18, with a median RRprev of 1.00 for

18 milar immunogenicity profile with respect to HPV 6, 11, 16, and 18.

19 tudy results suggest that the acquisition of HPV 6, 11, 16, and/or 18 in males is common and that man

20 of subsequent incident genital infections by HPV 6, 11, 16, or 18 in men.

21 h a reduction in subsequent incident genital HPV 6, 11, and 16 infections.

22 The RRprev were greater for HPV 6, 11, and 18 than for HPV 16 for all scenarios inve

23 rivalent HPV vaccine prevents infection with HPV-6, 11, 16, and 18 and the development of related ext

24 lation and generated an antibody response to HPV-6, 11, 16, and 18 that was noninferior to that gener

25 Antibody responses to HPV-6, 11, 16, and 18 were noninferior to those generate

26 cy with respect to persistent infection with HPV-6, 11, 16, or 18 and detection of related DNA at any

27 al intraepithelial neoplasia associated with HPV-6, 11, 16, or 18 infection in men who have sex with

28 al intraepithelial neoplasia associated with HPV-6, 11, 16, or 18 was 50.3% (95% confidence interval

29 ulation, efficacy against lesions related to HPV-6, 11, 16, or 18 was 90.4% (95% CI, 69.2 to 98.1).

30 ithelial neoplasia related to infection with HPV-6, 11, 16, or 18 was reduced by 54.2% (95% CI, 18.0

31 ding risks of persistent anal infection with HPV-6, 11, 16, or 18 were reduced by 59.4% (95% CI, 43.0

32 95% CI, 45.8 to 78.6) for lesions related to HPV-6, 11, 16, or 18.

33 sia or anal cancer related to infection with HPV-6, 11, 16, or 18.

34 dence of external genital lesions related to HPV-6, 11, 16, or 18.

35 t human papillomavirus (HPV) vaccine series (HPV-6, -11, -16, -18) is immunogenic and safe in young w

36 against all of the different HPVs evaluated (HPV-6, -11, -16, -31, -35, -39, -45, -58, and -59 as pse

37 Seroconversion rates were 100% for HPV-6, -11, -16, and -18 among participants taking ART.

38 quadrivalent vaccine (4vHPV), which prevents HPV-6, -11, -16, and -18 infection.

39 ral rinses for HPV DNA and baseline sera for HPV-6, -11, -16, and -18 L1 antibodies.

40 asured neutralizing antibodies (NAb) against HPV-6, -11, -16, and -18 using the pseudovirion-based ne

41 termined the prevalence of vaccine-type HPV (HPV-6, -11, -16, and -18) among all, vaccinated, and unv

42 types targeted by the quadrivalent vaccine (HPV-6, -11, -16, and -18) will be one of the first measu

43 may be protected against up to 4 genotypes (HPV-6, -11, -16, and -18).

44 ters (GMTs) and (2) seroconversion rates for HPV-6, -11, -16, and -18, among those seronegative and H

45 tic efficacy against disease associated with HPV-6, -11, -16, and -18.

46 ting cervical and genital disease related to HPV-6, -11, -16, and -18.

47 -HPV responses were summarized as serum anti-HPV-6, -11, -16, or -18 geometric mean titers 1 month af

48 aled that men with circulating antibodies to HPV-6, -11, -16, or -18 were not less likely to acquire

49 4-19 years, the vaccine-type HPV prevalence (HPV-6, -11, -16, or -18) decreased from 11.5% (95% confi

50 dies (hazard ratio for the risk of acquiring HPV-6, -11, -16, or -18, 1.63; 95% confidence interval,

51 rabbit antisera to L1 VLPs corresponding to HPV-6, -11, -18, -31, -33, -35, -39, and -45 were assaye

52 st time to detection among men with incident HPV 6/11 infection.

53 to human papillomavirus (HPV) 16/18 but not HPV 6/11 infections or disease.

54 ive incidence of GWs among men with incident HPV 6/11 infections was 14.6% (95% confidence interval [

55 tion among men with incident infections with HPV 6/11 only (6.2 months; 95% CI, 5.6-24.2 months).

56 HPV 6/11 plays an important role in GW development, with

57 /35/39/45/51/52/56/58/59 and seronegative to HPV 6/11/16/18 at day 1, and had a normal Pap result at

58 Maximal reductions of approximately 90% for HPV 6/11/16/18 infection, approximately 90% for genital

59 We used a mathematical model of HPV 6/11/16/18 sexual transmission within an MSM populat

60 placebo recipients who were DNA negative to HPV 6/11/16/18/31/33/35/39/45/51/52/56/58/59 and seroneg

61 We determined seroprevalence of HPV 6/11/16/18/31/33/45/52/58 among 4943 persons aged 14

62 ntibody and cell-mediated immune response to HPV-6/11 have been observed.

63 ion of a pregnant woman who has condyloma or HPV-6/11 infection with the quadrivalent HPV vaccine wil

64 dence interval) was 34.5% (11.3 to 51.8) for HPV-6/11, 34.9% (9.1 to 53.7) for HPV-6, 30.3% (-45.0 to

65 HPV-6/11/16/18 vaccine reduced the risk of CIN2-3/AIS as

66 After the prophylactic HPV-6/11/16/18 vaccine was licensed in the United States

67 (HPV)-6/11/16/18 vaccine reduces the risk of HPV-6/11/16/18-related cervical intraepithelial neoplasi

68 ive to the efficacy already observed against HPV-6/11/16/18-related disease, because women may have >

69 bsequent infection for a combined measure of HPV-6/11/31/33/35/45/52/58 in female subjects (pooled RR

70 ections with a number of low-risk HPV types (HPV-6/11/74), which are responsible for the majority of

71 lower for each type, with 6.3% observed for HPV-6, 2.0% for HPV-11, 5.1% for HPV-16, and 1.5% for HP

72 51.8) for HPV-6/11, 34.9% (9.1 to 53.7) for HPV-6, 30.3% (-45.0 to 67.5) for HPV-11, and 49.5% (21.0

73 HPV 6 (43.8%), HPV 11 (10.7%), and HPV 16 (9.8%) were th

74 anged from 92.3% (for HPV-18) to 100.0% (for HPV-6) among participants not taking ART.

75 cident and 6-month persistent infections for HPV 6 and 11 did not differ by baseline serostatus.

76 PV 16, 18, 31, and 45) and in genital warts (HPV 6 and 11).

77 unt for 70% of cases of cervical cancer, and HPV 6 and 11, which cause 90% of the cases of anogenital

78 in a high neutralizing antibody response to HPV 6 and HPV 11 in her serum, and these antibodies tran

79 -uninfected homosexual men were screened for HPV-6 and -16 capsid antibodies.

80 By capture ELISA with HPV-6 and -16 L1 capsids, 47% of subjects were seroposit

81 ction detection of HPV DNA and prevalence of HPV-6 and -16 serum antibodies, was investigated in 149

82 1alpha release than those that bound poorly (HPV-6 and an HPV-16 E7 24gly mutant).

83 the surface area of AGWs and viral load for HPV-6 and HPV-11.

84 Human papillomavirus type 6 (HPV-6) and HPV-11 are the etiological agents of approxim

85 , such as human papillomavirus (HPV) type 6 (HPV-6) and HPV-11, induce benign genital warts that rare

86 ted with cancer, low-risk HPV types, such as HPV 6, are associated with benign warts.

87 HPV-6 B1 variants are more prevalent in genital swabs th

88 We observed significant association of HPV-6 B1 variants detection with GW development.

89 HPV-6 B1 variants prevalence was increased in GWs and ge

90 assays (EMSAs), we have shown that CDP binds HPV-6 both upstream and downstream of the E6, E7, and E1

91 t month 7, but not for HPV-18 by month 24 or HPV-6 by month 36.

92 d and neck cancers, and low-risk HPVs (e.g., HPV-6) cause benign hyperproliferative disease.

93 ths of DNA detection, but seroconversion for HPV-6 coincided with DNA detection.

94 HPV-6 DNA detection and the presence of anal warts were

95 er, suggesting that YY1 negatively regulates HPV-6 E1 promoter activity.

96 tein (CDP) binds the differentiation-induced HPV-6 E1 promoter and negatively regulates its activity

97 ve regulators of the differentiation-induced HPV-6 E1 promoter and thereby the HPV life cycle.

98 inhibit HPV replication in vitro, binds the HPV-6 E1 promoter.

99 We show that the HPV 6 E2 DBD is structurally more similar to the HPV 18

100 e compared the DNA binding properties of the HPV 6 E2 DNA binding domain (DBD) and a mutant lacking t

101 he minimal DNA-binding domain (DBD) from the HPV 6 E2 protein.

102 The low-risk HPV-6 E6 and E7 proteins did not cause any significant c

103 The low-risk HPV-6 E6 and E7 proteins did not induce such abnormaliti

104 ith a plasmid expressing luciferase from the HPV-6 E6, E7, or E1 regulatory region and a plasmid carr

105 y regulates the human papillomavirus type 6 (HPV-6) E6 promoter.

106 oduced a high-affinity pRB-binding site into HPV-6 E7 (6E7G22D) and showed that, in human foreskin ke

107 Despite this heterogeneity in phenotype, HPV-6 E7 and/or L1-specific WIL, as determined by lympho

108 nt DNA replication, whereas the nononcogenic HPV-6 E7 had reduced effects.

109 st that the shared activity of HPV-16 E7 and HPV-6 E7 to destabilize p130 and decrease or delay diffe

110 Second, we analyzed the ability of wild-type HPV-6 E7 to destabilize the other pRB family members, p1

111 Binding of HPV-6 E7 to p130 was necessary but not sufficient to dec

112 HPV-6 E7, like HPV-16 E7, decreased the level of p130 pr

113 HPV-11 E7ER and, much less efficiently, HPV-6 E7ER also promoted S-phase reentry by differentiat

114 howed that, in human foreskin keratinocytes, HPV-6 E7G22D decreased the level of pRB protein but not

115 Moreover, the HPV-6 epitopic peptides recognized by WIL differed to so

116 gnificant decline in the mean viral loads of HPV-6 (from 0.011 x 108 to 0.00000154 x 108 copies/mg of

117 n the Mw group but only in the viral load of HPV-6 (from 1.41 x 108 to 0.004 x 108 copies/mg of tissu

118 The impact of HPV-6 genetic heterogeneity on persistence and progressi

119 tion in Men (HIM) Study participants who had HPV-6 genital swabs and/or GWs preceded by a viable norm

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

121 Since HPV-6 infections are confined to the epithelium, such an

122 the control of human papillomavirus type 6 (HPV-6) infections is an appealing premise, but their act

123 Human papillomavirus type 6 (HPV-6) is a low-risk HPV whose replication cycle, like t

124 hierarchy of E2 sites within the HPV 16 and HPV 6 LCRs are different.

125 d HPV 16, 1 PeIN III lesion was positive for HPV 6 only.

126 Condyloma primarily contained HPV 6 or 11.

127 l now not been demonstrated for the low-risk HPV-6 or HPV-11 E7 proteins.

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

129 ined genital warts among women with incident HPV-6 or HPV-11 infection was 64.2% (95% CI, 50.7%-77.4%

130 .1%) among 46 men with incident detection of HPV-6 or HPV-11 infection, 2.0% (95% CI, 0.5%-7.9%) amon

131 P) is caused by human papillomavirus type 6 (HPV-6) or HPV-11.

132 t CDP represses transcription from all three HPV-6 promoters.

133 f high-risk HPV-16, but not that of low-risk HPV-6, reduced miR-218 expression, and conversely, RNA i

134 nd HPV-18-related cancers, the prevention of HPV-6-related and HPV-11-related genital warts and juven

135 HPV-6 variants distribution differed between countries a

136 e intervals for the risk of GWs according to HPV-6 variants were calculated.

137 ere detected in 3.4% of female participants; HPV-6 was detected in 1.3% (95% CI, 0.8%-2.3%), HPV-11 i

138 5 men developed incident oral HPV infection (HPV-6 was detected in 7, HPV-11 in 0, HPV-16 in 17, and

139 HPV-6 was found in 130/195, HPV-11 in 63/195, and HPV-6/

140 e E6 and E7 proteins from the low-risk virus HPV-6 were not able to bypass any of the growth arrest s

141 ype in the lesions from control patients was HPV 6, while lesions from immunosuppressed types most of