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 objectives are to compare antibody titers to HPV 6, 11, 16, and 18 and rate of abnormal cytology betw

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

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

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

11 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

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

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

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

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

16 Seroconversion to HPV 6, 11, 16, and 18 occurred in 83%, 84%, 90%, and 62%

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 95% CI, 45.8 to 78.6) for lesions related to HPV-6, 11, 16, or 18.

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

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

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

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

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

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

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

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

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

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

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

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

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

48 ts analyzed, 31 (0.2%) detected vaccine-type HPV-6, -11, -16, and -18.

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

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

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

52 4-19 years, the vaccine-type HPV prevalence (HPV-6, -11, -16, or -18) decreased from 11.5% (95% confi

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

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

55 e of quadrivalent HPV vaccine (4vHPV) types (HPV 6,11,16,18) and other HPV-type categories and determ

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

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

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

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

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

61 irus immune-therapeutic capable of enhancing HPV 6/11-specific T cell immunity.

62 /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

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

64 HPV 6/11/16/18 serum antibody was detected using a multi

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

66 PRs for HPV 6/11/16/18 were 0.56 (95% confidence interval [CI],

67 sistence with >=1 quadrivalent vaccine type (HPV 6/11/16/18) between vaccinated (>=1 dose at baseline

68 We detected quadrivalent (HPV 6/11/16/18) vaccine-preventable types in 0.3% (95% C

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

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

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

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

73 first observable clinical outcome following HPV-6/11 infection, the strains targeted by vaccination.

74 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

75 genital warts (AGWs), commonly attributed to HPV-6/11.

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

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

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

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

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

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

82 any site were statistically significant with HPV-6, -16, -18, -31, and -56; odds ratios (ORs) ranged

83 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

84 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

85 nt HPV genotype (5%, 95% CI 4-7) followed by HPV-6 (4%, 3-5).

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

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

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

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

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

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

92 Two common human papillomaviruses (HPVs), HPV-6 and -11, are implicated in most cases, but it is s

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

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

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

96 1alpha release than those that bound poorly (HPV-6 and an HPV-16 E7 24gly mutant).

97 Blood assessments revealed HPV-6 and HPV-11 antigen-specific T-cell induction.

98 se of prophylactic HPV vaccine that includes HPV-6 and HPV-11 antigens has been studied.

99 notherapy designed to elicit T-cells against HPV-6 and HPV-11, was evaluated in a 52-week Phase 1/2 s

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

101 Genital HPV is common among men, with HPV-6 and HPV-16 being the most common genotypes.

102 The most common genotypes were HPV-6 and HPV-16 for both anatomical locations, although

103 ncordance was statistically significant with HPV-6 and HPV-31 (ORs, 4.89 [95% CI, 1.09-21.9] and 65.0

104 The proportion of GWs among HPV-6 and/or -11-positive patients remained constant acr

105 Thirty-two eligible adults with HPV-6 and/or HPV-11 RRP, requiring >=2 surgical interven

106 INO-3107 provides clinical benefit to HPV-6 and/or HPV-11-associated RRP adults and is well-to

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

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

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

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

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

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

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

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

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

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

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

118 IgG antibodies against HPV-6 E and L proteins are transferred from mothers to t

119 to HPV-6 L1 at 12 months (median) and to the HPV-6 E proteins between 23 and 35 months was observed.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 ed immunoglobulin G (IgG) antibodies against HPV-6 early (E2, E4, E6, E7) and late (L1) proteins in c

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

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

143 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

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

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

146 ection rates for quadrivalent vaccine types (HPV-6, HPV-11, HPV-16, and HPV-18) and related types (HP

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

148 ur in early childhood, as a sign of acquired HPV-6 infection by vertical or horizontal transmission s

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

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

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

152 l antibodies had vanished, seroconversion to HPV-6 L1 at 12 months (median) and to the HPV-6 E protei

153 Seropositivity of HPV-6 L1 in the neonates declined during the first 6 mon

154 Seroconversion against HPV-6 L1, E2, E4, E6, and E7 does occur in early childho

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

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

157 Condyloma primarily contained HPV 6 or 11.

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

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

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

161 .1%) among 46 men with incident detection of HPV-6 or HPV-11 infection, 2.0% (95% CI, 0.5%-7.9%) amon

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

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

164 Maternal antibodies to all tested HPV-6 proteins were transferred to neonates, concordance

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

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

167 HPV-6 variants distribution differed between countries a

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

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

170 5 men developed incident oral HPV infection (HPV-6 was detected in 7, HPV-11 in 0, HPV-16 in 17, and

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

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

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