ライフサイエンスコーパス: HPV-31

1 HPV 31 was the least accurately detected by participatin

2 HPV-31 early transcripts were found to utilize a heterog

3 he most prevalent types were HPV 16 (4.13%), HPV 31 (4.12%) and HPV 51 (3.39%), while HPV 18 (1.70%)

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

5 E2 protein, as did human papillomavirus 31 (HPV-31) E2, which also colocalized with FGFR3 within the

6 apsid genes of human papillomavirus type 31 (HPV-31) are expressed late in the differentiation-depend

7 apsid genes of human papillomavirus type 31 (HPV-31) are expressed upon keratinocyte differentiation

8 that maintain human papillomavirus type 31 (HPV-31) episomes have been examined.

9 in the context of the complete HPV type 31 (HPV-31) genome.

10 cells reduced human papillomavirus type 31 (HPV-31) transcription, whereas depletion of SETD6 in int

11 In human papillomavirus type 31 (HPV-31), the E1--E4 and E5 open reading frames are expre

12 induced in a smaller subset of HPV type 31 (HPV-31)-positive cells at this time point.

13 four oncogenic non-vaccine HPV types-HPV-33, HPV-31, HPV-45, and HPV-51-in different trial cohorts re

14 fection) was seen across cohorts for HPV-33, HPV-31, HPV-45, and HPV-51.

15 entified included HPV-16 in 10 tumors (48%), HPV-31 in 5 tumors, HPV-33 in 1 tumor, HPV-35 in 2 tumor

16 st prevalent persistence and HPV-33 (53.8%), HPV-31 (46.7%), and HPV-16 (42.6%) the highest incident

17 ne, which targets HPV-16 and HPV-18, against HPV-31, -33, and -45 infection and an increased incidenc

18 Both schedules elicited antibodies against HPV-31 and HPV-45 up to 5 years after first dose.

19 Vaccine efficacy against HPV-31/33/45 for two-dose women who received their secon

20 to provide partial cross-protection against HPV-31, -33, -35, -45, -52, and possibly -58, that is, a

21 When an HPV 31 genome (31E1*) containing a missense mutation in

22 CIN 612-9E cells, which were derived from an HPV-31-infected patient and harbor HPV-31 extrachromosom

23 n against incident infection with HPV 45 and HPV 31.

24 Between BPV-1 and HPV-31 E2, 8 of the 11 tyrosines are conserved in the N-

25 ive mutant form of FGFR3 decreased BPV-1 and HPV-31 transient replication although this result also o

26 Both BPV-1 and HPV-31 Y102E are similar in that neither binds the C ter

27 quired HR-HPV types were HPV-52, HPV-16, and HPV-31; and their incidence was increased significantly

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

29 at weaker or absent from other types such as HPV-31, HPV-33, and HPV-51.

30 HPV 16 was most common (49.1%), followed by HPV 31 (10.4%) and HPV 52 (9.7%).

31 ing pathogenesis using recircularized cloned HPV 31 genomes that were transfected together with a dru

32 kin keratinocytes with recircularized cloned HPV-31 genomic sequences resulted in a high frequency of

33 ization of primary keratinocytes with cloned HPV-31 genomes.

34 re introduced in the context of the complete HPV 31 genome.

35 ne expression in the context of the complete HPV-31 genome, recombinant genomes were constructed that

36 %), HPV-16/18 significantly declined, as did HPV-31 among HMs.

37 -16 and its genetically related types (i.e., HPV-31, -33, -35, -52, and -58).

38 revalence of all type categories, especially HPV 31/33/45/52/58 among females, varied by race/ethnici

39 for HPV-16 to 634 (95% CI, 28.5-14 087) for HPV-31.

40 version ranged from 4% for HPV-52 to 36% for HPV-31.

41 ranged from 4.7% (for HPV-59) to 29.5% (for HPV-31), and the risk of > or =CIN3 ranged from 0.0% (fo

42 ranged from 0.0% (for HPV-59) to 14.8% (for HPV-31).

43 was noted for HPV-33 in all cohorts, and for HPV-31 in the ATP-E and TVC-naive.

44 ompared with the 3-dose schedule, except for HPV-31 at 4-4(1/2) years after the first dose and HPV-33

45 correlate with sequence variations found for HPV-31, -35, -52, and -58.

46 Reductions were most notable for HPV-31.

47 nd similar type specificity was observed for HPV-31 and -45.

48 different from that previously reported for HPV-31 was found to be activated or repressed by HPV-11.

49 ch mutated VLP had residues substituted from HPV-31 or HPV-52 L1 sequences to the HPV-16 L1 backbone.

50 .68-56.51) against cross-reactive genotypes (HPV 31, 33, 45), respectively.

51 d from an HPV-31-infected patient and harbor HPV-31 extrachromosomally, exhibited the same switch in

52 the region of amino acids (aa) 107 to 175 in HPV-31 E2.

53 We observed significant declines in HPV-31 (all women and heterosexual men), HPV-45 (all wom

54 s demonstrate that capsid gene expression in HPV-31 requires an inefficient early poly(A) signal whic

55 ce of R-loops at the viral early promoter in HPV-31 (CIN612) and HPV-16 (W12) episomal HPV cell lines

56 The reduction in HPV-31/33/45/52/58 infection and CIN1-3/AIS was 25.0% (9

57 Although a modest reduction in HPV-31/33/45/52/58-related CIN2 or worse was observed, t

58 ependent polyadenylation and read-through in HPV-31.

59 Vaccine efficacy against incident HPV-31/33/45 infections for three doses was 59.7% (56.0-

60 uppressed in cell lines that stably maintain HPV 31 or 16 episomes, as well as cervical cancer lines

61 Infection of cells which maintain HPV 31 DNA episomally with E2 recombinant adenoviruses r

62 FGFR3 depletion in cell lines that maintain HPV-31 episomes increased viral copy number.

63 l lines were isolated that stably maintained HPV 31 DNA as episomes and underwent terminal differenti

64 alized cell lines are capable of maintaining HPV-31 DNA as episomes and induce the synthesis of virio

65 a similar fashion, genomes containing mutant HPV 31 E7 genes, including a translation termination mut

66 that cell lines immortalized with the mutant HPV-31 expressed transcripts which were similar in size

67 d multiple, integrated copies of the mutated HPV-31 DNA.

68 ries failed to detect high concentrations of HPV 31 and, to a lesser extent, to detect HPV types 35,

69 The prevalence of HPV 31, 33, and 45 decreased significantly by 54% (RR 0.

70 evidence indicating that tyrosine (Y) 138 of HPV-31 E2 is a substrate of FGFR3.

71 previously reported that tyrosine (Y) 138 of HPV-31 E2 is phosphorylated by the fibroblast growth fac

72 5 did not significantly alter the ability of HPV-31 genomes to replicate transiently in keratinocytes

73 DNase I hypersensitivity analysis of HPV-31 chromatin in cell lines that maintain viral genom

74 ing from dichotomic branching in the case of HPV-31 to star phylogenies of the other three types.

75 Vaccination reduced the incidence of HPV-31/45 infection by 40.3% (95% confidence interval [C

76 We characterized mutations of HPV-31 E2 for interactions with relevant cellular bindin

77 the initiation of treatment, a population of HPV-31-positive cells that were resistant to interferon

78 tion affect the immortalization potential of HPV-31.

79 Vaccination reduced the rate of HPV-31/33/45/52/58 infection by 17.7% (95% confidence in

80 Vaccination also reduced the rate of HPV-31/58/59-related CIN1-3/AIS by 26.0% (95% CI, 6.7% t

81 xamine the effect of Y102 phosphorylation on HPV-31 E2 biology.

82 ytes >4-fold more effectively than HPV-16 or HPV-31 and >20-fold more efficiently than HPV-11 or cont

83 transfected with wild-type HPV-31 genomes or HPV-31 genomes containing mutations in HDAC binding sequ

84 apillomavirus BPV-1 and alpha papillomavirus HPV-31 E2.

85 ere similar to those observed with high-risk HPV-31, microarray analysis of 7,075 expressed sequences

86 ected using the E1 promoter of the high-risk HPV-31.

87 ated quasiviruses containing G418-selectable HPV-31 genomes with phosphodeficient phenylalanine mutan

88 This demonstrated the ability to synthesize HPV 31 virions from transfected DNA templates and allowe

89 Our studies demonstrate that HPV-31 late gene expression is regulated in a large part

90 The HPV-31-positive cells which expressed filaggrin did not

91 functionally active target sequences in the HPV-31 E1 and E2 open reading frames.

92 This is in contrast to the deletion of the HPV-31 early AAUAAA element, which resulted in a dramati

93 ctable marker was inserted into L1/L2 of the HPV-31 genome, creating HPV-31neo.

94 Mutations were created on the HPV-31 and -52 L1 proteins to determine if HPV-16 type-s

95 We previously reported that the HPV-31 E2 Y138 mutation to glutamic acid did not bind to

96 a reporter assay, it was determined that the HPV-31 early polyadenylation sequences allowed significa

97 plasia grade 2/3, vaginal cancer) related to HPV 31, 33, 45, 52, and 58 and non-inferiority (excludin

98 vical, vulvar and vaginal disease related to HPV 31, 33, 45, 52, and 58 was 0.5 cases per 10 000 pers

99 ne against infections and disease related to HPV 31, 33, 45, 52, and 58, and non-inferior HPV 6, 11,

100 lesions, and cervical procedures related to HPV 31, 33, 45, 52, and 58.

101 ted by SETD6, displayed decreased binding to HPV-31 E2, suggesting that SETD6 methylation of Brd4 als

102 t persistent infection and/or CIN 2/3 due to HPV-31 A/B and HPV-31C variants were -7.1% (95% confiden

103 infections and provided cross-protection to HPV-31/33/45.

104 vical, vulvar, or vaginal disease related to HPV-31, 33, 45, 52, and 58 in a prespecified per-protoco

105 e prevented infection and disease related to HPV-31, 33, 45, 52, and 58 in a susceptible population a

106 Specific CD4+ T-cell and B-cell responses to HPV-31 and HPV-45 at month 36 were similar across groups

107 at these methodologies are not restricted to HPV-31 but are applicable to other HPV types, including

108 n VE was observed by variant among transient HPV-31 infections (P = .68).

109 Although transfected wild-type HPV 31 genomes, as well as genomes containing an E6 tran

110 eratinocytes were transfected with wild-type HPV-31 genomes or HPV-31 genomes containing mutations in

111 V type, and infection with non-vaccine types HPV 31 and HPV 45 over 7 years of follow-up.

112 39.5%-97.08%) against cross-protective types HPV-31/33/45.

113 V-11, HPV-16, and HPV-18) and related types (HPV-31, and HPV-45) decreased year over year, with the l

114 plicate in a transient in vitro assay, while HPV-31 Y102E binds E1 and was able to replicate, albeit

115 cy against 6-month persistent infection with HPV 31 (65.8%, 96.2% CI 24.9-85.8) and HPV 45 (70.7%, 96

116 cy against 6-month persistent infection with HPV 31 (79.1%, 97.7% CI 27.6-95.9) and HPV 45 (76.9%, 18

117 common and best-studied type, together with HPV-31, -33, -35, -52, -58, and -67.