ライフサイエンスコーパス: HPV-31

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

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

3 tion affect the immortalization potential of HPV-31.

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

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

6 Reductions were most notable for HPV-31.

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

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

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

10 .68-56.51) against cross-reactive genotypes (HPV 31, 33, 45), respectively.

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

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

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

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

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

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

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

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

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

20 -16 and its genetically related types (i.e., HPV-31, -33, -35, -52, and -58).

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

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

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

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

25 39.5%-97.08%) against cross-protective types HPV-31/33/45.

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

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

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

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

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

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

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

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

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

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

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

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

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

39 %), HPV-16/18 significantly declined, as did HPV-31 among HMs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 5 did not significantly alter the ability of HPV-31 genomes to replicate transiently in keratinocytes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 HPV 31 was the least accurately detected by participatin

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

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

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