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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

28 -16 and its genetically related types (i.e., HPV-31, -33, -35, -52, and -58).

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

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

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

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

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

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

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

36 Reductions were most notable for HPV-31.

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

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

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

40 .68-56.51) against cross-reactive genotypes (HPV 31, 33, 45), respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 5 did not significantly alter the ability of HPV-31 genomes to replicate transiently in keratinocytes

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

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

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

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

61 tion affect the immortalization potential of HPV-31.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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