ライフサイエンスコーパス: Sabin

1 Sabin strains of poliovirus used in the manufacture of o

2 Sabin strains used in the manufacture of oral polio vacc

3 Sabin strains were identified up to 5-8 weeks after the

4 campaign in all towns; in Aguascalientes, 1 Sabin 3 was isolated 16 weeks after the campaign, follow

5 her titers than attenuated counterparts PV(1)Sabin and PV(2)W-2, respectively, in primary human monoc

6 cell line, PV(1)Mahoney replicated but PV(1)Sabin did not, while both grew well in HeLa cells.

7 ecular recombinants of PV(1)Mahoney and PV(1)Sabin were assessed, a correlation between neurovirulenc

8 ed by dilution analysis of poliovirus type 2 Sabin in cerebrospinal fluid.

9 V(3)Leon grew weakly, while PV(3)Sabin, PV(2)Sabin, and PV(2) P712 did not replicate in these cells,

10 Although the type 3 Sabin strain is an effective vaccine, polioviruses with

11 PV(3)Leon grew weakly, while PV(3)Sabin, PV(2)Sabin, and PV(2) P712 did not replicate in t

12 Virus 31043 had a Sabin-derived type 3-type 2-type 1 recombinant genome wi

13 ion), even though all were protected against Sabin-1.

14 sociated with increased seroresponses to all Sabin types, especially to Sabin type 3.

15 nd rotavirus) infections, interference among Sabin vaccine viruses, and preexisting poliovirus antibo

16 nucleotide difference between the MEF-1 and Sabin 2 strains, resulting in 72 amino acid substitution

17 e entire 5' noncoding regions of Sabin 1 and Sabin 2 were replaced exactly with that of one of the ty

18 similar for Sabin isolate-Sabin isolate and Sabin isolate-non-Sabin enterovirus recombination after

19 each other and from those of WT Mahoney and Sabin type 3 viruses.

20 for attenuated oral polio vaccines (OPV) and Sabin types 1, 2, and 3.

21 eraction of the IRESs of PV type 3 (PV3) and Sabin type 3 (Sabin3) with polypyrimidine tract-binding

22 ence difference between 7 type 1 strains and Sabin type 1 vaccine strain was found.

23 Poliovirus isolates were identified as Sabin-like or wild type through real-time polymerase cha

24 at experimental IPV produced from attenuated Sabin strain (sIPV) of serotype 1 poliovirus induced ser

25 In attenuated Sabin strains, point mutations within stem-loop V of the

26 progressing rapidly, and the live attenuated Sabin strains in the oral poliovirus vaccine (OPV) are b

27 xperimental IPV produced from the attenuated Sabin strain (sIPV) with those of conventional IPV (cIPV

28 d that a 1,000-fold excess of the attenuated Sabin strain of poliovirus was protective against diseas

29 can enhance viral titers of both attenuated (Sabin strain) and wild-type polioviruses, a finding that

30 rable in efficacy to the currently available Sabin type 1 vaccine strain, but have the added advantag

31 ributable to interference of Sabin type 3 by Sabin type 2.

32 study, simulating 1 year of tOPV cessation, Sabin 2 transmission was higher in household contacts of

33 itch, 58% of environmental samples contained Sabin poliovirus; starting 6 weeks after the switch, Sab

34 1 possesses broader immunogenicity than does Sabin 2.

35 Committee dealing with these agents--Enders,Sabin, Dalldorf, Syverton--have passed on, but the work

36 e-derived poliovirus (cVDPV) is 300 days for Sabin-like virus type 1, 210 days for Sabin-like virus t

37 ys for Sabin-like virus type 1, 210 days for Sabin-like virus type 2, and 390 days for Sabin-like vir

38 or Sabin-like virus type 2, and 390 days for Sabin-like virus type 3.

39 hat VP1 substitution rates are increased for Sabin-like isolates relative to the rate for the wild ty

40 We combine our observations for Sabin-like virus evolution with the molecular clock for

41 DPV, the recombination rates are similar for Sabin isolate-Sabin isolate and Sabin isolate-non-Sabin

42 ntibodies, and stool samples were tested for Sabin strain polioviruses.

43 rived poliovirus (cVDPV2; >1% divergent from Sabin 2) occurred during July 2005-June 2010, a period w

44 virus (VDPV) with a 1.1% sequence drift from Sabin type 1 vaccine strain in the VP1 coding region 6 m

45 igenic divergence of the iVDPV variants from Sabin 1 followed two major independent evolutionary path

46 quences in neutralizing epitopes varied from Sabin 1 and Mahoney, with little variation among WPV1 is

47 In 8 patients who had Sabin-Feldman dye test titers >64 and for whom the infec

48 ssion analysis, fecal shedding of homologous Sabin strains was associated with increased seroresponse

49 Key determinants of attenuation in Sabin 1 had reverted in the iVDPV isolates, and represen

50 in humans, we studied molecular evolution in Sabin-like poliovirus isolates from Nigerian acute flacc

51 d mutagenesis of the miR-134 binding site in Sabin-1 IRES relieved miR-134-mediated repression indica

52 ve of recently acquired T. gondii infection (Sabin-Feldman dye test [DT] titers from 1:256 to 1:32,00

53 bination rates are similar for Sabin isolate-Sabin isolate and Sabin isolate-non-Sabin enterovirus re

54 hermore, the T cells also recognize and kill Sabin 1 vaccine-infected targets.

55 valent oral poliovirus vaccine (OPV) lacking Sabin 2.

56 gammaglobulinemic patient received monotypic Sabin 3 vaccine in 1962.

57 adjuvant for currently used and proposed new Sabin IPVs.

58 fter the campaign, following 7 weeks with no Sabin strains detected.

59 isolate-Sabin isolate and Sabin isolate-non-Sabin enterovirus recombination after accounting for the

60 ants shows that while recombination with non-Sabin enteroviruses is associated with cVDPV, the recomb

61 wed miR-134 binding to Sabin-1 and 3 but not Sabin-2 IRES.

62 34) can regulate Sabin-1 replication but not Sabin-2 or Sabin-3 via direct interaction with the PV 5'

63 ine point mutation at nucleotide (nt) 472 of Sabin oral poliovirus vaccine (OPV) type 3 is found in c

64 tropism of poliovirus and the attenuation of Sabin vaccine strains.

65 ruses sharing a 367-nucleotide (nt) block of Sabin 1-derived sequence spanning the VP1 and 2A genes c

66 Comparison of Sabin-like virus recombinants with known Nigerian vaccin

67 OPV formulations with higher doses of Sabin type 3 could improve immunogenicity among infants

68 transcripts containing the IRES elements of Sabin type 1 poliovirus or encephalomyocarditis virus, c

69 The evolution of Sabin 3 throughout the entire period of virus excretion

70 amples containing up to a 100-fold excess of Sabin vaccine strain-related sequences of the same serot

71 ssion to observe prevalence and incidence of Sabin 2 virus.

72 as primarily attributable to interference of Sabin type 3 by Sabin type 2.

73 Six pairs of Sabin strain-specific recombinant primers were designed

74 ained the temperature-sensitive phenotype of Sabin 1.

75 e in some way to the attenuated phenotype of Sabin type I.

76 ated and temperature-sensitive phenotypes of Sabin 3.

77 Polioviruses of Sabin types 2 and 3 reverted more easily than those of t

78 the structural and nonstructural proteins of Sabin strains may equally contribute to the attenuation

79 in which the entire 5' noncoding regions of Sabin 1 and Sabin 2 were replaced exactly with that of o

80 Replication of Sabin strains used in oral poliovirus vaccine (OPV) in t

81 mechanism of miR-134-mediated repression of Sabin-1.

82 We aimed to assess the risk of Sabin 2 transmission after a polio vaccination campaign

83 The pI's of Sabin types 1, 2, and 3 viruses were 7.4, 7.2, and 6.3,

84 ive mOPV2, as assessed by faecal shedding of Sabin 2 by reverse transcriptase quantitative PCR (RT-qP

85 However, faecal shedding of Sabin 2 in household contacts was increased significantl

86 Faecal shedding of Sabin 2 in infants who did not receive the mOPV2 challen

87 l 1991) isolates completely matched those of Sabin 1.

88 of a miR-134 mimic repressed translation of Sabin-1 5'UTR driven luciferase validating the mechanism

89 ps indicated transient local transmission of Sabin-like virus type 3 and, possibly, Sabin-like virus

90 All isolates were antigenic variants of Sabin 1, having multiple amino acid substitutions within

91 ceived OPV were found to contain variants of Sabin vaccine viruses.

92 o end game, which includes the withdrawal of Sabin strains, starting with type 2, and the introductio

93 New poliovirus vectors based on Sabin 1 and 2 vaccine strain viruses were constructed, a

94 ion-PCR (qRT-PCR) assay for detection of OPV Sabin strains 1, 2, and 3 directly in stool samples with

95 ulate Sabin-1 replication but not Sabin-2 or Sabin-3 via direct interaction with the PV 5'UTR.

96 risk of transmission of type 2 poliovirus or Sabin 2 virus on re-introduction or resurgence of type 2

97 on of Sabin-like virus type 3 and, possibly, Sabin-like virus type 1 during periods of low wild polio

98 lts from the toxoplasma serological profile (Sabin-Feldman dye test, conventional IgM and IgA ELISAs,

99 ween these two tests, a serological profile (Sabin-Feldman dye test, IgA and IgE antibody tests, diff

100 d considerable divergence from the prototype Sabin strain in all cases.

101 the type 1 live-attenuated poliovirus (PV) (Sabin) vaccine containing a human rhinovirus type 2 (HRV

102 the type 1 live-attenuated poliovirus (PV) (Sabin) vaccine containing a human rhinovirus type 2 (HRV

103 that microRNA-134-5p (miR-134) can regulate Sabin-1 replication but not Sabin-2 or Sabin-3 via direc

104 ss-protection following DENV infection since Sabin's challenge studies in the 1940s.

105 lower than those against the vaccine strain Sabin-1, two genetically distinct WPV1s isolated in 1965

106 liovirus; starting 6 weeks after the switch, Sabin polioviruses were rarely isolated, and if they wer

107 The Sabin vaccine strains used in prevention of poliomyeliti

108 sequence (nt 3271 to 3637) derived from the Sabin 1 oral poliovirus vaccine strain spanning the 3'-t

109 o poliovirus populations, differing from the Sabin 1 vaccine strain by approximately 10%, differing f

110 The iVDPV isolates differed from the Sabin type 1 oral poliovirus vaccine (OPV) strain at 1.8

111 differences in nucleotide sequence from the Sabin type 1 strain.

112 uence for antigenic site 3a derived from the Sabin type 2 strain.

113 differences in nucleotide sequence from the Sabin type 3 vaccine.

114 own to be caused by viruses derived from the Sabin vaccine strains.

115 e IgM ELISA, 71 (46.4%) were negative in the Sabin-Feldman dye test.

116 Like the Sabin-Feldman dye test, the new test is based on complem

117 poliovirus strains derived from Mahoney, the Sabin 1 vaccine strain and the mouse-adapted LS-a virus.

118 % correlation with the reference method, the Sabin-Feldman dye test for the detection of Toxoplasma I

119 two major determinants of attenuation of the Sabin 2 oral poliovirus vaccine strain (A481 in the 5'-u

120 The RdRp of the Sabin I vaccine strain has Thr-362 changed to Ile.

121 h the attenuating IRES point mutation of the Sabin serotype 1 vaccine strain.

122 ucleotide 480-G was identical to that of the Sabin strain.

123 Neuron-specific propagation deficits of the Sabin strains are partially encrypted within a confined

124 own that the attenuated viral genomes of the Sabin strains direct levels of viral protein synthesis l

125 ces were not closely related to those of the Sabin strains or 53 diverse contemporary wild poliovirus

126 ontinued because of the inherent risk of the Sabin strains to revert to neurovirulence and reacquire

127 amino acids within the capsid region of the Sabin type 2 oral poliovirus vaccine strain with corresp

128 to-U mutation at base 472 in the IRES of the Sabin type 3 poliovirus vaccine strain, known to attenua

129 n directing the attenuation phenotype of the Sabin vaccine strain of poliovirus type 1.

130 All three serotypes of the Sabin vaccine strains and the P3/Leon strain of poliovir

131 tral nervous system (CNS) attenuation of the Sabin vaccine strains of poliovirus (PV) are located wit

132 er and interpret data about evolution of the Sabin viruses used in OPV in regions where cVDPV has occ

133 merges due to the genetic instability of the Sabin viruses used in the oral polio vaccine (OPV) in po

134 to 97% nucleotide sequence identity) to the Sabin type 2 oral poliovirus vaccine (OPV) strain and un

135 Despite their effectiveness as vaccines, the Sabin strains retain a neuropathogenic potential in anim

136 tics are observed in cells infected with the Sabin 1 vaccine strain.

137 A translation defect associated with the Sabin type 3 IRES was observed in all organs examined.

138 Samples were tested with the Sabin-Feldman dye test and a range of agglutination assa

139 globulin G (IgG) and IgM IMx assays with the Sabin-Feldman dye test and an IgM enzyme-linked immunoso

140 test were similar to those obtained with the Sabin-Feldman dye test run in parallel.

141 new test which were not perceptible with the Sabin-Feldman dye test.

142 s for attenuating point mutations within the Sabin strains.

143 he 5' UTR and P1 genomic region in all three Sabin serotypes, as well as vaccine-related viruses with

144 n simply and quantitatively detect all three Sabin strains directly in stool samples to approximate s

145 Binding of miR-134 to Sabin-1 IRES caused degradation of the IRES transcript i

146 abin type 1, 97% to Sabin type 2, and 61% to Sabin type 3 vaccines.

147 Seroresponses were 86% to Sabin type 1, 97% to Sabin type 2, and 61% to Sabin type

148 roresponses were 86% to Sabin type 1, 97% to Sabin type 2, and 61% to Sabin type 3 vaccines.

149 ypochromicity data showed miR-134 binding to Sabin-1 and 3 but not Sabin-2 IRES.

150 oresponses to all Sabin types, especially to Sabin type 3.

151 Although stem-loop V Sabin mutations have been proposed to alter RNA secondar

152 The primary outcome was Sabin 2 incidence in the 10 weeks after the campaign in

153 tional recombination beyond the initial wild-Sabin recombination event.

154 e the phased cessation of OPV (starting with Sabin type 2) and emphasized the need for affordable IPV