ライフサイエンスコーパス: FCV

1 FCV attachment and entry is mediated by feline junctiona

2 FCV formation required intracytoplasmic replication of b

3 FCV infection resulted in the cleavage of the SG-nucleat

4 FCV proteinase-dependent processing of Pro-Pol in the in

5 FCV was isolated from 33 of 116 cats sampled over a 15-m

6 FCV-derived sequence from these clones mapped to a regio

7 FCVs are multimembranous structures that accumulate mono

8 exchanged for the equivalent sequences in an FCV Urbana strain infectious cDNA clone.

9 While FCoV and FCV belong to two distinct virus families, the Coronavir

10 itors against the 3CLpro enzymes of FCoV and FCV have not been previously identified.

11 luated for their activities against FCoV and FCV.

12 e proteinases (r3CL(pro)) from norovirus and FCV were found to cleave poly(A)-binding protein (PABP)

13 a structural platform for anti-FIPV and anti-FCV drug development.

14 with a covalently immobilized layer of anti-FCV mAbs.

15 In enzyme-linked immunosorbent assays, FCV binding to fJAM-A ectodomain was concentration depen

16 d significantly decreased capacities to bind FCV.

17 s a means to selectively tag substrate-bound FCV.

18 The surface-bound FCVs are subsequently coupled with an extrinsic Raman la

19 12 (genus Norovirus) and feline calicivirus (FCV) (genus Vesivirus), to investigate potential strateg

20 Feline calicivirus (FCV) and murine norovirus (MNV) are used as models to un

21 of the VPg proteins from feline calicivirus (FCV) and murine norovirus (MNV), which have been determi

22 nd of the genomic RNA of feline calicivirus (FCV) encodes a small (12.2-kDa) minor structural protein

23 trated by the capture of feline calicivirus (FCV) from cell culture media that is exposed to a gold s

24 ng frame 2 (ORF2) of the feline calicivirus (FCV) genome encodes a capsid precursor that is posttrans

25 longitudinal analysis of feline calicivirus (FCV) infection in an animal rescue shelter can be used a

26 e examined the effect of feline calicivirus (FCV) infection on SG accumulation.

27 The genome of feline calicivirus (FCV) is an approximately 7.7-kb single-stranded positive

28 Feline calicivirus (FCV) nonstructural proteins are translated as part of a

29 ion of the region of the feline calicivirus (FCV) ORF1 encoded by nucleotides 3233 to 4054 in an in v

30 y the active form of the feline calicivirus (FCV) RNA-dependent RNA polymerase (RdRP).

31 Feline calicivirus (FCV) strains can show significant antigenic variation wh

32 n which the LC region of feline calicivirus (FCV) was placed under the control of the cytomegalovirus

33 Feline calicivirus (FCV), a member of the Caliciviridae, produces its major

34 Feline calicivirus (FCV), a member of the Vesivirus genus, provides a tracta

35 CRFK cells infected with Feline Calicivirus (FCV), a virus released by cell lysis, not requiring vesi

36 major capsid protein of feline calicivirus (FCV), an expression library containing random, short (10

37 of a related vesivirus, feline calicivirus (FCV), highlighted potentially important differences rela

38 pesvirus type 1 (FHV-1), feline calicivirus (FCV), Mycoplasma felis, Chlamydophila felis, and Bordete

39 cute gastroenteritis and feline calicivirus (FCV), which causes respiratory illness and stomatitis in

40 system was isolated from feline calicivirus (FCV)-infected cells.

41 the extensively studied feline calicivirus (FCV).

42 nfectious viral entry of feline calicivirus (FCV).

43 functional receptor for feline calicivirus (FCV).

44 ned the entry process of feline calicivirus (FCV).

45 onaviruses (FCoVs) and feline caliciviruses (FCVs), respectively, and are important infectious diseas

46 ay is correlated with the number of captured FCV, determined by atomic force microscopy, as a means o

47 To characterize FCV binding to surface-expressed fJAM-A, we transfected

48 t is possible to recover engineered chimeric FCV strains that possess altered antigenic characteristi

49 ve component of this fraction was designated FCV replication complexes (RCs), by analogy to other pos

50 actions that regulate stress pathways during FCV infection.

51 c voltammetric determination of famciclovir (FCV).

52 CR positive for FHV-1, 7 for M. felis, 5 for FCV, 1 for C. felis, and 0 for B. bronchiseptica.

53 Only D1 was necessary for FCV binding to cells; all other domains could be replace

54 ntly identified as a functional receptor for FCV.

55 oprecipitation of radiolabeled proteins from FCV-infected feline kidney cells with serum raised again

56 centration dependent and saturable; however, FCV bound D1 alone weakly and was unable to bind D2.

57 Furthermore, SGs did not accumulate in FCV-infected cells that were stressed with arsenite or h

58 Changes in FCV capsid conformation following its interaction with f

59 NA molecules similar to those synthesized in FCV-infected cells.

60 idylated by the viral NS7 polymerase (Y24 in FCV, Y26 in MNV) occurs in a conserved position within t

61 productive FCV infection and (ii) individual FCV isolates differ in the factors they require.

62 deletions were introduced into an infectious FCV cDNA clone in order to evaluate the functional impor

63 ach of these cleavage sites in an infectious FCV cDNA clone was lethal for the virus, indicating that

64 d into the LC coding region of an infectious FCV cDNA clone.

65 to alanines by mutagenesis of an infectious FCV cDNA clone.

66 e ectodomain or D1 was sufficient to inhibit FCV infection in plaque reduction assays.

67 articles could be rescued from a full-length FCV cDNA clone encoding a nonfunctional VP2 when VP2 was

68 inimizing nonspecific binding and maximizing FCV binding efficiency.

69 In contrast to our finding that D1 mediated FCV binding, we found that all domains of fJAM-A were ne

70 mapped using a new 3.6-A structure of native FCV.

71 Analysis of FCV-infected feline kidney cells showed that the levels

72 Remarkably, while the core of FCV VPg contains a well-defined three-helix bundle, the

73 uccessfully applied for the determination of FCV in pure solutions and pharmaceutical preparations.

74 We found that preincubation of FCV with the ectodomain or D1 was sufficient to inhibit

75 mino acid sequences in the capsid protein of FCV (designated regions C and E) that were postulated to

76 show that a region of the capsid protein of FCV that rearranges following receptor engagement is not

77 from 11 other cats infected with a range of FCV isolates was also determined.

78 ere found to be critical for the recovery of FCV with a characteristic cytopathic effect in feline ki

79 evalence and presence of multiple strains of FCV within the shelter, the spread of such pathogens may

80 the mutations within the capsid structure of FCV was mapped using a new 3.6-A structure of native FCV

81 ed thus far, is quite different from that of FCV.

82 Formation of FCVs was significantly inhibited by 3-methyladenine, con

83 ctivity with antisera produced against other FCV strains.

84 s from three antigenically distinct parental FCV strains (CFI, KCD, and NADC) were exchanged for the

85 led with data showing that both the parental FCV and the srr mutants underwent increases in hydrophob

86 ssion of fJAM-A was not sufficient to permit FCV infection by all of the isolates we investigated.

87 ar factors are required to permit productive FCV infection and (ii) individual FCV isolates differ in

88 Here, we show that the infectivity of some FCV isolates is neutralized following incubation with th

89 ng interest in fuel cell vehicle technology (FCV) has engendered a growing need and realization to de

90 t 37 degrees C, these findings indicate that FCV likely undergoes conformational change upon interact

91 pathways and dominant-negative mutants, that FCV infects cells via clathrin-mediated endocytosis.

92 We have also observed that FCV permeabilizes cell membranes early during infection

93 We show that FCV infection impairs the assembly of SGs despite an inc

94 sly (E(960)/A(961) and E(1071)/S(1072)), the FCV ORF1 polyprotein contains five cleavage sites that d

95 e kidney cells with serum raised against the FCV ORF1 C-terminal region showed that this "3CD-like" p

96 Using mutational analysis, we identified the FCV-induced cleavage site within G3BP1, which differs fr

97 These structural changes in the FCV capsid have been shown to allow the assembly of a po

98 volution within hypervariable regions of the FCV capsid gene in individual cats ranged from 0.05 to 1

99 ds to the outer face of the P2 domain of the FCV capsid protein VP1, inducing conformational changes

100 dom, short (100- to 200-bp) fragments of the FCV F9 capsid gene was constructed.

101 roduced into an infectious cDNA clone of the FCV genome, and transfection of RNA derived from these c

102 -amino-acid insertion in the sequence of the FCV major capsid protein that forms a "cantilevered arm"

103 egion encoding the C-terminal portion of the FCV ORF1 (amino acids 942 to 1761) in bacteria allowed d

104 esponding to amino acids 1072 to 1763 of the FCV polyprotein encoded by open reading frame 1 of the g

105 Multiple active forms of the FCV RdRP were identified.

106 esting that Pro-Pol is an active form of the FCV RdRP.

107 ments led to improved reconstructions of the FCV-fJAM-A complex both before and after the induced con

108 poliovirus (PV) 3C(pro) cleavage, while the FCV r3CL(pro) products differed due to cleavage at an al

109 luorescence microscopy, we observed that the FCVs contained morphologically intact bacteria, despite

110 ons that could be specifically attributed to FCV, M. felis, or C. felis were seen, although interpret

111 e contributions of the virus and the host to FCV RNA replication.

112 A were necessary to confer susceptibility to FCV infection.

113 oles called Francisella-containing vacuoles (FCVs).

114 nd virulent, systemic feline calicivirus (vs-FCV) causes a highly fatal disease in cats for which no

115 dentify regions of fJAM-A that interact with FCV, we purified recombinant fJAM-A ectodomain and D1 an