ライフサイエンスコーパス: CSFV

1 e modified by site-directed mutagenesis of a CSFV Brescia infectious clone (BICv).

2 In addition, CSFV infection induced a biphasic activation of ERK1/2,

3 r MEK1/2/ERK1/2, whereas MEK2 did not affect CSFV replication after blocking the interferon-induced J

4 only a few host restriction factors against CSFV, including interferon-stimulated genes (ISGs), have

5 ial for the antiviral action of GBP1 against CSFV replication, and the binding of the NS5A protein to

6 are commonly induced by type I IFNs against CSFV in lentivirus-delivered cell lines, resulting in th

7 n 1 (GBP1) as a potent antiviral ISG against CSFV.

8 aking our findings together, GBP1 is an anti-CSFV ISG whose action depends on its GTPase activity.

9 However, anti-CSFV ISGs are poorly documented.

10 tudy will facilitate the development of anti-CSFV therapeutic agents by targeting host factors and ma

11 te-binding protein 1 (GBP1) as a potent anti-CSFV ISG.

12 We further show that the anti-CSFV action of GBP1 depends on its GTPase activity.

13 The assay detected CSFV, representing different phylogenetic groupings, but

14 he second cysteine of the CCFV motif (CCFV > CSFV), but not the first, abrogated both Wrch-1 membrane

15 e loss of virus-mediated IRF3 degradation in CSFV-infected cells.

16 upregulated at the transcriptional level in CSFV-infected PK-15 cells and in various organs of CSFV-

17 Our work reveals a novel role of MEK2 in CSFV infection and sheds light on the molecular basis by

18 rain, indicating a significant role of p7 in CSFV virulence.

19 ed small hairpin RNAs dramatically inhibited CSFV replication.

20 A panel of recombinant mutant CSFVs was created using alanine scanning mutagenesis of

21 and accurate test permits rapid detection of CSFV in affected herds.

22 and the MEK2/ERK1/2 cascade in the growth of CSFV for the first time.

23 infected domestic swine, the natural host of CSFV host, we observed that the virus was now completely

24 ctivity, was essential for the inhibition of CSFV replication.

25 tions of the cysteines in the TRASH motif of CSFV N(pro) abolished the interaction of N(pro) with IRF

26 nfected PK-15 cells and in various organs of CSFV-infected pigs.

27 that GBP1 acted mainly on the early phase of CSFV replication and inhibited the translation efficienc

28 which is clearly involved in the process of CSFV virulence in swine.

29 The E1 protein of CSFV strain Brescia contains six cysteine residues at po

30 a novel binding partner of the E2 protein of CSFV using yeast two-hybrid screening.

31 hat GBP1 interacted with the NS5A protein of CSFV, and this interaction was mapped in the N-terminal

32 , this negatively affects the replication of CSFV and BDV.

33 MEK2 positively regulates the replication of CSFV through inhibiting the JAK-STAT signaling pathway.

34 Furthermore, the replication of CSFV was markedly inhibited in PK-15 cells treated with

35 K2 significantly promoted the replication of CSFV, whereas knockdown of MEK2 by lentivirus-mediated s

36 iency of the internal ribosome entry site of CSFV.

37 on of E1-E2 heterodimers and their effect on CSFV viability in vitro and in vivo remain unclear.

38 ely than translation dependent on the HCV or CSFV internal ribosome entry sites, which do not require

39 ine relative to the highly virulent parental CSFV Brescia strain, indicating a significant role of p7

40 nce of the NS4B protein of highly pathogenic CSFV strain Brescia (BICv) identified a putative Toll/in

41 mall interfering RNAs significantly promoted CSFV growth.

42 Notably, we demonstrate that MEK2 promotes CSFV replication through inhibiting the interferon-induc

43 Recombinant CSFVs containing mutations in different residues of FPII

44 We show that MEK2 positively regulates CSFV replication.

45 an IFN-induced GTPase, remarkably suppressed CSFV replication, whereas knockdown of endogenous GBP1 e

46 c reticulum lipid composition confirmed that CSFV p7 is a pore-forming protein, and that pore-forming

47 terious for virus growth, demonstrating that CSFV p7 function is critical for virus production in cel

48 0S ribosomal complex containing eIF3 and the CSFV IRES.

49 escia, indicating a significant role for the CSFV E2 glycoprotein in swine virulence.

50 ures, while persistence was probable for the CSFV-like case.

51 nlike in SVV, the deletion of IIId2 from the CSFV and BDV IRES elements impairs initiation of transla

52 lthough the position and interactions of the CSFV IRES with the 40S subunit in this complex are simil

53 swine was unwarranted while response to the CSFV-like pathogen was generally effective.

54 ere identified by virus isolation, while the CSFV real-time RT-PCR assay identified all four infected

55 ngth infectious clone of the highly virulent CSFV strain Brescia (BICv) was used to evaluate how amin

56 e of E2 glycosylation of the highly virulent CSFV strain Brescia in infection of the natural host.

57 protected swine from challenge with virulent CSFV strain Brescia at 3 and 28 days postinfection.

58 o pestiviruses, classical swine fever virus (CSFV) and border disease virus (BDV), are required for 8

59 virus (HCV) and classical swine fever virus (CSFV) coordinate cap-independent assembly of eukaryotic

60 l protein p7 of classical swine fever virus (CSFV) is a small hydrophobic polypeptide with an apparen

61 Classical swine fever virus (CSFV) is the causative agent of classical swine fever (C

62 Classical swine fever virus (CSFV) is the causative agent of classical swine fever (C

63 virus (HCV) and classical swine fever virus (CSFV) messenger RNAs contain related (HCV-like) internal

64 determinants of classical swine fever virus (CSFV) virulence and host range, chimeras of the highly p

65 e PCR assay for classical swine fever virus (CSFV) was developed and evaluated in experimentally infe

66 se (RT) PCR for classical swine fever virus (CSFV) was evaluated for diagnostic sensitivity and speci

67 replication of classical swine fever virus (CSFV), a devastating porcine pestivirus.

68 replication of classical swine fever virus (CSFV), a fatal pestivirus of pigs, remain unknown.

69 glycoprotein of classical swine fever virus (CSFV), is involved in several critical virus functions,

70 iruses, such as classical swine fever virus (CSFV), target IRF3 for ubiquitination and subsequent pro

71 ral proteins of classical swine fever virus (CSFV), the etiological agent of a severe, highly lethal

72 rrhea virus and classical swine fever virus (CSFV), use the viral protein N(pro) to subvert host cell

73 l protein E2 of classical swine fever virus (CSFV).

74 lycoproteins of classical swine fever virus (CSFV).

75 lycoproteins of classical swine fever virus (CSFV).