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1                                              CSFV E2DeltaDCTN6v showed reduced replication, compared
2                                              CSFV has been shown to antagonise the induction of type
3                               In addition, a CSFV infectious clone harboring the E2 Q316L substitutio
4 e modified by site-directed mutagenesis of a CSFV Brescia infectious clone (BICv).
5                                 In addition, CSFV infection induced a biphasic activation of ERK1/2,
6 r MEK1/2/ERK1/2, whereas MEK2 did not affect CSFV replication after blocking the interferon-induced J
7 valent vaccine is safe and effective against CSFV or PCV2 challenge.
8  only a few host restriction factors against CSFV, including interferon-stimulated genes (ISGs), have
9 ial for the antiviral action of GBP1 against CSFV replication, and the binding of the NS5A protein to
10  are commonly induced by type I IFNs against CSFV in lentivirus-delivered cell lines, resulting in th
11 n 1 (GBP1) as a potent antiviral ISG against CSFV.
12 ted a novel bivalent subunit vaccine against CSFV and PCV2.
13 aking our findings together, GBP1 is an anti-CSFV ISG whose action depends on its GTPase activity.
14                                However, anti-CSFV ISGs are poorly documented.
15 tudy will facilitate the development of anti-CSFV therapeutic agents by targeting host factors and ma
16 te-binding protein 1 (GBP1) as a potent anti-CSFV ISG.
17                We further show that the anti-CSFV action of GBP1 depends on its GTPase activity.
18 re, we characterized the interaction between CSFV E2 and swine protein Torsin-1A during virus infecti
19                           The assay detected CSFV, representing different phylogenetic groupings, but
20 tein interaction is a critical factor during CSFV replication.
21 Torsin-1A protein-protein interaction during CSFV replication and provides a potential pathway toward
22  a critical role for that interaction during CSFV replication.IMPORTANCE Structural glycoprotein E2 i
23 he second cysteine of the CCFV motif (CCFV > CSFV), but not the first, abrogated both Wrch-1 membrane
24 e loss of virus-mediated IRF3 degradation in CSFV-infected cells.
25  the E2-DCTN6 protein-protein interaction in CSFV virulence and provides possible mechanisms of virus
26  upregulated at the transcriptional level in CSFV-infected PK-15 cells and in various organs of CSFV-
27     Our work reveals a novel role of MEK2 in CSFV infection and sheds light on the molecular basis by
28 1A and E2 proteins was confirmed to occur in CSFV-infected swine cells using three independent method
29 rain, indicating a significant role of p7 in CSFV virulence.
30 interaction between DCTN6 and E2 proteins in CSFV-infected swine cells by using two additional indepe
31 ed small hairpin RNAs dramatically inhibited CSFV replication.
32                A panel of recombinant mutant CSFVs was created using alanine scanning mutagenesis of
33 n period, which suggests that the ability of CSFV E2 to bind host DCTN6 protein efficiently during in
34 glycoprotein E2 is an important component of CSFV due to its involvement in many virus activities, pa
35 and accurate test permits rapid detection of CSFV in affected herds.
36 and the MEK2/ERK1/2 cascade in the growth of CSFV for the first time.
37 infected domestic swine, the natural host of CSFV host, we observed that the virus was now completely
38 ctivity, was essential for the inhibition of CSFV replication.
39 tions of the cysteines in the TRASH motif of CSFV N(pro) abolished the interaction of N(pro) with IRF
40 nfected PK-15 cells and in various organs of CSFV-infected pigs.
41 that GBP1 acted mainly on the early phase of CSFV replication and inhibited the translation efficienc
42  which is clearly involved in the process of CSFV virulence in swine.
43                            The E1 protein of CSFV strain Brescia contains six cysteine residues at po
44 a novel binding partner of the E2 protein of CSFV using yeast two-hybrid screening.
45 hat GBP1 interacted with the NS5A protein of CSFV, and this interaction was mapped in the N-terminal
46 , this negatively affects the replication of CSFV and BDV.
47 MEK2 positively regulates the replication of CSFV through inhibiting the JAK-STAT signaling pathway.
48              Furthermore, the replication of CSFV was markedly inhibited in PK-15 cells treated with
49 K2 significantly promoted the replication of CSFV, whereas knockdown of MEK2 by lentivirus-mediated s
50 iency of the internal ribosome entry site of CSFV.
51 on of E1-E2 heterodimers and their effect on CSFV viability in vitro and in vivo remain unclear.
52 ely than translation dependent on the HCV or CSFV internal ribosome entry sites, which do not require
53 ine relative to the highly virulent parental CSFV Brescia strain, indicating a significant role of p7
54 nce of the NS4B protein of highly pathogenic CSFV strain Brescia (BICv) identified a putative Toll/in
55 mall interfering RNAs significantly promoted CSFV growth.
56   Notably, we demonstrate that MEK2 promotes CSFV replication through inhibiting the interferon-induc
57                                A recombinant CSFV E2 mutant protein with a Q316L substitution failed
58                                A recombinant CSFV harboring mutations disrupting the E2-DCTN6 interac
59                                A recombinant CSFV mutant, E2DeltaDCTN6v, harboring specific substitut
60                                  Recombinant CSFVs containing mutations in different residues of FPII
61       We show that MEK2 positively regulates CSFV replication.
62 an IFN-induced GTPase, remarkably suppressed CSFV replication, whereas knockdown of endogenous GBP1 e
63 c reticulum lipid composition confirmed that CSFV p7 is a pore-forming protein, and that pore-forming
64 terious for virus growth, demonstrating that CSFV p7 function is critical for virus production in cel
65 0S ribosomal complex containing eIF3 and the CSFV IRES.
66                           In conclusion, the CSFV/PCV2 bivalent vaccine is safe and effective against
67 escia, indicating a significant role for the CSFV E2 glycoprotein in swine virulence.
68 ures, while persistence was probable for the CSFV-like case.
69 nlike in SVV, the deletion of IIId2 from the CSFV and BDV IRES elements impairs initiation of transla
70 lthough the position and interactions of the CSFV IRES with the 40S subunit in this complex are simil
71  is an important structural component of the CSFV particle.
72  swine was unwarranted while response to the CSFV-like pathogen was generally effective.
73 ere identified by virus isolation, while the CSFV real-time RT-PCR assay identified all four infected
74                 The results showed that this CSFV/PCV2 bivalent vaccine elicited a high level of neut
75 ssion of N(pro) and infection with wild-type CSFV were found to antagonise the mitochondrial localisa
76 virals for control of outbreaks in typically CSFV-free countries.
77 ngth infectious clone of the highly virulent CSFV strain Brescia (BICv) was used to evaluate how amin
78 e of E2 glycosylation of the highly virulent CSFV strain Brescia in infection of the natural host.
79 protected swine from challenge with virulent CSFV strain Brescia at 3 and 28 days postinfection.
80 rotein in classical swine fever (CSF) virus (CSFV) is the major virus structural glycoprotein and is
81 o pestiviruses, classical swine fever virus (CSFV) and border disease virus (BDV), are required for 8
82                 Classical swine fever virus (CSFV) and porcine circovirus type 2 (PCV2) are two of th
83 virus (HCV) and classical swine fever virus (CSFV) coordinate cap-independent assembly of eukaryotic
84             The classical swine fever virus (CSFV) glycoprotein E2 is the major structural component
85 l protein p7 of classical swine fever virus (CSFV) is a small hydrophobic polypeptide with an apparen
86                 Classical swine fever virus (CSFV) is the causative agent of classical swine fever (C
87                 Classical swine fever virus (CSFV) is the causative agent of classical swine fever (C
88                 Classical swine fever virus (CSFV) is the causative agent of classical swine fever, a
89 virus (HCV) and classical swine fever virus (CSFV) messenger RNAs contain related (HCV-like) internal
90 determinants of classical swine fever virus (CSFV) virulence and host range, chimeras of the highly p
91 e PCR assay for classical swine fever virus (CSFV) was developed and evaluated in experimentally infe
92 se (RT) PCR for classical swine fever virus (CSFV) was evaluated for diagnostic sensitivity and speci
93  replication of classical swine fever virus (CSFV), a devastating porcine pestivirus.
94  replication of classical swine fever virus (CSFV), a fatal pestivirus of pigs, remain unknown.
95 glycoprotein of classical swine fever virus (CSFV), is involved in several critical virus functions,
96 iruses, such as classical swine fever virus (CSFV), target IRF3 for ubiquitination and subsequent pro
97 ral proteins of classical swine fever virus (CSFV), the etiological agent of a severe, highly lethal
98 rrhea virus and classical swine fever virus (CSFV), use the viral protein N(pro) to subvert host cell
99 l protein E2 of classical swine fever virus (CSFV).
100 lycoproteins of classical swine fever virus (CSFV).
101 lycoproteins of classical swine fever virus (CSFV).
102            Remarkably, animals infected with CSFV E2DeltaDCTN6v remained clinically normal during the

 
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