ライフサイエンスコーパス: MHV

1 MHV-68 lytic infection upregulates Fos expression, AP-1

2 MHV-68-infected mice deficient in miR-155 exhibited decr

3 MHV-Brts31 has near-normal levels of RNA synthesis at th

4 with the CoV mouse hepatitis virus strain 1 (MHV-1) induces an acute respiratory disease with a high

5 tic basis of mouse hepatitis virus strain 1 (MHV-1) pneumovirulence.

6 Intranasal mouse hepatitis virus type 1 (MHV-1) infection of mice induces lung pathology similar

7 Intranasal mouse hepatitis virus-1 (MHV-1) infection of susceptible mouse strains mimics som

8 obesity and murine hepatitis virus strain-3 (MHV-3)-induced fulminant hepatitis due to excessive macr

9 ive regulator of murine gammaherpesvirus 68 (MHV-68 or gammaHV-68) lytic gene expression and replicat

10 reactivation of murine gammaherpesvirus 68 (MHV-68) in the lungs of major histocompatibility complex

11 re susceptible to acute gammaherpesvirus 68 (MHV-68) replication at day 7 after infection.

12 (HSV-1), and/or murine gammaherpesvirus 68 (MHV-68) with influenza virus, West Nile virus (WNV), or

13 with studies on murine gammaherpesvirus 68 (MHV-68), complete tegumentation and secondary envelopmen

14 c infection with murine gammaherpesvirus 68 (MHV-68).

15 response against murine gammaherpesvirus 68 (MHV-68).

16 ion of mice with murine gammaherpesvirus 68 (MHV-68).

17 f latency during mouse gamma-herpesvirus 68 (MHV-68) infection.

18 and function of murine gamma-herpesvirus 68 (MHV-68)-specific CD4(+) T cells using gp150-specific TCR

19 ring persistent murine gamma-herpesvirus-68 (MHV-68) infection.

20 We used this model to analyze a MHV-68 mutant lacking the expression of all miRNAs.

21 howed that mouse hepatitis virus strain A59 (MHV-A59) with a mutated catalytic site (N1348A) replicat

22 limination of nsp1 and nsp2 does not abolish MHV viability.

23 During acute MHV-A59 infection, oligodendrocytic Cx47, which is mainl

24 is required to prevent thromboembolism after MHV replacement, its value in patients receiving BHVs is

25 These CD4(+) T cells were protective against MHV-68 infection in the absence of CD8(+) T cells and B

26 16 (bCEA), which encode proposed alternative MHV receptors, revealed low ceacam2 expression in microg

27 rced expression of Vsig4 in mice ameliorates MHV-3-induced viral fulminant hepatitis.

28 5 was also increased by pRb in vitro, and an MHV with mutations in the LXCXE/D-motif, named vLC, exhi

29 neither CEACAM2 nor PSG16 is likely to be an MHV receptor on neurons, and the mechanism for CEACAM1a-

30 which exogenous PDEs were expressed from an MHV backbone lacking the gene for a functional NS2 prote

31 ruses, at an upstream genomic position in an MHV-A59/S chimera restored IFN resistance.

32 sis reveals that the N-terminal region of an MHV N SR-rich linker peptide (residues 198 to 230) binds

33 ning all of the MHV-1 structural genes on an MHV-A59 background were able to reproduce the severe acu

34 all of the MHV-1 structural proteins, on an MHV-A59 background.

35 complicated pregnancy in 10 patients with an MHV (4.7%).

36 Only 58% of the patients with an MHV had a pregnancy free of serious adverse events compa

37 Women with an MHV have only a 58% chance of experiencing an uncomplica

38 ity occurred in 1.4% of the patients with an MHV, in 1.5% of patients with a tissue heart valve (P=1.

39 events occurred in 23.1% of patients with an MHV, in 5.1% of patients with a tissue heart valve (P<0.

40 he pregnancy outcome of 212 patients with an MHV.

41 BCoV Nsp1 coding region directly yielded an MHV wt-like phenotype, which demonstrates a cognate inte

42 btle structural differences between BCoV and MHV NTDs, primarily involving different conformations of

43 completely interchangeable between BCoV and MHV.

44 in L2 cells treated with IFN-alpha/beta, and MHV had the ability to rescue only SeV replication.

45 her, most of the pFP mutants of SARS-CoV and MHV also failed to mediate membrane fusion, suggesting t

46 eins of 3 beta-CoVs, MERS-CoV, SARS-CoV, and MHV, and demonstrated that they were essential for media

47 Although KSHV and MHV-68 are closely related, the findings provide new ins

48 We show that KSHV LANA and MHV-68 LANA proteins bind LBS DNA using strikingly diffe

49 nhibition varied among tested cell lines and MHV S proteins, suggesting a role for metalloprotease us

50 e processes in expression of VSV protein and MHV-68 immediate-early genes.

51 orous MHV-1-specific CD8 T cell response, as MHV-1 infection of C3.SW-H2(b)/SnJ mice, which mount an

52 ty against HCV but not other viruses such as MHV-68.

53 In contrast, substitution of alanine at MHV nsp14 D330 did not affect viral replication, sensiti

54 bacterial artificial chromosome (BAC)-based MHV reverse genetics system.

55 l, these results indicate that the BAC-based MHV reverse genetics system will be useful for studies o

56 ceptible C3H/HeJ mice mount robust and broad MHV-1-specific CD4 T cell responses, whereas in resistan

57 owed that induction of TNF-alpha and IL-6 by MHV-A59 infection was mediated through activation of the

58 te gene core promoters could be activated by MHV-68 lytic replication, indicating that the mechanisms

59 tially blocked NF-kappaB activity induced by MHV infection and inhibition of NF-kappaB activity by a

60 sequent IFN-alpha/beta production induced by MHV infection.

61 acid-inducible gene I (RIG-I) was induced by MHV infection.

62 critical role in IFN-alpha/beta induction by MHV infection in oligodendrocytes.

63 ctivities that are specifically inhibited by MHV, and possibly by other coronaviruses, remain to be i

64 sponsive promoter was partially inhibited by MHV; however, IRF-3 was transported to the nucleus and b

65 We used a chimeric MHV system (MHV(Mut)) in which exogenous PDEs were expre

66 In the context of recombinant chimeric MHV expressing inactive ns2, VP3-CTD restored the abilit

67 -producing CD8(+) T cells arising in chronic MHV-68 infection in the absence of CD4(+) T cell help be

68 Our results demonstrate that the conserved MHV N7-MTase SAM-binding-site residues are not required

69 - or B cell-deficient mice failed to contain MHV CNS infection and developed progressive demyelinatin

70 or novel protein specificity in contemporary MHV.

71 ling is critically important for controlling MHV-induced pathology and regulation of the immune respo

72 s (UTRs) of the mouse hepatitis coronavirus (MHV) and bovine coronavirus (BCoV), separate species in

73 t 3' UTR in the mouse hepatitis coronavirus (MHV) for virus replication, thus demonstrating common 3'

74 irus (BCoV) and mouse hepatitis coronavirus (MHV) recognize sugar and protein receptors, respectively

75 Mouse hepatitis coronavirus (MHV) uses the N-terminal domain (NTD) of its spike prote

76 e previously showed that murine coronavirus (MHV) accessory protein ns2, a 2H phosphoesterase superfa

77 However, TMPRSS2 overexpression decreased MHV structural protein expression, release of infectious

78 A similarly defective MHV N mutant bearing an insertion of the SR region from

79 completely protected following a lethal-dose MHV-1 challenge despite mounting only a modest secondary

80 Thus, RNase L activation during MHV infection is cell type specific and correlates with

81 ather than direct antiviral mediator, during MHV-induced encephalitis.

82 Ag-specific CD4(+) T cell populations during MHV-68 infection.

83 tically active ns2 is required for efficient MHV replication in macrophages, as well as for the induc

84 with the CS3 p4-p1 amino acids in engineered MHV mutants switches specificity from PLP1 to PLP2 at CS

85 -3.6%) and 18.2% (+/-9.5%) for the enveloped MHV and varphi6, respectively, and mean recoveries of 55

86 macrophages and mouse embryonic fibroblasts, MHV replication was significantly reduced by the IFN-alp

87 Despite its galectin fold, MHV NTD does not bind sugars, but instead binds mCEACAM1

88 ell types producing IFN-alpha/beta following MHV CNS infection.

89 e) experienced more severe disease following MHV infection, with reduced survival, increased spread o

90 For MHV, this domain has now been shown to promote multiple

91 ion of novel CD4 and CD8 T cell epitopes for MHV-1 permitted high-resolution analyses of pulmonary T

92 Surprisingly, the PS was not essential for MHV viability, nor did its elimination have a severe eff

93 infected in vivo, the canonical receptor for MHV, the carcinoembryonic antigen family member CEACAM1a

94 The PDE activity of ns2 is required for MHV replication in macrophages and for hepatitis.

95 M-binding-site residues are not required for MHV viability and suggest that the determinants of CoV N

96 n this region is the absence of gene 5a from MHV-S.

97 mediated Western blot detection of nsp6 from MHV-infected cells.

98 sential role in the assembly of a functional MHV replication-transcription complex.

99 t 2 h after infection than for the fusogenic MHVs.

100 tency in vivo using murine gammaherpesvirus (MHV-68) infection.

101 n be modeled using murine gamma-herpesvirus (MHV)-68 in mice lacking CD4(+) T cells.

102 transported to the nucleus and bound DNA in MHV-infected cells superinfected with SeV.

103 investigation of the role of nsp3 domains in MHV viral replication.

104 ave identified novel CD4 and CD8 epitopes in MHV-1-infected susceptible and resistant strains of mice

105 uses, but evolved new structural features in MHV for mCEACAM1a binding.

106 galectin (galactose-binding lectin) fold in MHV NTD.

107 ion defines a major RNA binding interface in MHV with site-directed spin labeling studies consistent

108 E able to functionally substitute for ns2 in MHV infection.

109 ated the role of the nucleocapsid protein in MHV-induced disease.

110 ein production were significantly reduced in MHV-infected Ifit2(-/-) relative to wt bone marrow-deriv

111 between the 5' UTR and Nsp1 coding region in MHV-like and BCoV-like betacoronaviruses that is cis act

112 sponse plays an important protective role in MHV-1-infected resistant B6 mice and that both CD4 and C

113 psid proteins, which play important roles in MHV pathogenicity in mice, are not responsible for the d

114 s showed that U48C and U48A substitutions in MHV SL2 were lethal, while a U48G substitution was viabl

115 al for efficient subgenomic RNA synthesis in MHV.

116 s, the number of double-membrane vesicles in MHV-Brts31-infected cells is reduced at the nonpermissiv

117 onor liver plasticity and (b) individualized MHV management for both donors and recipients based on f

118 he parental wild-type recombinant virus, inf-MHV-A59.

119 On the other hand, exogenous BMP2 inhibits MHV-68 lytic growth but did not affect VSV growth.

120 Interestingly, MHV has a cell-type-dependent ability to resist the anti

121 dity and lung pathology following intranasal MHV-1 infection of susceptible C3H/HeJ and A/J mice.

122 frequencies of spleen cells harboring latent MHV-68 genomes were the same in both miR-155-deficient a

123 Results showed that Penn-98-1 behaved like MHV-2, thus establishing a role for the spike protein in

124 reported that murine gammaherpesvirus-68 (M1-MHV-68) induces pulmonary artery (PA) neointimal lesions

125 ivity occurs in S100A4 mice, 7 days after M1-MHV-68, unrelated to inflammation or viral load and befo

126 A particular strain of MHV, MHV-S, exhibited orders-of-magnitude higher sensitivity

127 induced by the dual hepato- and neurotropic MHV-A59.

128 enhanced entry, of the highly neurovirulent MHV strain JHM.SD relative to their effects on the refer

129 antly more genomic RNAs for the nonfusogenic MHVs were detected in the endoplasmic reticulum (ER) wit

130 congestion volumes of risky versus nonrisky MHV types (49%+/-6% and 34%+/-7% vs. 29%+/-8% and 33%+/-

131 Here, we show that replacing the 209-nt MHV 5' UTR with the approximately 63%-sequence-identical

132 A maximum of 3.7% of MHV and 2% of MS2 could be recovered from the solids.

133 The ability of MHV to delay SeV-mediated ISG production may partially i

134 These data imply that the ability of MHV to replicate in macrophages is a prerequisite for re

135 Sequence analysis of MHV-Brts31 RNA indicated that a single G-to-A transition

136 which enables effective long-term control of MHV-68.

137 m to maintain effective long-term control of MHV-68.

138 inding domains as a principal determinant of MHV packaging signal recognition.

139 We initiated a dissection of MHV nsp3 aimed at identifying those activities or struct

140 tructure of three tandemly linked domains of MHV nsp3, including the papain-like protease 2 (PLP2) ca

141 sufficient for mediating the enhancement of MHV-68 lytic replication by Tpl2.

142 dues 198 to 230) binds to the acidic face of MHV nsp3a containing the acidic alpha2 helix with an aff

143 Furthermore, the hepatotropism of MHV-JHM depends not on the spike protein and viral entry

144 nd substantially our structural knowledge of MHV nsp3, providing a platform for further investigation

145 se studies reveal that the SR-rich linker of MHV N is necessary but not sufficient to maintain this h

146 tly increased on CD8 T cells in the lungs of MHV-68-infected CII(-/-), CD40(-/-), or CD80/86(-/-) mic

147 A computationally derived model of MHV PLP2 bound to ubiquitin was generated, and the poten

148 replication in myeloid cells, as a mutant of MHV (ns2(H126R)) encoding an inactive PDE fails to antag

149 Creation of a gene 5a knockout mutant of MHV-A59 demonstrated that a major component of IFN resis

150 nstructed BCoV chimeras and other mutants of MHV nsp3 and obtained complementary genetic evidence for

151 In addition, mutation of MHV nonstructural protein 2 (ns2) abrogates the ability

152 emonstrated that the genetic organization of MHV-1 was similar to that of other strains of MHV.

153 to investigate the genotype and phenotype of MHV quasispecies selected for resistance to a broad-spec

154 fect of altering the Ubl adjacent to PLP2 of MHV on enzyme activity, viral replication, and pathogene

155 9/S(MHV-1)) increased the pneumovirulence of MHV-A59, and mice infected with this recombinant virus d

156 ranial inoculation, efficient replication of MHV in the brain is not dependent on an enzymatically ac

157 enzymatically active, rescue replication of MHV(Mut) in bone marrow-derived macrophages, and inhibit

158 he basis for the enhanced IFN sensitivity of MHV-S was found to map entirely to the region downstream

159 that MDA5 signaling reduces the severity of MHV-induced disease, at least in part by reducing the in

160 ddition to the organization and stability of MHV-induced double-membrane vesicles.

161 proteolipid protein at the chronic stage of MHV-A59 infection.

162 d the catalytic residue in the JHM strain of MHV (JHMV), which causes acute and chronic encephalomyel

163 s demonstrate that a demyelinating strain of MHV causes concomitant axonal loss and macrophage-mediat

164 A particular strain of MHV, MHV-S, exhibited orders-of-magnitude higher sensiti

165 However, in vitro, most strains of MHV are largely resistant to the action of this cytokine

166 HV-1 was similar to that of other strains of MHV.

167 recently determined the crystal structure of MHV NTD complexed with its protein receptor murine carci

168 Here we present the crystal structure of MHV NTD complexed with its receptor murine carcinoembryo

169 g the mild encephalitis and 100% survival of MHV-A59-infected wild-type (wt) mice, nearly 60% of infe

170 -TRS determinants are distinct from those of MHV NTD, rapid helix destabilization activity of CoV N N

171 type and complementation profile as those of MHV-Brts31.

172 ow in this article that adoptive transfer of MHV-68-specific CD8(+) T cells was ineffective at reduci

173 Therefore, our results on MHV-68 establish a solid foundation for mechanistic stud

174 Despite the numerous functional studies on MHV and its nsp3 domain, the structure of only one domai

175 n IFN-treated cells infected with MHV-A59 or MHV-S.

176 Lys194, a residue conserved among all other MHV strains.

177 roperties and the potential of a recombinant MHV-68 (AC-RTA) in which the genes required for persiste

178 Previous analysis of chimeric recombinant MHVs in which the spike gene, encoding the protein that

179 ionally, PDEs encoded by OC43 and BEV rescue MHV(Mut) replication and restore pathogenesis in wild-ty

180 o those observed with MHV-1, although rA59/S(MHV-1) was significantly less virulent.

181 S gene within the MHV-A59 background (rA59/S(MHV-1)) increased the pneumovirulence of MHV-A59, and mi

182 increased pneumovirulence relative to rA59/S(MHV-1), but were still much less virulent than MHV-1.

183 hile the highly neurovirulent strain JHM.SD (MHV-4) causes fatal encephalitis with extensive neuronal

184 her sensitivity to IFN than prototype strain MHV-A59.

185 s virus (MHV) neurotropism varies by strain: MHV-A59 causes mild encephalomyelitis and demyelination,

186 We used a chimeric MHV system (MHV(Mut)) in which exogenous PDEs were expressed from an

187 owed that, at the nonpermissive temperature, MHV-Brtsc31 was not able to proteolytically process eith

188 V-1), but were still much less virulent than MHV-1.

189 using isothermal titration calorimetry, that MHV N219, an N construct that extends into the SR-rich l

190 ction fluorescence microscopy confirmed that MHV-A59 used microtubules (MTs) as a conduit to reach th

191 These results demonstrate that MHV is recognized by both RIG-I and MDA5 and induces IFN

192 We present evidence that MHV infection can delay interferon-stimulated gene (ISG)

193 -bet and produced IFN-gamma, indicating that MHV-68 infection triggered differentiation of CD4(+) T c

194 We show that MHV infection activated both transcription factors, the

195 We showed that MHV and varphi6 remained infective on the time scale of

196 the action of this cytokine, suggesting that MHV encodes one or more functions that antagonize or eva

197 This observation suggests that MHV must inhibit an alternative IFN-induced pathway that

198 The MHV accessory protein, ns2, antagonizes the type I inter

199 The MHV PS is an RNA structure that maps to the region of th

200 elect chimeric viruses containing either the MHV-1 S gene or genes encoding all of the MHV-1 structur

201 results suggest that the proposed SL4 in the MHV 5'UTR functions in part as a spacer element that ori

202 between these two BCoV regions, which in the MHV genome act in a fully interspecies-compliant manner.

203 gly, the 30-nt inter-stem-loop domain in the MHV genome can be deleted and viral progeny, although de

204 e genetics to replace its counterpart in the MHV genome.

205 s tested by replacing its counterpart in the MHV genome.

206 These results identify a new cistron in the MHV replicase gene locus and show that nsp3 has an essen

207 grammed death-1 but were not enriched in the MHV-68-specific compartment, nor were they uniformly CD4

208 model structure and then engineered into the MHV genome with [nsp14-ExoN(+)] or without [nsp14-ExoN(-

209 in, we expressed a series of segments of the MHV N protein as fusions with green fluorescent protein

210 To explore other domain interactions of the MHV N protein, we expressed a series of segments of the

211 NMR studies of the MHV NTD.TRS complex revealed that this region defines a

212 tand the role and mechanism of action of the MHV PS in its native genomic locus, we constructed viral

213 Sequencing of the 3' one-third of the MHV-1 genome demonstrated that the genetic organization

214 are contained within the 3' one-third of the MHV-1 genome, but additional important virulence factors

215 in mice demonstrated that expression of the MHV-1 S gene within the MHV-A59 background (rA59/S(MHV-1

216 Chimeras containing all of the MHV-1 structural genes on an MHV-A59 background were abl

217 he MHV-1 S gene or genes encoding all of the MHV-1 structural proteins, on an MHV-A59 background.

218 mouse hepatitis virus (MHV), we replaced the MHV N gene with its counterpart from the closely related

219 firmed previous work that suggested that the MHV-1 HE is a pseudogene.

220 fines a new complementation group within the MHV replicase gene locus.

221 at expression of the MHV-1 S gene within the MHV-A59 background (rA59/S(MHV-1)) increased the pneumov

222 to provide a distinct selective advantage to MHV.

223 ral and nonstructural proteins contribute to MHV liver pathogenesis and support previous reports that

224 Exposure to MHV-68 causes a persistent infection, along with infecti

225 by treating them with immune serum prior to MHV-1 infection.

226 nd mortality during subsequent reexposure to MHV-1.

227 s observed for R80A/E82A-ExoN(-) relative to MHV-ExoN(-), indicating that the decreased-fidelity phen

228 susceptible to VSV infection but less so to MHV-68 infection.

229 3H/HeJ mice, which are highly susceptible to MHV-1-induced disease, we demonstrate that both CD4 and

230 to stimulate the infectivity of transfected MHV genomic RNA (gRNA).

231 ant of Murine hepatitis virus, Bristol ts31 (MHV-Brts31), that defines a new complementation group wi

232 produce a recombinant virus, Bristol tsc31 (MHV-Brtsc31), which has the same RNA-negative ts phenoty

233 ed the viral protein production by wild-type MHV but not by vLC.

234 The replication of wild-type MHV strain A59 (A59) and a mutant with an inactive phosp

235 N activity are more sensitive than wild-type MHV to restriction by exogenous IFN-beta and that viruse

236 Unexpectedly, MHV NTD contains a core structure that has the same beta

237 In this study, we use MHV infection of the liver as a model to demonstrate tha

238 regnant women with a mechanical heart valve (MHV) are at a heightened risk of a thrombotic event, and

239 heart valve exist: mechanical heart valves (MHV), which are implanted surgically, and bioprosthetic

240 lized management of the middle hepatic vein (MHV).

241 r by the elaboration of a broad and vigorous MHV-1-specific CD8 T cell response, as MHV-1 infection o

242 , and a DNA virus, murine gammaherpes virus (MHV-68).

243 40 nucleotides of the mouse hepatitis virus (MHV) 5' untranslated region (5'UTR) are predicted to con

244 lease activity of the mouse hepatitis virus (MHV) A59 Nsp15 was also increased by pRb in vitro, and a

245 he murine coronavirus mouse hepatitis virus (MHV) activates the pattern recognition receptors melanom

246 enus Betacoronavirus, mouse hepatitis virus (MHV) and MERS-CoV, encode 2',5'-phosphodiesterases (2',5

247 ll, our data suggest murine hepatitis virus (MHV) ExoN activity is required for resistance to the inn

248 Murine hepatitis virus (MHV) has long served as a model system for the study of

249 he murine coronavirus mouse hepatitis virus (MHV) have distinct, S-dependent organ and tissue tropism

250 ave demonstrated that mouse hepatitis virus (MHV) hepatotropism is determined largely by postentry ev

251 the model coronavirus mouse hepatitis virus (MHV) in which all or part of the M protein was replaced

252 defective mutant of murine hepatitis virus (MHV) in which the N gene was replaced with that of its c

253 he murine coronavirus mouse hepatitis virus (MHV) induced the expression of type I interferon (alpha/

254 Thus, during mouse hepatitis virus (MHV) infection, hepatitis, which damages the parenchyma,

255 prototype coronavirus mouse hepatitis virus (MHV) is carried out by a replicase-transcriptase compose

256 Mouse hepatitis virus (MHV) isolates JHM.WU and JHM.SD promote severe central n

257 ific ISGs against the mouse hepatitis virus (MHV) members of the coronaviruses are largely unknown.

258 Mouse hepatitis virus (MHV) neurotropism varies by strain: MHV-A59 causes mild

259 he murine coronavirus mouse hepatitis virus (MHV) nonstructural protein 2 (ns2) is a 2',5'-phosphodie

260 We modeled the CoV murine hepatitis virus (MHV) nsp12-RdRp structure and superimposed it on solved

261 ineered mutations in murine hepatitis virus (MHV) nsp14 N7-MTase at residues D330 and G332 and determ

262 ce (NMR) structure of mouse hepatitis virus (MHV) nsp3a and show, using isothermal titration calorime

263 ly that mutations in murine hepatitis virus (MHV) nsp4 loop 1 that alter nsp4 glycosylation are assoc

264 tagenesis of the CoV murine hepatitis virus (MHV) nsp5, we identified a new temperature-sensitive (ts

265 Murine hepatitis virus (MHV) PLP2 and orthologs recognize and cleave at a positi

266 n of the CNS with the mouse hepatitis virus (MHV) provides a unique model situation in which the exte

267 The Murine hepatitis virus (MHV) strain A59 ns2 protein is a 30-kDa nonstructural pr

268 gene point mutants of mouse hepatitis virus (MHV) that were defective in growth and assembled virions

269 ) for the coronavirus mouse hepatitis virus (MHV) was originally identified as an element that confer

270 a/beta) receptor with mouse hepatitis virus (MHV), a murine coronavirus.

271 e rJHM strain (rJ) of mouse hepatitis virus (MHV), a neurotropic coronavirus that causes acute enceph

272 ical Betacoronavirus, mouse hepatitis virus (MHV), and by Middle East respiratory syndrome-associated

273 e murine coronavirus, mouse hepatitis virus (MHV), causes acute hepatitis in its natural host and pro

274 In mouse hepatitis virus (MHV), the NTD binds the transcriptional regulatory seque

275 he model coronavirus, mouse hepatitis virus (MHV), to investigate the genotype and phenotype of MHV q

276 the model coronavirus mouse hepatitis virus (MHV), we constructed mutants in which each RNA-binding d

277 ns in the coronavirus mouse hepatitis virus (MHV), we replaced the MHV N gene with its counterpart fr

278 ion is altered due to mouse hepatitis virus (MHV)-A59 infection both in vivo and in vitro; however, i

279 on by the coronavirus mouse hepatitis virus (MHV).

280 avirus (SARS-CoV) and mouse hepatitis virus (MHV).

281 , and the murine CoV, mouse hepatitis virus (MHV).

282 navirus model system, mouse hepatitis virus (MHV).

283 s into the genome of murine hepatitis virus (MHV-A59) containing ExoN activity [ExoN(+)] at positions

284 g murine coronavirus (mouse hepatitis virus [MHV]) infection of myeloid cells correlates with high ba

285 Murine coronavirus (mouse hepatitis virus [MHV]) nonstructural protein 2 (ns2) is a 2',5'-phosphodi

286 infection with a recombinant -herpes virus, MHV-68, engineered to express SIINFEKL peptide, the liga

287 ing behavior of two model enveloped viruses (MHV and varphi6) and two nonenveloped bacteriophages (MS

288 iated by both SeV and IFN-beta but only when MHV infection precedes SeV or IFN-beta exposure.

289 s, we explored potential mechanisms by which MHV-A59 infection alters Cx43 localization and examined

290 n why BCoV NTD does not bind CEACAM1 and why MHV NTD does not bind sugar.

291 Indeed, CD4-depleted mice infected with MHV-68 express increased levels of IL-10, a cytokine cap

292 activated in IFN-treated cells infected with MHV-A59 or MHV-S.

293 ion to the nucleus in cultures infected with MHV.

294 iral late gene promoters upon infection with MHV-68.

295 ceacam1a knockout mice were inoculated with MHV to determine the extent to which CEACAM1a-independen

296 syndrome (SARS)-like pathology observed with MHV-1 and reproducibly increased pneumovirulence relativ

297 ons that were similar to those observed with MHV-1, although rA59/S(MHV-1) was significantly less vir

298 en, or inhibition by IFN-beta compared to WT MHV.

299 II, III, and IV, yielded near-wild-type (wt) MHV phenotypes when used by reverse genetics to replace

300 each immediately enabled near-wild-type (wt) MHV-like progeny, thus behaving similarly to comparable

301 eased peak titers relative to wild-type (WT) MHV.