ライフサイエンスコーパス: MHV

1 MHV infection in mice provides an efficient cause-effect

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

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

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

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

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

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

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

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

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

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

12 Murine gammaherpesvirus-68 (MHV-68) intraperitoneal infection is a gammaherpesvirus

13 Murine gammaHV-68 (MHV-68) is an important tool for understanding immune fa

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

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

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

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

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

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

20 Antibiotic suppression markedly accelerated MHV-68 pathology causing pulmonary consolidation and hem

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

22 disease severity and improved survival after MHV-68 infection.

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

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

25 16 (bCEA), which encode proposed alternative MHV receptors, revealed low ceacam2 expression in microg

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

27 5 was also increased by pRb in vitro, and an MHV with mutations in the LXCXE/D-motif, named vLC, exhi

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

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

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

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

32 dramatically decrease the replication of an MHV that is sensitive to PARP activity.

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

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

46 e performed at our Transplant Institute, and MHV tributaries of the 640 right lobe liver grafts were

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 ansition mutations across the genome in both MHV and MERS-CoV.

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

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

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

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

61 gly, inoculation with the RSA59 (P)-carrying MHV significantly reduced demyelination at the chronic s

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

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

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

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

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

67 or novel protein specificity in contemporary MHV.

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

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

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

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

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

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

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

75 Using this proline-deleted MHV strain, here we investigated whether intracranial in

76 proline residue in the FP of a demyelinating MHV strain, we found that two central, consecutive proli

77 d in the FP of the recombinant demyelinating MHV strain plays a crucial role in translocation of the

78 7 reduced pulmonary pathology and detectable MHV-68 with increased CD3 and CD8 cells.

79 We determined MHV-68-specific CD8 T cells in latently infected mice us

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

81 TiPARP functions in a proviral manner during MHV infection.

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

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

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

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

86 To test this hypothesis, we engineered MHV-ExoN-AA with 1, 2, or 3 nucleotide mutations along g

87 -3.6%) and 18.2% (+/-9.5%) for the enveloped MHV and varphi6, respectively, and mean recoveries of 55

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

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

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

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

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

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

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

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

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

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

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

99 es an immunodominant CD8 T cell epitope from MHV-68.

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 , and the presence of communicating veins if MHV resection is necessary.

103 virulence in vivo Despite these impairments, MHV- and SARS-CoV ExoN motif I AA mutants (ExoN-AA) have

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

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

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

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

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

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

110 investigate the gut bacterial microbiome in MHV-68 infection.

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

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

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

114 ve demonstrated that the spike has a role in MHV pathogenesis and retrograde axonal transport.

115 FPs) in the spike protein play a key role in MHV pathogenesis.

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

117 al for efficient subgenomic RNA synthesis in MHV.

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

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

120 NHC inhibited MHV lacking ExoN proofreading activity similarly to wild

121 NHC inhibited MHV only when added early during infection, decreased vi

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

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

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

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

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

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

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

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

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

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

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

135 r studies define a structural determinant of MHV entry in the brain parenchyma important for altered

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 9/S(MHV-1)) increased the pneumovirulence of MHV-A59, and mice infected with this recombinant virus d

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

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

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

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

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

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

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

159 yed RSA59 (an isogenic recombinant strain of MHV-A59)-induced experimental neuroinflammation model to

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

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

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

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

164 n or competitive fitness compared to that of MHV-ExoN-AA.

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

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

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

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

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

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

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

172 ast, a low-passage-number (passage 10 [P10]) MHV-ExoN-AA showed increased replication and competitive

173 bserved that the proline-deleted recombinant MHV strain is restricted to the optic nerve, is unable t

174 Studies with recombinant MHV strains that differ in the gene encoding the spike p

175 Reconstructed MHV tributaries were removed due to AVG infection in 25

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

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

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

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

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

181 O1) drives AhR activation in other settings, MHV infection induced equal expression of downstream gen

182 ronavirus (mouse hepatitis virus A59 strain [MHV-A59]) developed severe encephalomyelitis with hind-l

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

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

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

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

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

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

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

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

191 We also show that MHV replication induced the expression of other genes kn

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

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

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

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

196 The MHV was resected in 6 patients, always sparing segments

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

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

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

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

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

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

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

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

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

206 Our previous crystal structure study of the MHV NTD/mCEACAM1a complex (G.

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

208 tein are triggered.IMPORTANCE Binding of the MHV S protein to the receptor mCEACAM1a triggers conform

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

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

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

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

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

214 to provide a distinct selective advantage to MHV.

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

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

217 s study, we identify multiple impediments to MHV-ExoN-AA reversion.

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

219 or modulation of the host immune response to MHV and plays a role in the expression of TiPARP, which

220 e for AhR activation in the host response to MHV infection.

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

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

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

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

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

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

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

228 Using MHV reverse genetics, we generated a series of mutant vi

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

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

231 tumor, with or without middle hepatic vein (MHV) invasion.

232 d for reconstruction of middle hepatic vein (MHV) tributaries in living donor liver transplantation (

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

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

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

236 at NHC inhibits both murine hepatitis virus (MHV) (50% effective concentration [EC(50)] = 0.17 muM) a

237 40 nucleotides of the mouse hepatitis virus (MHV) 5' untranslated region (5'UTR) are predicted to con

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

239 he murine coronavirus mouse hepatitis virus (MHV) activated the NLRP3 inflammasome and inflammatory c

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

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

242 de substitutions) in murine hepatitis virus (MHV) and severe acute respiratory syndrome (SARS)-CoV yi

243 strain RSA59 (PP) of mouse hepatitis virus (MHV) contains two central, consecutive prolines in the F

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

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

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

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

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

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

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

251 Mouse hepatitis virus (MHV) is a murine betacoronavirus (m-CoV) that causes a w

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

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

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

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

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

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

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

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

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

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

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

263 Mouse hepatitis virus (MHV) uses its N-terminal domain (NTD) of the viral spike

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

265 n cells infected with mouse hepatitis virus (MHV), a coronavirus (CoV), and contributes to the upregu

266 owing infection with murine hepatitis virus (MHV), a model coronavirus.

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

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

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

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

271 ototypic coronavirus, mouse hepatitis virus (MHV), resulting in the expression of several effector ge

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

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

274 sis of a ts strain of mouse hepatitis virus (MHV), tsNC11, focusing on the role of mutations in the m

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

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

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

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

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

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

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

282 Mouse hepatitis virus (MHV; murine coronavirus) causes meningoencephalitis, mye

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

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

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

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

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

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

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

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

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

292 We further demonstrate that infection with MHV induces a severe attack on host cell NAD(+) and NADP

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

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

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

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

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

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

299 reading activity similarly to wild-type (WT) MHV, suggesting an ability to evade or overcome ExoN act

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.