ライフサイエンスコーパス: SARS-CoV

1 SARS-CoV caused a worldwide epidemic infecting more than

2 SARS-CoV encodes several proteins that modulate innate i

3 SARS-CoV is a pathogenic coronavirus that emerged from a

4 SARS-CoV nsp12, the canonical RNA-dependent RNA polymera

5 SARS-CoV-specific memory CD8 T cells persisted for up to

6 The 2003 SARS-CoV outbreak began in Guangdong Province in China a

7 se from cells; however, we also identified a SARS-CoV protein that inhibits BST-2 function.

8 le nAbs or dual nAb combinations to target a SARS-CoV RBD epitope that shows plasticity may have limi

9 Previously, we demonstrated that a SARS-CoV lacking the E protein was attenuated in vivo.

10 A mouse model of acute SARS-CoV infection has been helpful in understanding the

11 nfected C57BL/6 (B6) mice with mouse-adapted SARS-CoV (MA15) or IAV (PR8), both of which cause severe

12 While SARS-CoV, mouse-adapted SARS-CoV (MA15), and chimeric SARS-CoVs bearing the spik

13 gainst challenge with virulent mouse-adapted SARS-CoV (MA15).

14 ce infected with a recombinant mouse-adapted SARS-CoV (rMA15) to better understand the contribution o

15 A mouse-adapted SARS-CoV (SARS-CoV-MA15) lacking the envelope (E) protei

16 of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone.

17 tional, independently isolated mouse-adapted SARS-CoVs.

18 to protection from severe lung disease after SARS-CoV infection.

19 ry CD8 T cells in mediating protection after SARS-CoV challenge has not been previously investigated.

20 D8 T cells persisted for up to 6 years after SARS-CoV infection, a time at which memory B cells and a

21 nhibitors exhibit antiviral activity against SARS-CoV infected Vero E6 cells and broadened specificit

22 ro inhibition and antiviral activity against SARS-CoV infected Vero E6 cells.

23 MERS-CoV (NA 01) and human antiserum against SARS-CoV, human CoV NL63, and human CoV OC43.

24 development into a potent antiviral against SARS-CoV and Ebola, Hendra, and Nipah viruses.

25 for possible therapeutic development against SARS-CoV.

26 een identified as protective factors against SARS-CoV disease, including STAT1 and MyD88.

27 l to become a new antiviral strategy against SARS-CoV infections.

28 nificantly greater neutralizing antibody and SARS-CoV-specific CD4 and CD8 T cell responses.

29 te kinetic analyses of purified MERS-CoV and SARS-CoV PLpros uncovered significant differences in the

30 for the convergent evolution of NL63-CoV and SARS-CoV.

31 Conversely, HKU4, HKU5, and SARS-CoV 3CL(pro) enzymes are tightly associated dimers.

32 tion revealed a progressive increase in anti-SARS-CoV antibodies in lung and serum that did not corre

33 However, the anti-SARS-CoV antibody response is short-lived in patients wh

34 Coronaviruses such as SARS-CoV and Middle East respiratory syndrome-associated

35 including severe respiratory viruses such as SARS-CoV.

36 The association SARS-CoV with aberrant cytokine, chemokine, and Interfer

37 of utilizing this pathway to both attenuate SARS-CoV infection and develop novel therapeutic treatme

38 scape from neutralization usually attenuates SARS-CoV infection.

39 of both SARS S-pseudotyped HIV and authentic SARS-CoV.

40 cantly dysregulated genes are common between SARS-CoV and MERS-CoV, including NFKBIA that is a key re

41 inhibitor of human cathepsin L that blocked SARS-CoV and Ebola pseudotype virus entry in human cells

42 st three independent strategies for blocking SARS-CoV entry, validates these mechanisms of inhibition

43 Both SARS-CoV and MERS-CoV are zoonotic infections, with bats

44 ate, demonstrating activity in blocking both SARS-CoV (IC(50) = 273 +/- 49 nM) and Ebola virus (IC(50

45 icancer drug imatinib, as inhibitors of both SARS-CoV and MERS-CoV in vitro Here we show that the ant

46 protein-ligand X-ray structure of 15 g-bound SARS-CoV PLpro and a corresponding model of 15 h docked

47 ed mechanisms of host receptor adaptation by SARS-CoV but also provide a molecular and structural bas

48 his study, we show that a protein encoded by SARS-CoV designated as open reading frame-9b (ORF-9b) lo

49 D regulate the ion-conducting pore formed by SARS-CoV E in artificial bilayers and the pathogenicity

50 mutations decreasing the tunnel space or by SARS-CoV mutations increasing the tunnel space.

51 s specific for a conserved epitope shared by SARS-CoV and MERS-CoV is a potential strategy for develo

52 RBD inhibits hACE2-dependent transduction by SARS-CoV spike protein, a successful application of the

53 mouse-adapted SARS-CoV (MA15), and chimeric SARS-CoVs bearing the spike genes of early human strains

54 re are still unanswered questions concerning SARS-CoV pathogenesis.

55 ged individuals at high risk for contracting SARS-CoV or IAV infections.

56 ry syndrome (SARS), caused by a coronavirus (SARS-CoV).

57 respiratory syndrome-associated coronavirus (SARS-CoV) and Middle East respiratory syndrome-associate

58 (HIV-1) and the SARS-associated Coronavirus (SARS-CoV) employ programmed -1 ribosomal frameshifting (

59 respiratory syndrome-associated coronavirus (SARS-CoV) epidemic was controlled by nonvaccine measures

60 The disease caused by a novel coronavirus (SARS-CoV) rapidly spread worldwide, causing more than 80

61 ly showed that recombinant SARS coronavirus (SARS-CoV) (Urbani strain based) lacking envelope (E) pro

62 disease that is caused by SARS coronavirus (SARS-CoV) and for which there are currently no approved

63 SARS coronavirus (SARS-CoV) causes severe acute respiratory tract disease

64 (around 50% vs. 10%) than SARS coronavirus (SARS-CoV) infection.

65 es have suggested that the SARS coronavirus (SARS-CoV) originated from animals.

66 coronavirus (NL63-CoV) and SARS coronavirus (SARS-CoV) receptor-binding domains (RBDs), each complexe

67 vere acute respiratory syndrome coronavirus (SARS-CoV) 3CL(pro), (R)-16, to have inhibitor activity a

68 vere acute respiratory syndrome coronavirus (SARS-CoV) 3Cpro and revealed a greater flexibility in it

69 vere acute respiratory syndrome coronavirus (SARS-CoV) accessory protein 6 (p6) is a 63-amino-acid mu

70 vere acute respiratory syndrome coronavirus (SARS-CoV) and Ebola, Hendra, and Nipah viruses are membe

71 vere acute respiratory syndrome coronavirus (SARS-CoV) and its orthologs in the alpha and beta corona

72 vere acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome (MERS)-Co

73 vere acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavir

74 vere acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavir

75 vere acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavir

76 vere acute respiratory syndrome coronavirus (SARS-CoV) and mouse hepatitis virus (MHV).

77 vere acute respiratory syndrome coronavirus (SARS-CoV) and reemerging influenza virus cause dispropor

78 vere acute respiratory syndrome coronavirus (SARS-CoV) and the NL63 coronaviruses are human respirato

79 vere acute respiratory syndrome coronavirus (SARS-CoV) caused an acute human respiratory illness with

80 vere acute respiratory syndrome coronavirus (SARS-CoV) causes a respiratory disease with a mortality

81 vere acute respiratory syndrome coronavirus (SARS-CoV) causes acute lung injury (ALI) that often lead

82 vere acute respiratory syndrome coronavirus (SARS-CoV) causes lethal disease in humans, which is char

83 vere acute respiratory syndrome coronavirus (SARS-CoV) causes severe respiratory distress in infected

84 vere acute respiratory syndrome coronavirus (SARS-CoV) emerged from zoonotic sources in 2002 and caus

85 vere acute respiratory syndrome coronavirus (SARS-CoV) emerged in 2003 in Southeast Asia and rapidly

86 vere acute respiratory syndrome coronavirus (SARS-CoV) epidemic, no patients under 24 years of age di

87 vere acute respiratory syndrome coronavirus (SARS-CoV) from palm civets has twice evolved the capacit

88 vere acute respiratory syndrome coronavirus (SARS-CoV) has developed strategies to inhibit host immun

89 vere acute respiratory syndrome coronavirus (SARS-CoV) in 2002 and Middle East respiratory syndrome c

90 vere acute respiratory syndrome coronavirus (SARS-CoV) in 2002 and, more recently, Middle Eastern res

91 vere acute respiratory syndrome coronavirus (SARS-CoV) in genomic sequence than others previously rep

92 vere acute respiratory syndrome coronavirus (SARS-CoV) infection can cause the development of severe

93 vere acute respiratory syndrome coronavirus (SARS-CoV) infection is limited, and little is known abou

94 vere acute respiratory syndrome coronavirus (SARS-CoV) is a highly pathogenic respiratory virus that

95 vere acute respiratory syndrome coronavirus (SARS-CoV) is a major target of protective immunity in vi

96 vere acute respiratory syndrome coronavirus (SARS-CoV) is an important emerging virus that is highly

97 vere acute respiratory syndrome Coronavirus (SARS-CoV) is composed of 16 non-structural proteins (nsp

98 vere acute respiratory syndrome coronavirus (SARS-CoV) PLpro, revealing prominent differences between

99 vere acute respiratory syndrome coronavirus (SARS-CoV) to modulate the host immune response mediated

100 vere acute respiratory syndrome coronavirus (SARS-CoV) to what has recently been found for MERS-CoV,

101 vere acute respiratory syndrome coronavirus (SARS-CoV) which causes acute respiratory and gastrointes

102 vere acute respiratory syndrome coronavirus (SARS-CoV), a biosafety level 3 (BSL-3) pathogen.

103 vere acute respiratory syndrome coronavirus (SARS-CoV), establish host shutoff via their nonstructura

104 vere acute respiratory syndrome coronavirus (SARS-CoV), it has been shown that virus entry requires t

105 vere acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus

106 vere acute respiratory syndrome coronavirus (SARS-CoV)-neutralizing antibody 80R with equilibrium dis

107 vere acute respiratory syndrome coronavirus (SARS-CoV).

108 vere acute respiratory syndrome coronavirus (SARS-CoV).

109 vere acute respiratory syndrome coronavirus (SARS-CoV).

110 vere acute respiratory syndrome coronavirus (SARS-CoV).

111 vere acute respiratory syndrome coronavirus (SARS-CoV).

112 vere acute respiratory syndrome-coronavirus (SARS-CoV) spike (S) glycoprotein (SARS-S).

113 vere acute respiratory syndrome-coronavirus (SARS-CoV), has been established; however, the large vira

114 steine proteases encoded by the coronavirus (SARS-CoV: PLpro; NL63: PLP1 and PLP2) represent potentia

115 identification of an associated coronavirus, SARS-CoV.

116 human severe acute respiratory syndrome CoV (SARS) CoV is angiotensin-converting enzyme 2 (ACE2).

117 A mouse-adapted SARS-CoV (SARS-CoV-MA15) lacking the envelope (E) protein (rSARS-C

118 igin: severe acute respiratory syndrome CoV (SARS-CoV) and Middle East respiratory syndrome CoV (MERS

119 ) and severe acute respiratory syndrome CoV (SARS-CoV) represent highly pathogenic human CoVs that sh

120 of S glycoproteins of 3 beta-CoVs, MERS-CoV, SARS-CoV, and MHV, and demonstrated that they were essen

121 Two zoonotic coronaviruses (CoVs)-SARS-CoV and MERS-CoV-have crossed species to cause seve

122 from other human CoVs (including the deadly SARS-CoV and MERS-CoV) and their related zoonotic CoVs,

123 e receptor-binding domain (RBD) of different SARS-CoV strains isolated from humans or civets.

124 ry lesions and fibrosis are generated during SARS-CoV infection are not known.

125 ost proteins that interact with nsp's during SARS-CoV infections.

126 n kinase 2 (Abl2), as required for efficient SARS-CoV and MERS-CoV replication in vitro These data de

127 obtain viable chimeras containing the entire SARS-CoV M protein as well as mutants with intramolecula

128 For example, SARS-CoV infection of cultured cells depends on endosoma

129 n to identify and characterize the bona fide SARS-CoV FP.

130 te to persistent lung inflammation following SARS-CoV infection.

131 cytokines, and antibody responses following SARS-CoV rechallenge in AGMs.

132 For SARS-CoV, the absence of this 2'-O-MTase activity result

133 ore the necessity of 2'-O-MTase activity for SARS-CoV pathogenesis and identify host immune pathways

134 region of the S protein that is crucial for SARS-CoV entry.

135 Utilizing models for SARS-CoV infection, key components of innate immune sign

136 A similar trend was observed for SARS-CoV PLpro, although it was much more efficient than

137 exposes a novel internal fusion peptide for SARS-CoV S, which may be conserved across the Coronaviri

138 interactions of SARS-S with the receptor for SARS-CoV, angiotensin converting enzyme 2 (ACE2); (ii) S

139 vo data showing that calcium is required for SARS-CoV S-mediated fusion.

140 ino acids 798-818 SFIEDLLFNKVTLADAGFMKQY for SARS-CoV, FP1).

141 ign a successful live-attenuated vaccine for SARS-CoV and opens avenues for treatment and prevention

142 Here, we use the known structural data from SARS-CoV E to infer the residues important for ion chann

143 cleavage of viral glycoproteins derived from SARS-CoV and Ebola, Hendra, and Nipah viruses that are r

144 otypes bearing the glycoprotein derived from SARS-CoV or Ebola, Hendra, or Nipah virus.

145 tured in vitro These two strains differ from SARS-CoV only in containing an extra open reading frame

146 ndicate that the virus differs markedly from SARS-CoV.

147 Therefore, the activity of PLPs from SARS-CoV, MERS-CoV, and mouse hepatitis virus was evalua

148 VRP(3000)-based vaccines were protected from SARS-CoV disease, while animals receiving the VRP(3014)-

149 eceptor (EGFR), is critical to recovery from SARS-CoV-induced tissue damage.

150 Similarly to SUD, the PL(pro)s from SARS-CoV, MERS-CoV, and HCoV-NL63 physically interact wi

151 lar and structural basis for tracking future SARS-CoV evolution in animals.

152 s infections, new respiratory viruses (e.g., SARS-CoV), and lung infections caused by antibiotic-resi

153 cal evaluation of a series of new generation SARS-CoV PLpro inhibitors are described.

154 ese mutations were naturally selected or how SARS-CoV evolved to adapt to different host receptors ha

155 However, SARS-CoV PLpro much preferred K48-linked polyubiquitin c

156 In SARS-CoV homologous rechallenge studies, 11 of the 12 an

157 c T cell response underlie severe disease in SARS-CoV-infected mice.

158 ore protective than a cathepsin inhibitor in SARS-CoV-infected mice.

159 e nsp10 surface that interacts with nsp14 in SARS-CoV replication, as several mutations that abolishe

160 As the function of ORF7a in SARS-CoV replication was previously unknown, we focused

161 The conserved epitope was also recognized in SARS-CoV- and MERS-CoV-infected human leukocyte antigen

162 ss the relevance of small non-coding RNAs in SARS-CoV pathology, we deep sequenced RNAs from the lung

163 to show that T cells play a crucial role in SARS-CoV clearance and that a suboptimal T cell response

164 tly higher in MERS-CoV-infected MDMs than in SARS-CoV-infected cells.

165 anted and an unadjuvanted double-inactivated SARS-CoV (DIV) vaccine, we demonstrate an eosinophilic i

166 Several viruses, including SARS-CoV, utilize virally encoded 2'-O-MTases to camoufl

167 During primary infection, SARS-CoV replicated in the AGM lung for up to 10 days.

168 that p53 inhibits replication of infectious SARS-CoV as well as of replicons and human coronavirus N

169 Mutations were introduced into SARS-CoV NSP16 within the conserved KDKE motif and effec

170 bat ACE2 gene map almost perfectly to known SARS-CoV interaction surfaces.

171 ceptible 8- to 10-month-old mice from lethal SARS-CoV challenge.

172 cells protect susceptible hosts from lethal SARS-CoV infection, but they also suggest that SARS-CoV-

173 rotected 8- to 10-month-old mice from lethal SARS-CoV infection.

174 emonstrate that IFN-I and IMM promote lethal SARS-CoV infection and identify IFN-I and IMMs as potent

175 hose susceptible and resistant to the lethal SARS-CoV infection, respectively.

176 Furthermore, like SARS-CoV nsp1, the mRNA degradation activity of MERS-CoV

177 for drugs, as inhibition of nsp1 would make SARS-CoV more susceptible to the host antiviral defenses

178 ation of the enzyme, 16-(R) is a noncovalent SARS-CoV 3CLpro inhibitor with moderate MW and good enzy

179 used by the silent codon change in Stem 3 of SARS-CoV changed the viral growth kinetics and affected

180 otection against infection in the absence of SARS-CoV-specific memory CD4 T or B cells.

181 tease operates as a portal for activation of SARS-CoV cell entry.

182 dotyped viruses in vitro and the cleavage of SARS-CoV spike glycoprotein in an in vitro cleavage assa

183 tor recognition, an important determinant of SARS-CoV infection and pathogenesis.

184 er, these data indicate that dimerization of SARS-CoV nsp9 at the GXXXG motif is not critical for RNA

185 Upon challenge with a lethal dose of SARS-CoV, virus-specific memory CD8 T cells efficiently

186 The emergence of SARS-CoV and MERS-CoV provides evidence that coronavirus

187 tential, as demonstrated by the emergence of SARS-CoV and Middle East respiratory syndrome (MERS)-CoV

188 t ACE2 utilization preceded the emergence of SARS-CoV-like viruses from bats.

189 This study shows that formulation of SARS-CoV spike protein or inactivated whole-virus vaccin

190 is further exacerbated by the formulation of SARS-CoV vaccines with alum adjuvants.

191 Recent identification of SARS-CoV NSP16 as a viral 2'-O-methyltransferase (2'-O-M

192 however, it was also found that infection of SARS-CoV could be strongly induced by trypsin treatment.

193 Finally, potent inhibitors of SARS-CoV PLpro were found to have no effect on MERS-CoV

194 of small molecule, nonpeptide inhibitors of SARS-CoV PLpro.

195 acterization of small-molecule inhibitors of SARS-CoV replication that block viral entry by three dif

196 to fibrotic lung disease in a mouse model of SARS-CoV infection.

197 Using mouse models of SARS-CoV pathogenesis, we have identified that the wound

198 V and each other, most of the pFP mutants of SARS-CoV and MHV also failed to mediate membrane fusion,

199 lar to the nonstructural protein 1 (nsp1) of SARS-CoV that inhibits host gene expression at the trans

200 The outbreaks of SARS-CoV and MERS-CoV and the continuing diagnosis of ne

201 unopathogenic basis for the fatal outcome of SARS-CoV infection in the AC70 mice.

202 aracterized and compared the pathogeneses of SARS-CoV infection in two of the most stable Tg lineages

203 red an important clue to the pathogenesis of SARS-CoV infection and illustrates the havoc that a smal

204 Here, we studied the priming of SARS-CoV S by elastase and show an important role for re

205 -nsp3.2) and N (svRNA-N) genomic regions of SARS-CoV.

206 uggesting that nsp10 is a major regulator of SARS-CoV replicase function.

207 he crystal structure at 3.38 A resolution of SARS-CoV nsp14 in complex with its cofactor nsp10 adds t

208 Our work suggests a potential risk of SARS-CoV re-emergence from viruses currently circulating

209 However, the role of SARS-CoV-specific memory CD8 T cells in mediating protec

210 1 plays an important role in the severity of SARS-CoV pathogenesis and that it is independent of the

211 ild-type SARS-CoV, a mouse-adapted strain of SARS-CoV (called MA15) was developed and was shown to ca

212 zation potency toward the icUrbani strain of SARS-CoV.

213 tro titers equivalent to epidemic strains of SARS-CoV.

214 The X-ray structure of SARS-CoV 3CLpro bound with 16-(R) was instrumental in gu

215 rated and compared to the X-ray structure of SARS-CoV PLpro to provide plausible explanations for dif

216 Many survivors of SARS-CoV infection develop pulmonary fibrosis (PF), with

217 of a coronavirus pandemic similar to that of SARS-CoV.

218 ction of titers that are lower than those of SARS-CoV.

219 earance, as intravenous adoptive transfer of SARS-CoV-immune splenocytes or in vitro-generated T cell

220 Treatment of SARS-CoV and MERS-CoV infection is limited to providing

221 With this greater understanding of SARS-CoV biology, many researchers have sought to identi

222 molecular basis for the extreme virulence of SARS-CoV remains elusive.

223 This panel of SARS-CoVs provides novel reagents that we have used to f

224 Each class of mutants clustered on SARS-CoV nsp1 surface and suggested nsp1 interacts with

225 red for pathogen clearance following primary SARS-CoV infection.

226 piratory syndrome coronavirus spike protein (SARS-CoV S) can be primed by a variety of host cell prot

227 Identifying host factors that regulate SARS-CoV pathogenesis is critical to understanding how t

228 We found that BST-2 does restrict SARS-CoV, but the loss of ORF7a leads to a much greater

229 termine if BST-2 has the ability to restrict SARS-CoV and if the SARS-CoV genome encodes any proteins

230 e found that BST-2 is capable of restricting SARS-CoV release from cells; however, we also identified

231 tif and effectively attenuated the resulting SARS-CoV mutant viruses both in vitro and in vivo.

232 tro and completely protected against several SARS-CoV strains containing substitutions associated wit

233 and aged mice within novel models of severe SARS-CoV pathogenesis.

234 cation of severe acute respiratory syndrome (SARS) CoV and murine CoV also inhibits the activity of M

235 trate for severe acute respiratory syndrome (SARS)-CoV an RNA synthesis and proofreading pathway thro

236 t notably severe acute respiratory syndrome (SARS)-CoV and Middle East respiratory syndrome (MERS)-Co

237 ch as the severe acute respiratory syndrome (SARS)-CoV and the Middle East respiratory syndrome-CoV,

238 a for the severe acute respiratory syndrome (SARS)-CoV E protein suggest that it assembles into a hom

239 y distant severe acute respiratory syndrome (SARS)-CoV employ the same receptor for host cell entry,

240 vation of severe acute respiratory syndrome (SARS)-CoV ExoN activity results in a stable mutator phen

241 The severe acute respiratory syndrome (SARS)-CoV was identified as the etiologic agent of the 2

242 Unlike severe acute respiratory syndrome (SARS)-CoV, which exclusively infects and releases throug

243 uction by severe acute respiratory syndrome (SARS)-CoV.

244 CCL-3, RANTES/CCL-5, and interleukin 8) than SARS-CoV.

245 ely and causes stronger p53 degradation than SARS-CoV PL(pro) alone.

246 responses in patients provided evidence that SARS-CoV pathogenesis is at least partially controlled b

247 active EGFR [EGFR(DSK5) mice], we find that SARS-CoV infection causes enhanced lung disease.

248 These results indicate that SARS-CoV ORF-9b manipulates host cell mitochondria and m

249 Here, we report that SARS-CoV nsp7 and nsp8 activate and confer processivity

250 Further in vitro analysis revealed that SARS-CoV RNA dimers assemble through 'kissing' loop-loop

251 Finally, we also show that SARS-CoV ORF7a blocks the restriction activity of BST-2

252 Overall, our results show that SARS-CoV-specific memory CD8 T cells protect susceptible

253 RS-CoV infection, but they also suggest that SARS-CoV-specific CD4 T cell and antibody responses are

254 The SARS-CoV M chimera exhibited a conditional growth defect

255 The SARS-CoV papain-like protease is encoded next to SUD wit

256 Using the SCHOOL approach and the SARS-CoV fusion peptide sequence, we rationally designed

257 2 interface is more compact than that at the SARS-CoV/hACE2 interface, and hence RBD/hACE2 binding af

258 ur potential BST-2 modulators encoded by the SARS-CoV genome: the papain-like protease (PLPro), nonst

259 the ability to restrict SARS-CoV and if the SARS-CoV genome encodes any proteins that modulate BST-2

260 rough a palindromic sequence embedded in the SARS-CoV Stem 3.

261 Moreover, the SARS-CoV N substitutions did not alter the fidelity of l

262 de further evidence of the bat origin of the SARS-CoV and highlight the likelihood of future bat coro

263 We show that the cytoplasmic tail of the SARS-CoV E protein is sufficient to redirect a plasma me

264 To dissect the targeting of the SARS-CoV E protein to the Golgi region, we exogenously e

265 Dissecting the mechanism of targeting of the SARS-CoV E protein will lead to a better understanding o

266 we generated and analyzed 38 mutants of the SARS-CoV nsp1, targeting 62 solvent exposed residues out

267 The endoribonuclease activity of the SARS-CoV Nsp15 (sNsp15) was stimulated by retinoblastoma

268 actions between the S1 and S2 domains of the SARS-CoV S glycoprotein.

269 d more structural constraint rather than the SARS-CoV RBD-like region(s) should have broader utility

270 We show that the SARS-CoV protein ORF7a inhibits BST-2 glycosylation, lea

271 on (IFN) antagonism screen, we show that the SARS-CoV proteome contains several replicase, structural

272 We used the SARS-CoV apo X-ray structure to develop a model of the N

273 Using the SARS-CoV reverse genetics system, we generated and chara

274 The degree of sex bias to SARS-CoV infection increased with advancing age, such th

275 y crystal structure of inhibitor 24-bound to SARS-CoV PLpro, a drug design template was created.

276 hese data indicate that svRNAs contribute to SARS-CoV pathogenesis and highlight the potential of svR

277 Enhanced susceptibility of male mice to SARS-CoV was associated with elevated virus titers, enha

278 e a key role of EGFR in the host response to SARS-CoV and how it may be implicated in lung disease in

279 s, especially IFN-alpha, than in response to SARS-CoV.

280 o address this age-related susceptibility to SARS-CoV and IAV, we infected C57BL/6 (B6) mice with mou

281 hat sex differences in the susceptibility to SARS-CoV in mice parallel those observed in patients and

282 owed that male mice were more susceptible to SARS-CoV infection compared with age-matched females.

283 Gene transcription signatures unique to SARS-CoV disease states have been identified, but host f

284 RTD-1-treated, SARS-CoV-infected mice displayed altered lung tissue cyt

285 l disease following infection with wild-type SARS-CoV, a mouse-adapted strain of SARS-CoV (called MA1

286 Here, we used SARS-CoV as a research model and examined the escape pat

287 n monocyte-derived macrophages (MDMs) versus SARS-CoV-infected MDMs.

288 a coronavirus PLP's interface with ISG15 via SARS-CoV PLpro in complex with the principle binding dom

289 We propose a novel mechanism whereby SARS-CoV fusion protein function can be controlled by sp

290 While SARS-CoV nsp1 is localized exclusively in the cytoplasm

291 While SARS-CoV, mouse-adapted SARS-CoV (MA15), and chimeric SA

292 However, while SARS-CoV uses the human angiotensin-converting enzyme 2

293 and female mice of different age groups with SARS-CoV and analyzed their susceptibility to the infect

294 us-specific CD8 T cells by immunization with SARS-CoV peptide-pulsed dendritic cells also resulted in

295 gen receptor signaling in mice infected with SARS-CoV.

296 protect the mice from lethal infection with SARS-CoV MA15, suggesting that further optimization of t

297 After infection with SARS-CoV, the acute lung injury caused by the virus must

298 red immune response following infection with SARS-CoV.

299 blocking of entry of HIV-1 pseudotyped with SARS-CoV surface glycoprotein S (SARS-S) but not that of

300 vities against a panel of human and zoonotic SARS-CoVs and neutralization escape mutants.