ライフサイエンスコーパス: SARS

1 SARS coronavirus (SARS-CoV) causes severe acute respirat

2 SARS is a threat which is similar to MERS virus, but the

3 SARS PLpro binds diUb(Lys48) in an extended conformation

4 SARS-CoV caused a worldwide epidemic infecting more than

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

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

7 Epidemiological data from the 2002-2003 SARS epidemic and recent Middle East respiratory syndrom

8 m which the causative agent of the 2002-2003 SARS pandemic is thought to have originated.

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

10 rombocytopenia Syndrome virus in China and a SARS-like coronavirus in the Middle East.

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

12 avirus (MERS-CoV), has caused outbreaks of a SARS-like illness with high case fatality rate.

13 Here we examine the disease potential of a SARS-like virus, SHC014-CoV, which is currently circulat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

28 for possible therapeutic development against SARS-CoV.

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

30 Furthermore, although SARS does not require NPC1 for entry, SARS entry also be

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

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

33 ticular concern (for example, HIV, Ebola and SARS).

34 Our findings suggest that both EBOV and SARS traffic deep into the endocytic pathway for entry a

35 It is notable that HIV and SARS similarly dysregulated 11 genes and 3 pathways.

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

37 how that the PLpro domains from the MERS and SARS coronaviruses can recognize and process the same su

38 gens such as Marburg virus, Nipah virus, and SARS coronavirus.

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

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

41 gence in human populations, zoonoses such as SARS cause occasional infections in human populations ex

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

43 including severe respiratory viruses such as SARS-CoV.

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

45 Importantly, available SARS monoclonal antibodies offered success in limiting v

46 Evaluation of available SARS-based immune-therapeutic and prophylactic modalitie

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

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

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

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

51 highly contagious disease that is caused by SARS coronavirus (SARS-CoV) and for which there are curr

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

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

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

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

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

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

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

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 vere acute respiratory syndrome coronavirus (SARS)) via interactions with their surface glycans.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 identification of an associated coronavirus, SARS-CoV.

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

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

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

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

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

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

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

107 Bats harbor genetically diverse SARS-like coronaviruses (SL-CoVs), and some of them have

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

109 therapeutics for future control of emerging SARS-like infections.

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

111 though SARS does not require NPC1 for entry, SARS entry also begins after colocalization with NPC1.

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

113 hods by: 1) identifying the sites explaining SARS coronavirus differences between human, bat and palm

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

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

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

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

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

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

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

121 Since the only endosomal requirement for SARS entry is cathepsin L activity, we tested and provid

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

123 NPC1(+) LE/Lys, as a therapeutic target for SARS and EBOV.

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

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

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

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

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

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

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

131 rt-lived in patients who have recovered from SARS, making it critical to develop additional vaccine s

132 ctable in individuals who had recovered from SARS.

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

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

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

136 enveloped viruses, including influenza, HIV, SARS, MERS, and Ebola.

137 Yet, how SARS evades innate immune responses to cause human disea

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

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

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

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

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

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

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

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

146 Multiple new coronaviruses, including SARS, have been identified in human samples just within

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

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

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

150 re the causative agents for AIDS, influenza, SARS, and other serious health threats.

151 iologic agent of the 2002-2003 international SARS outbreak.

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

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

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

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

156 s partially protected these mice from lethal SARS.

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

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

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

160 Moreover, SARS and HIV infections dysregulate 4 genes (ANXA3, GNS,

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

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

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

164 eumonia in China, and the causative agent of SARS was identified to be a novel coronavirus, severe ac

165 The virus caused 8,096 confirmed cases of SARS and 774 deaths (a case fatality rate of approximate

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

167 duces promising leads for the development of SARS therapeutics.

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

169 gen--as reflected by the recent emergence of SARS and Influenza for example.

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

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

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

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

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

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

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

177 ts later and does not affect interactions of SARS-S with ACE2 or the enzymatic functions of cathepsin

178 of action, by blocking early interactions of SARS-S with the receptor for SARS-CoV, angiotensin conve

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

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

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

182 014, and there was a significant outbreak of SARS in 2003.

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

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

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

186 , a host protease required for processing of SARS-S during viral entry; and (iii) SSAA09E3 [N-(9,10-d

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

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

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

190 iling strongly suggests that the response of SARS affected patients seems to be mainly an innate infl

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

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

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

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

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

196 y, we report the 2.85 A crystal structure of SARS PLpro bound to a diUb(Lys48) activity-based probe.

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

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

199 We identified 32 studies of SARS coronavirus infection and severe influenza.

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

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

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

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

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

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

206 We previously showed that recombinant SARS coronavirus (SARS-CoV) (Urbani strain based) lackin

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

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

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

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

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

212 otyped with SARS-CoV surface glycoprotein S (SARS-S) but not that of HIV-1 pseudotyped with vesicular

213 f humans, severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), as we

214 agents of severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), provi

215 hat cause severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), two p

216 including severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS).

217 s causing severe acute respiratory syndrome (SARS) and the recently emerged Middle East respiratory s

218 from the severe acute respiratory syndrome (SARS) coronavirus (CoV) that stimulated -1 PRF.

219 The severe acute respiratory syndrome (SARS) coronavirus papain-like protease (PLpro) is a DUB

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

221 Severe acute respiratory syndrome (SARS) emerged in November 2002 as a case of atypical pne

222 Severe acute respiratory syndrome (SARS) is an infectious and highly contagious disease tha

223 idemic of Severe Acute Respiratory Syndrome (SARS) led to the identification of an associated coronav

224 series of severe acute respiratory syndrome (SARS) main protease (3CLpro) inhibitors led to the ident

225 ed by the severe acute respiratory syndrome (SARS) outbreak in 2003, China has prioritised the contro

226 dly, that severe acute respiratory syndrome (SARS) S-mediated entry also begins only after a 30-min l

227 at caused severe acute respiratory syndrome (SARS), cause significant morbidity and mortality in huma

228 us (HCV), Severe acute respiratory syndrome (SARS), coxsackie viruses, and rhinoviruses.

229 tbreak of Severe Acute Respiratory Syndrome (SARS), providing new insights into the early stage of th

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

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

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

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

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

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

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

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

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

239 ts harbor severe acute respiratory syndrome (SARS)-like coronaviruses (SL-CoVs) from which the causat

240 breaks of severe acute respiratory syndrome (SARS)-like illness with a high mortality rate, raising c

241 ng on the severe acute respiratory syndrome (SARS)-like viruses, the results indicate that the WIV1-c

242 ter named severe acute respiratory syndrome (SARS).

243 za A, and severe acute respiratory syndrome (SARS).

244 ) against severe acute respiratory syndrome (SARS).

245 rude fatality rate (around 50% vs. 10%) than SARS coronavirus (SARS-CoV) infection.

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

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

248 activity against PEDV 3CL(pro), despite that SARS-3CL(pro) and PEDV 3CL(pro) share only 45.4% sequenc

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

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

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

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

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

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

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

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

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

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

259 at the homodimeric RNA complex formed by the SARS pseudoknot occurs in the cellular environment and t

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

261 st the papain-like protease (PLpro) from the SARS coronavirus (CoV).

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

263 gand that was found to inhibit -1 PRF in the SARS coronavirus on the conformational dynamics of the S

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

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

266 avirus on the conformational dynamics of the SARS pseudoknot.

267 ucture and function of the third stem of the SARS pseudoknot.

268 an efficiently use multiple orthologs of the SARS receptor human angiotensin converting enzyme II (AC

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

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

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

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

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

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

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

276 ty of residues involved in (R)-16 binding to SARS-3CL(pro) are conserved in PEDV-3CL(pro); however, t

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

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

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

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

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

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

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

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

287 CHY1) as an interacting partner of the viral SARS-unique domain (SUD) and papain-like protease (PL(pr

288 sis, influenza, respiratory syncytial virus, SARS-Coronavirus and pneumonia.

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

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

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

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

293 Using mice infected with SARS (severe acute respiratory syndrome)-CoV, we show th

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

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

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

297 red immune response following infection with SARS-CoV.

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

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

300 tory disease, and is related to the zoonotic SARS and MERS betacoronaviruses, which have high fatalit