ライフサイエンスコーパス: arenavirus

1 r virus (a retrovirus) and Machupo virus (an arenavirus).

2 stically altered the phylogeny of the family Arenavirus.

3 Espinosa virus (OCEV) is a novel, uncultured arenavirus.

4 anarito virus (GTOV), a distantly related NW arenavirus.

5 contrast to those of 14 other nonpathogenic arenaviruses.

6 rg virus GP2 despite CASV genome homology to arenaviruses.

7 a novel strategy to combat human-pathogenic arenaviruses.

8 FN suppression mechanism shared by all known arenaviruses.

9 V) GP does not cluster with New or Old World arenaviruses.

10 ween New World (Junin) and Old World (Lassa) arenaviruses.

11 ng extracellular matrix proteins and certain arenaviruses.

12 n provide heterologous protection against NW arenaviruses.

13 st LASV, but not those specific to New World arenaviruses.

14 otent and defined immunotherapeutics against arenaviruses.

15 vaccine candidates against human-pathogenic arenaviruses.

16 of ambisense-derived transcripts of multiple arenaviruses also stalled XRN1.

17 MACV, another highly pathogenic NW arenavirus, also activated IFN responses.

18 o virus (MACV), another highly pathogenic NW arenavirus, also induces an IFN response.

19 rs of both Old World (OW) and New World (NW) arenaviruses, also inhibits the nuclear translocation an

20 Machupo virus (MACV) is a New World (NW) arenavirus and causative agent of Bolivian hemorrhagic f

21 with the glycoproteins (GPs) of a prototypic arenavirus and hantavirus and show that the lectin endop

22 vergent from the classical Old and New World arenaviruses and also differ substantially from each oth

23 ody cocktail with antibodies targeting three arenaviruses and demonstrated protective efficacy agains

24 Arenaviruses and hantaviruses cause severe human disease

25 o provides insights into the pathogenesis of arenaviruses and may facilitate the design of vaccines a

26 help dictate the outcome of infections with arenaviruses and other DC-replicating viruses and shed l

27 the innate immune evasion mechanisms between arenaviruses and other hemorrhagic fever-causing viruses

28 e mechanism shared by the diverse pathogenic arenaviruses and thus shed important light on the pathog

29 ory setting to include Ebola virus, Tacaribe arenavirus, and HHV-8, and we propose ARB as a broad-spe

30 lian cells with Ebola virus (EBOV), Tacaribe arenavirus, and human herpesvirus 8 (HHV-8).

31 choriomeningitis virus (LCMV), the prototype arenavirus, and Lassa virus (LASV), the causative agent

32 oped RNA viruses, filoviruses, flaviviruses, arenaviruses, and bunyaviruses, cause hemorrhagic fevers

33 thogenic RNA viruses, including filoviruses, arenaviruses, and coronaviruses, suggests the potential

34 ished that efficient budding of filoviruses, arenaviruses, and other viruses is critically dependent

35 athogenic potential of known and/or emerging arenaviruses, and reveals a novel target for the develop

36 Budding of filoviruses, arenaviruses, and rhabdoviruses is facilitated by subver

37 Arenaviruses are an important family of emerging viruses

38 Related arenaviruses are beginning to spread in human population

39 Arenaviruses are emerging viruses including several caus

40 Arenaviruses are enveloped negative-strand RNA viruses t

41 Arenaviruses are enveloped viruses with a bisegmented ne

42 Arenaviruses are enveloped, negative-stranded RNA viruse

43 Concerns about human-pathogenic arenaviruses are exacerbated because of the lack of FDA-

44 Concerns about human-pathogenic arenaviruses are exacerbated because of the lack of FDA-

45 North American arenaviruses are generally considered nonpathogenic, but

46 Many of the NW arenaviruses are highly pathogenic viruses that cause sy

47 Arenaviruses are important emerging human pathogens main

48 Arenaviruses are important emerging human pathogens that

49 Arenaviruses are important emerging human pathogens that

50 pathway that is subverted by JUNV.IMPORTANCE Arenaviruses are important human pathogens for which FDA

51 esponses to highly pathogenic New World (NW) arenaviruses are not well understood.

52 Arenaviruses are responsible for acute hemorrhagic fever

53 Several arenaviruses are responsible for causing viral hemorrhag

54 Arenaviruses are responsible for severe and often fatal

55 Old World arenaviruses are significant human pathogens that often

56 Outside of the order Nidovirales, arenaviruses are the only RNA viruses that encode an Exo

57 All known pathogenic NW arenaviruses are transmitted in South America by their h

58 Mammalian arenaviruses are zoonotic viruses that cause asymptomati

59 a support the development of live-attenuated arenaviruses as broadly protective pan-arenavirus vaccin

60 the host immune system and highly pathogenic arenaviruses as well as distinct mechanisms underlying v

61 molecular and cellular biology of New World arenaviruses, as well as a discussion of the current ani

62 used as universal molecular determinants of arenavirus attenuation for the rapid development of safe

63 to document a general molecular strategy for arenavirus attenuation that can facilitate the rapid dev

64 to develop a general molecular strategy for arenavirus attenuation.

65 erve as a universal molecular determinant of arenavirus attenuation.

66 ified into OW (Old World) and NW (New World) arenaviruses based on their antigenicity, phylogeny, and

67 BIBD-associated arenaviruses (BIBDAV) are genetically divergent from the

68 vered boid inclusion body disease-associated arenaviruses (BIBDAV) of reptiles have drastically alter

69 a lectin-independent mechanism, traffics to arenavirus budding sites, and is incorporated into virio

70 es derived from the GPCs of newly discovered arenavirus by the SKI-1/S1P of humans or any other speci

71 ether the glycoprotein of any newly emerging arenavirus can be efficiently processed by human SKI-1/S

72 Arenaviruses can cause lethal hemorrhagic fevers in huma

73 a against MACV.IMPORTANCE Multiple New World arenaviruses can cause severe disease in humans, and som

74 Arenaviruses can cause severe hemorrhagic fever diseases

75 The reason why some arenaviruses can cause severe human diseases while other

76 ected cells provides the first evidence that arenaviruses can reshape apoptotic signaling according t

77 pigs with Pichinde virus (PICV), a prototype arenavirus, can serve as a surrogate small animal model

78 The nucleoprotein (NPs) of all arenaviruses carry a unique exoribonuclease (RNase) doma

79 Arenaviruses cause fatal hemorrhagic disease in humans.

80 Several arenaviruses cause hemorrhagic fever disease in humans a

81 At least five New World (NW) arenaviruses cause hemorrhagic fevers in South America.

82 Hemorrhagic fever arenaviruses cause lethal infections in humans and, in t

83 Arenaviruses cause severe hemorrhagic fever diseases in

84 Several arenaviruses cause severe hemorrhagic fever in humans an

85 Several arenaviruses cause severe hemorrhagic fever in humans an

86 he design of vaccines and treatments against arenavirus-caused diseases.

87 Several arenaviruses, chiefly Lassa virus (LASV), cause hemorrha

88 Several arenaviruses, chiefly Lassa virus (LASV), cause hemorrha

89 nt of AHF is Junin virus (JUNV); a New World arenavirus classified as a National Institute of Allergy

90 nt of AHF is Junin virus (JUNV); a New World arenavirus classified as an NIAID/CDC category A priorit

91 iomeningitis virus--a prototype of Old World arenaviruses closely related to Lassa fever virus--elici

92 The glycoprotein complex (GPC) of arenaviruses, composed of stable signal peptide, GP1, an

93 ERGIC-53 is required for arenavirus, coronavirus, and filovirus propagation; in i

94 ions in this region affect the entry of each arenavirus differently.

95 ncluding filoviruses (Ebola and Marburg) and arenaviruses (e.g., Lassa and Junin) which cause severe

96 ght to better understand how closely related arenaviruses elude cross-species neutralization by inves

97 from Junin virus (JUNV), a hemorrhagic fever arenavirus endemic in central Argentina.

98 ach to assess the compatibility of New World arenaviruses, endemic in rodents, with the host TfR1 ent

99 Arenaviruses enter the host cell by fusion of the viral

100 es for biochemical and structural studies of arenavirus entry and its inhibition.

101 ically distinct small-molecule inhibitors of arenavirus entry have recently been identified and shown

102 Arenavirus entry into the host cell is promoted by the v

103 membrane fusion, a characteristic feature of arenavirus entry.

104 ad small-molecule inhibitors that target the arenavirus envelope glycoprotein (GPC) have recently bee

105 ntly been identified and shown to act on the arenavirus envelope glycoprotein (GPC) to prevent membra

106 presents direct verification that New World arenaviruses exhibit class I viral membrane fusion machi

107 The arenavirus family consists of several highly pathogenic

108 The arenavirus family includes several important pathogens t

109 The arenavirus family includes several members that are high

110 ruses, such as Ebola virus or members of the arenavirus family, rapidly cause severe hemorrhagic dise

111 he glycoproteins of several human-pathogenic arenaviruses found in South America, including JUNV, MAC

112 Transmission of hemorrhagic fever New World arenaviruses from their rodent reservoirs to human popul

113 ding intergenic region (IGR) present in each arenavirus genome segment, the S and L segments (S-IGR a

114 irus, illustrates the unique assembly of the arenavirus glycoprotein spike, and provides a much-neede

115 Old World arenavirus glycoproteins (GPs) mainly engage alpha-dystr

116 inst pseudoviruses bearing Old and New World arenavirus glycoproteins but not against viruses from ot

117 SKI-1/S1P to characterize the processing of arenavirus glycoproteins in a quantitative manner.

118 e the efficiency and subcellular location of arenavirus GPC processing.

119 Viral entry into cells is mediated by arenavirus GPC that consists of an SSP, the receptor-bin

120 SKI-1/S1P to characterize the processing of arenavirus GPC-derived target sequences by human SKI-1/S

121 ERGIC-53 binds to arenavirus GPs through a lectin-independent mechanism, t

122 the early exocytic pathway, associates with arenavirus, hantavirus, coronavirus, orthomyxovirus, and

123 tively, our data suggest that North American arenaviruses have a higher potential to cause human dise

124 Arenaviruses have a significant impact on public health

125 On the other hand, NW arenaviruses have also developed several strategies to c

126 superinfection exclusion, whether New World arenaviruses have evolved such a mechanism remains uncle

127 underlying disease severity and virulence in arenavirus hemorrhagic fever are largely unknown, partic

128 serve as a surrogate small animal model for arenavirus hemorrhagic fevers.

129 ane fusion may be useful in the treatment of arenavirus hemorrhagic fevers.

130 Hemorrhagic fever arenaviruses (HFA) are important human pathogens that ca

131 Hemorrhagic fever arenaviruses (HFA) cause high morbidity and mortality, a

132 Hemorrhagic fever arenaviruses (HFA) pose important public health problems

133 Hemorrhagic fever arenaviruses (HFAs) cause high rates of morbidity and mo

134 Hemorrhagic fever arenaviruses (HFAs) pose important public health problem

135 R1 as a cellular receptor for North American arenaviruses, highlight an "arms race" between these vir

136 as a cell-surface receptor, while New World arenaviruses hijack transferrin receptor.

137 n pressure on the TfR1 of the North American arenavirus host species.

138 of Argentine hemorrhagic fever (AHF), is an arenavirus identified as a category A high-priority agen

139 investigated the sequence plasticity of the arenavirus IGR.

140 NA vaccine approach to generate a potent pan-arenavirus immunotherapeutic.

141 tified pathogens in human samples containing arenavirus in addition to animal samples containing flav

142 ollowing the identification of several novel arenaviruses in diseased snakes.

143 eningitis virus) and New World (Junin virus) arenaviruses in rodent, monkey, and human cell lines.

144 Importantly, both pathogenic NW arenaviruses, in contrast to the OW highly pathogenic ar

145 Arenaviruses include several causative agents of hemorrh

146 A hallmark of arenavirus infection (e.g., LASV) is general immunosuppr

147 e discuss the early host immune responses to arenavirus infection and the recently discovered molecul

148 lammatory and proapoptotic host responses to arenavirus infection could ameliorate disease severity.

149 tween the host innate immune response and NW arenavirus infection in vitro and in vivo, with emphasis

150 NW arenavirus infection induces a variety of host innate im

151 Current chemotherapy for arenavirus infection is limited to the nucleoside analog

152 A crucial step in productive arenavirus infection of human cells is the processing of

153 Although Old World arenavirus infection results in down-regulation of its v

154 this to contrasting clinical outcomes during arenavirus infection, specifically to samples obtained f

155 represent a viable therapeutic strategy for arenavirus infection.

156 hly specific, novel therapeutic strategy for arenavirus infection.

157 therapeutics or vaccines available to combat arenavirus infection.

158 DA-licensed vaccines are available to combat arenavirus infections and antiarenaviral therapy is limi

159 Concerns posed by arenavirus infections are aggravated by the lack of U.S.

160 organization for the treatment of pathogenic arenavirus infections in humans.

161 DA-licensed vaccines are available to combat arenavirus infections, while antiarenaviral therapy is l

162 biosynthesis inhibitors for the treatment of arenavirus infections.

163 Arenaviruses initially target macrophages and dendritic

164 We show that all six North American arenaviruses investigated utilize host species TfR1 orth

165 protects against a broad range of New World arenaviruses is desirable for purposes of simplicity, co

166 st response to infection by these pathogenic arenaviruses is distinct in many aspects.

167 The glycoprotein (GP) of arenaviruses is glycosylated at 11 conserved N-glycosyla

168 nfection by Lassa virus, a highly pathogenic arenavirus, is toxic and prone to treatment failure, we

169 shed a culture system for a novel lineage of arenaviruses isolated from boa constrictors diagnosed wi

170 The New World arenavirus Junin virus (JUNV) is the causative agent of

171 riomeningitis virus (LCMV) and the New World arenavirus Junin virus (JUNV) strain Candid #1.

172 eviously shown that the highly pathogenic NW arenavirus, Junin virus (JUNV), induced an IFN response

173 virus, but a stronger receptor for two other arenaviruses, Junin and Sabia viruses.

174 st, infections with the highly pathogenic NW arenavirus JUNV are associated with high levels of IFNs

175 e immune responses to infections with the NW arenaviruses JUNV and MACV and to infection with the OW

176 IFN responses toward infections with the NW arenaviruses JUNV and MACV are quite different from resp

177 However, the NW arenaviruses JUNV and MACV readily trigger an IFN respon

178 Here we report that infection with NW arenaviruses JUNV and MACV, but not OW LASV, activated P

179 strate for the first time that pathogenic NW arenaviruses JUNV and MACV, but not the OW arenavirus LA

180 The arenavirus Lassa causes severe hemorrhagic fever and a s

181 ogenic viruses, including the Old World (OW) arenavirus Lassa fever virus (LASV) and the New World (N

182 The highly pathogenic Old World (OW) arenavirus Lassa fever virus (LASV) is the causative age

183 y lethal human disease that is caused by the arenavirus Lassa virus (LASV).

184 The arenavirus Lassa virus causes hundreds of thousands of i

185 V relative is not another bunyavirus but the arenavirus Lassa virus instead, suggesting that current

186 s JUNV and MACV and to infection with the OW arenavirus LASV and provides important insights into the

187 ent from responses to infections with the OW arenavirus LASV, a discovery that needs to be further in

188 W arenaviruses JUNV and MACV, but not the OW arenavirus LASV, activated the dsRNA-dependent PKR, anot

189 ses, in contrast to the OW highly pathogenic arenavirus LASV, readily elicited an IFN response in hum

190 ntry mediated by the glycoproteins of the HF arenaviruses LASV and Junin virus (JUNV).

191 on of recombinant versions of the prototypic arenavirus LCMV encoding codon-deoptimized viral nucleop

192 Here we have used the prototypic arenavirus LCMV to document a general molecular strategy

193 During the arenavirus life cycle, processing of the viral envelope

194 l factor interactions that contribute to the arenavirus life cycle.

195 esults suggest that, despite being primarily arenavirus like, the transmembrane subunit of CASV is ex

196 lts open a new avenue for the development of arenavirus live attenuated vaccines based on rearrangeme

197 A genetically unique arenavirus, Lujo virus, was recently discovered as the c

198 th the nucleoproteins (NPs) of the Old World arenavirus lymphocytic choriomeningitis virus (LCMV) and

199 es that the worldwide-distributed prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) is

200 es that the worldwide-distributed prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) is

201 es that the worldwide-distributed prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) is

202 tes that the globally distributed prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) is

203 We used the prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) to

204 e investigated the ability of the prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) to

205 ated the ability of the prototypic Old World arenavirus lymphocytic choriomeningitis virus (LCMV) to

206 ded the nucleoprotein (NP) of the prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) wit

207 loci within the S segment of the prototypic arenavirus lymphocytic choriomeningitis virus (LCMV).

208 atelet depleted mice infected with the mouse arenavirus lymphocytic choriomeningitis virus (LCMV).

209 onstrate that recombinants of the prototypic arenavirus lymphocytic choriomeningitis virus (rLCMVs),

210 Here we show that the arenaviruses lymphocytic choriomeningitis virus (LCMV) a

211 es that the worldwide-distributed prototypic arenavirus, lymphocytic choriomeningitis virus (LCMV), i

212 The prototypic arenavirus, lymphocytic choriomeningitis virus (LCMV), p

213 that the Z proteins of all known pathogenic arenaviruses, lymphocytic choriomeningitis virus (LCMV)

214 , makes human TfR1 a weaker receptor for one arenavirus, Machupo virus, but a stronger receptor for t

215 eutralizing antibodies against two New World arenaviruses, Machupo virus (MACV) and Junin virus (JUNV

216 The arenavirus matrix protein Z is highly multifunctional an

217 The arenavirus matrix protein Z is multifunctional, with at

218 thologs and present evidence consistent with arenavirus-mediated selection pressure on the TfR1 of th

219 Arenaviruses merit significant interest as important hum

220 that modest changes in other North American arenaviruses might allow these viruses to infect humans.

221 more efficient than ribavirin in controlling arenavirus multiplication and that the A3 inhibitory eff

222 table for HTS to rapidly identify inhibitors arenavirus multiplication.

223 use severe disease in humans, newly emerging arenaviruses must be able to hijack human SKI-1/S1P effi

224 In the present study, we produced arenavirus neutralizing antibodies by DNA vaccination of

225 Here we document that the arenavirus noncoding intergenic region (IGR) has a high

226 of TCRV NP and Pichinde virus (PICV) NP, an arenavirus NP with potent anti-IFN function.

227 etailed map of the host machinery engaged by arenavirus NPs and identify an antiviral pathway that is

228 document that efficient interaction between arenavirus nucleoprotein (NP) and RNA-dependent RNA poly

229 The arenavirus nucleoprotein (NP) can suppress induction of

230 Accordingly, the arenavirus nucleoprotein (NP) has been identified as a p

231 evious structural and functional analyses of arenavirus nucleoproteins (NPs) revealed a conserved DED

232 , the extensive human protein interactome of arenavirus nucleoproteins and uncovers a potent antivira

233 ic clade B viruses, as well as nonpathogenic arenaviruses of the same clade, use transferrin receptor

234 Transfer of arenavirus- or protein-specific CD8+ T cells or NK cells

235 st numerous viruses, including bunyaviruses, arenaviruses, paramyxoviruses, coronaviruses and flavivi

236 effective treatment in humans infected with arenaviruses, particularly species found in South Americ

237 n mitigate the severity of disease caused by arenaviruses, particularly species found in South Americ

238 ant insights into the potential mechanism of arenavirus pathogenesis, provides a convenient way to ev

239 Arenavirus pathogens cause a wide spectrum of diseases i

240 Several arenavirus pathogens, such as Lassa and Junin viruses, i

241 t light on the pathogenic mechanism of human arenavirus pathogens.

242 arget for developing antiviral drugs against arenavirus pathogens.

243 velopment of antivirals against deadly human arenavirus pathogens.

244 Using a prototype arenavirus, Pichinde virus (PICV), we characterized the

245 ng a reverse genetics system of a prototypic arenavirus, Pichinde virus (PICV), we have shown for the

246 In contrast, the Pichinde arenavirus (PICV) is a BSL2 pathogen that can cause hemo

247 Hemorrhagic fever arenaviruses pose significant threats to public health a

248 to accomplish the viral life cycle, so each arenavirus protein likely plays unappreciated accessory

249 r mechanistic understanding of the conserved arenavirus proteins in viral infection.

250 trate that infection is independent of known arenavirus receptor genes.

251 In conclusion, therapeutically administered arenavirus replicates in cancer cells and induces tumour

252 ver, the functional roles of the NP RNase in arenavirus replication and host immune suppression have

253 We show that all known human-pathogenic arenaviruses share an innate immune suppression mechanis

254 Arenavirus species are responsible for severe life-threa

255 dered mainly rodent-borne viruses, with each arenavirus species having its own reservoir host.

256 ity of convalescent antisera between related arenavirus species, weak or no cross-neutralization occu

257 s greatly accelerated the discovery of novel arenavirus species.

258 make humans or rodents susceptible to other arenavirus species.

259 This reaction is inhibited by arenavirus-specific monoclonal antibodies and small-mole

260 viral virulence in vivo IMPORTANCE: Several arenaviruses, such as Lassa fever virus, can cause sever

261 Arenaviruses, such as Lassa, Lujo, and Machupo viruses,

262 ow that a close relative of a North American arenavirus suggested to have caused human fatalities, th

263 el of pathogenic and nonpathogenic New World arenaviruses, suggesting that GPC cleavage represents no

264 These results suggest that pathogenic arenaviruses suppress NF-kappaB-mediated proinflammatory

265 ical roles of the Z protein in an infectious arenavirus system and have shed important light on the d

266 an active exoribonuclease domain of Tacaribe arenavirus (TCRV) NP.

267 sis of Lujo virus (LUJV), a recently emerged arenavirus that caused an outbreak of severe viral hemor

268 Lujo virus (LUJV) is an arenavirus that emerged in 2008 associated with a cluste

269 velopment of therapeutics against pathogenic arenaviruses that can infect hundreds of thousands of in

270 ween Lassa and Mopeia viruses, two Old World arenaviruses that differ by 40% in nucleic acid sequence

271 Among pathogenic arenaviruses, the OW LASV usually does not elicit an int

272 ith potent activity against a broad panel of arenaviruses, three of which were completely novel.

273 hTfR1 use is a key determinant for a NW arenavirus to cause hemorrhagic fevers in humans.

274 n vitro proof of the considerable ability of arenaviruses to cross species barriers.

275 The ability of newly emerging arenaviruses to hijack human SKI-1/S1P appears, therefor

276 ing armamentarium to combat human-pathogenic arenaviruses underscores the importance of developing no

277 kely occurs because the pathogenic New World arenaviruses use human transferrin receptor 1 to enter c

278 We show that these North American arenaviruses use the TfR1 orthologs of their rodent host

279 cerbated because of the lack of FDA-licensed arenavirus vaccines and because current antiarenaviral t

280 cerbated because of the lack of FDA-licensed arenavirus vaccines and because current antiarenaviral t

281 f U.S. Food and Drug Administration-licensed arenavirus vaccines and current antiarenaviral therapy b

282 There are no licensed arenavirus vaccines and current antiarenavirus therapy i

283 Food and Drug Administration (FDA)-licensed arenavirus vaccines are available.

284 Currently, there are no FDA-licensed arenavirus vaccines available, and current antiarenavira

285 t, but the development of safe and effective arenavirus vaccines has remained elusive, and currently,

286 To date, there have been no FDA-approved arenavirus vaccines, and current antiarenaviral therapy

287 safe, stable, and protective live-attenuated arenavirus vaccines.

288 a novel strategy to develop live-attenuated arenavirus vaccines.

289 uated arenaviruses as broadly protective pan-arenavirus vaccines.

290 y against viruses with the Old and New World arenavirus viral glycoprotein complex but not against en

291 To identify host factors associated with arenavirus virulence, we used a cynomolgus macaque model

292 Using Pichinde virus as a model arenavirus, we attempted to design glycoprotein-derived

293 velope glycoprotein of the hemorrhagic fever arenaviruses, we have shown that GPC is unique among cla

294 Prior to their discovery, known arenaviruses were considered mainly rodent-borne viruses

295 This is in contrast to orthomyxoviruses and arenaviruses, where resistance is ablated in animals dep

296 fusion glycoprotein of a nonpathogenic model arenavirus, which demonstrates antiviral activity and no

297 een host non-self RNA sensors and pathogenic arenaviruses, which also provides insights into the path

298 stigate the receptor usage of North American arenaviruses, whose entry proteins share greatest simila

299 s, support the association of North American arenavirus with fatal human infections, and suggest that

300 -IFN activity is thought to be shared by all arenaviruses with the exception of Tacaribe virus (TCRV)