ライフサイエンスコーパス: arenavirus

1 stically altered the phylogeny of the family Arenavirus.

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

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

4 otent and defined immunotherapeutics against arenaviruses.

5 vaccine candidates against human-pathogenic arenaviruses.

6 contrast to those of 14 other nonpathogenic arenaviruses.

7 rg virus GP2 despite CASV genome homology to arenaviruses.

8 a novel strategy to combat human-pathogenic arenaviruses.

9 FN suppression mechanism shared by all known arenaviruses.

10 -specific RdRP activation extends beyond the arenaviruses.

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

12 ng extracellular matrix proteins and certain arenaviruses.

13 n provide heterologous protection against NW arenaviruses.

14 e GPC spike from Old World but not New World arenaviruses adopts a distinct, pH-independent conformat

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

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

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

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

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

20 e rearrangements are restricted to Old World arenaviruses and are not induced solely by the pH change

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

22 smic tail (CT) is relatively conserved among arenaviruses and is known to interact with the SSP to re

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

24 e immune response to these highly pathogenic arenaviruses and open new directions for future studies.

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

26 chain ferritin and CD71 largely overlap with arenaviruses and Plasmodium vivax binding regions in the

27 Arenaviruses and the malaria parasite exploit CD71 for c

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

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

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

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

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

36 Arenaviruses are an important family of emerging viruses

37 Arenaviruses are emerging viruses including several caus

38 Arenaviruses are enveloped negative-strand RNA viruses t

39 Arenaviruses are enveloped viruses with a bisegmented ne

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

41 North American arenaviruses are generally considered nonpathogenic, but

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

43 Arenaviruses are important emerging human pathogens main

44 Arenaviruses are important emerging human pathogens that

45 Arenaviruses are important emerging human pathogens that

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

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

48 Arenaviruses are responsible for severe and often fatal

49 Old World arenaviruses are significant human pathogens that often

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

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

52 Mammalian arenaviruses are zoonotic viruses that cause asymptomati

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

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

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

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

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

58 erve as a universal molecular determinant of arenavirus attenuation.

59 to develop a general molecular strategy for arenavirus attenuation.

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

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

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

63 c tail (CT) of GP2 is highly conserved among arenaviruses, but its functional role in viral replicati

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

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

66 Arenaviruses can cause lethal hemorrhagic fevers in huma

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

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

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

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

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

72 Arenaviruses cause fatal hemorrhagic disease in humans.

73 Several arenaviruses cause hemorrhagic fever disease in humans a

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

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

76 Arenaviruses cause severe hemorrhagic fever diseases in

77 Several arenaviruses cause severe hemorrhagic fever in humans an

78 Several arenaviruses cause severe hemorrhagic fever in humans an

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

80 Arenavirus cell entry is mediated by the viral glycoprot

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

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

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

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

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

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

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

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

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

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

91 L protein of Lassa virus, a human-pathogenic arenavirus endemic in West Africa.

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

93 Arenaviruses enter the host cell by fusion of the viral

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

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

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

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

98 glycoprotein spike complex displayed on the arenavirus envelope is a key determinant of species trop

99 The arenavirus family consists of several highly pathogenic

100 The arenavirus family includes several important pathogens t

101 The arenavirus family includes several members that are high

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

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

104 The emergence of Old and New World arenaviruses from rodent reservoirs persistently threate

105 owever, despite the fact that all pathogenic arenaviruses from South America utilize transferrin rece

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

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

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

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

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

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

112 Viral entry is mediated by the arenavirus GP complex, which consists of the stable sign

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

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

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

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

117 Arenaviruses have a significant impact on public health

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

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

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

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

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

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

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

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

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

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

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

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

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

131 investigated the sequence plasticity of the arenavirus IGR.

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

133 sults of a study on the dynamics of Morogoro arenavirus in a population of multimammate mice (Mastomy

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

135 t, which is also the reservoir host of Lassa arenavirus in West Africa, is known for its strong seaso

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

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

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

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

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

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

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

143 ter coronavirus, flavivirus, rhabdovirus, or arenavirus infection induced a long-lasting enhancement

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

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

146 Nevertheless, the function of NP ExoN in arenavirus infection remains to be defined.

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

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

149 represent a viable therapeutic strategy for arenavirus infection.

150 hly specific, novel therapeutic strategy for arenavirus infection.

151 therapeutics or vaccines available to combat arenavirus infection.

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

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

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

155 SARS, MERS, Ebola, Nipah and an array of arenavirus infections sporadically spillover into human

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

157 biosynthesis inhibitors for the treatment of arenavirus infections.

158 innate immune responses to highly pathogenic arenavirus infections.IMPORTANCE Arenavirus NPs contain

159 Arenaviruses initially target macrophages and dendritic

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

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

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

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

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

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

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

167 cellular binding and entry of the New World arenaviruses Junin and Tacaribe virus, suggesting that z

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

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

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

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

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

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

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

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

176 The arenavirus Lassa causes severe hemorrhagic fever and a s

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

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

179 Recent occurrences of filoviruses and the arenavirus Lassa virus (LASV) in overlapping endemic are

180 The arenavirus Lassa virus causes hundreds of thousands of i

181 The arenaviruses Lassa virus (LASV), Junin virus (JUNV), and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

207 e RNA-dependent RNA-polymerase (RdRP) of the arenavirus Machupo (MACV), we demonstrate that the 5' ge

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

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

210 The arenavirus matrix protein Z is highly multifunctional an

211 The arenavirus matrix protein Z is multifunctional, with at

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

213 Arenaviruses merit significant interest as important hum

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

215 In situ hybridisation localised arenavirus mostly to blood cells.

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

217 table for HTS to rapidly identify inhibitors arenavirus multiplication.

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

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

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

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

222 pathogenic arenavirus infections.IMPORTANCE Arenavirus NPs contain a highly conserved DEDDh ExoN mot

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

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

225 Arenavirus nucleoproteins (NPs) contain a highly conserv

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

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

228 acts by blocking hemorrhagic fever New World arenavirus (NWA) entry into cells.

229 Several clade B New World arenaviruses (NWAs) can cause severe and often fatal hem

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

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

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

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

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

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

236 Arenavirus pathogens cause a wide spectrum of diseases i

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

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

239 ive-attenuated viral vaccines against deadly arenavirus pathogens.

240 arget for developing antiviral drugs against arenavirus pathogens.

241 velopment of antivirals against deadly human arenavirus pathogens.

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

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

244 ng a reverse genetics system of a prototypic arenavirus, Pichinde virus (PICV), we show that the GP2

245 Due to their efficient transmission, arenaviruses pose a severe risk for outbreaks and might

246 Hemorrhagic fever arenaviruses pose significant threats to public health a

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

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

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

250 und cultured Chinook salmon revealed a novel arenavirus, reovirus and nidovirus.

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 n essential biological role of the GP2 CT in arenavirus replication and suggest it as a potential nov

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

255 Arenavirus species are responsible for severe life-threa

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

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

258 s greatly accelerated the discovery of novel arenavirus species.

259 make humans or rodents susceptible to other arenavirus species.

260 ly to be a feasible approach for eliminating arenaviruses such as Lassa virus from Mastomys populatio

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

262 viral vaccine candidates.IMPORTANCE Several arenaviruses, such as Lassa virus (LASV), can cause seve

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

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

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

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

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

268 vian hemorrhagic fever (BHF), is a New World arenavirus that was first isolated in Bolivia from a hum

269 Certain arenaviruses that circulate in rodent populations can ca

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

271 ive molecule is highly effective against all arenaviruses that were tested, offering a universal ther

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

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

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

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

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

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

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

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

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 Sequencing revealed two different arenavirus variants which each infect wild Chinook and s

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

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

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

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 tional design approach to target TfR1-tropic arenaviruses with high potency and breadth.