ライフサイエンスコーパス: mutant virus

1 risk of the emergence of treatment-resistant mutant virus.

2 but not CLDN1, were infectable only with the mutant virus.

3 nd the infectivity of a class II IN deletion mutant virus.

4 genetically engineered CTL epitope-deficient mutant virus.

5 ouse studies show extreme attenuation of the mutant virus.

6 ored replication and virulence of the dNSP16 mutant virus.

7 in RAL IC50 than that of the IN-G140S/Q148H mutant virus.

8 s recruited in the airways compared with the mutant virus.

9 ited higher infectivity than either parental mutant virus.

10 dly diminished in cells infected with EBNA3A mutant virus.

11 the acquisition of transmissibility by this mutant virus.

12 liver in comparison to those produced by the mutant virus.

13 lial cells following infection with the UL78 mutant virus.

14 ntly decreased following reactivation of the mutant virus.

15 genes) or after infection with the DeltaICP0 mutant virus.

16 tly delayed in cells infected with the pUL25 mutant virus.

17 HA) mRNA nuclear export was seen with an NS1 mutant virus.

18 RNA in virions of wild-type, but not escape mutant, virus.

19 y to evaluate the antigenic phenotype of the mutant viruses.

20 athology following intranasal infection with mutant viruses.

21 multiple mutations were less fit than single-mutant viruses.

22 teracting with the MAbs, we generated escape mutant viruses.

23 d in cells infected with wild-type and ORF12 mutant viruses.

24 from mice infected with wild-type or glycan mutant viruses.

25 nds, the attenuated VACV was replaced by the mutant viruses.

26 e characteristics were unchanged for the two mutant viruses.

27 study, confirmed potency and selectivity of mutant viruses.

28 a dominant-negative, deacetylase-dead point mutant virus (AAV-HDAC3(Y298H)-v5), we found that select

29 press the DUB mutant and showed that the DUB mutant virus activated an earlier type I interferon resp

30 Thus, this mutant virus adapted to the loss of CLDN1 by developing

31 reated or IFN-treated cells infected by this mutant virus (AdEasyE1Sub19) contained much higher stead

32 we engineered a recombinant KSHV ORF52-null mutant virus and found that loss of ORF52 results in red

33 Using reverse genetics, we engineered Ubl mutant viruses and found that AM2 (V787S) and AM3 (V785S

34 g rates of wild-type virus, fitness costs of mutant virus, and growth rates of both viruses.

35 Since wt virions could not complement the mutant viruses, and the mutant viruses did not effective

36 and most viral gene expression of the L4-33K mutant virus are comparable to those of the wild-type vi

37 e not required for effective host control of mutant virus as all N1347A virus-infected mice survived

38 ectron microscopy to reveal that the gH-null mutant virus assembled and exited from cells normally, c

39 eceptor homolog, with the infectivity of one mutant virus being >500-fold less with the quail TVA rec

40 ers was associated with the selection of the mutant virus both in humans and in vitro.

41 ffectively attenuated the resulting SARS-CoV mutant viruses both in vitro and in vivo.

42 of PACT compromised IFN-I activation by the mutant virus, but not wild-type virus, a finding consist

43 ile in IFN-deficient Vero cells, both WT and mutant viruses can replicate at relatively high levels.

44 A mutant virus carrying a truncation deletion of the C-ter

45 us in virus-specific antiserum gives rise to mutant viruses carrying mutations A125T+A151T+L217Q in t

46 re explained in part by the observation that mutant viruses carrying NNRTI plus INSTI resistance muta

47 Characterization of mutant viruses carrying phenylalanine (Phe)-to-alanine (

48 Mutant viruses carrying substitutions at residue 145 sho

49 ated from lesions of animals inoculated with mutant virus contained mutations in the area of 3A that

50 The mutant viruses contained mutations in the hr1 region of

51 The mutant virus containing a substitution of Ala for Arg in

52 An LR mutant virus containing stop codons at the amino terminu

53 ing the latency-reactivation cycle because a mutant virus containing stop codons at the amino terminu

54 tal virus, SAT2/ZIM/7/83, indicated that the mutant virus containing the TQQS-to-ETPV mutation in the

55 In vitro susceptibility measurements with mutant viruses containing amino acid substitutions K70G,

56 infection of JCPyV by generating a panel of mutant viruses containing amino acid substitutions of th

57 ortant for these cellular processes and that mutant viruses containing mutations of CrPV-1A attenuate

58 in autophagic responses to wild-type or F17 mutant viruses could be detected, with autophagic activi

59 ication, as evidenced by the fact that their mutant viruses could not be rescued.

60 owth of a B1-deficient temperature-sensitive mutant virus (Cts2 virus) in U2OS osteosarcoma cells.

61 hree antibodies had neutralizing activity to mutant viruses deficient in gp41 carbohydrate attachment

62 ompare the phenotypes of an EBNA3A hypomorph mutant virus (Delta3A) and wild-type EBV.

63 of IFN-alpha/betaR-/- mice with the G50DblKo mutant virus demonstrated partial rescue of (i) acute vi

64 that recombinant E119D and E119A/D/G/-H274Y mutant viruses demonstrated reduced inhibition by all of

65 s; further, the recombinant T205-substituted mutant viruses described here would appear to be the fir

66 An infectious clone of one such mutant virus, designated rP11, appeared to be geneticall

67 nduced by infection with an E1B 19K deletion mutant virus did not repress macrophage proinflammatory

68 d not complement the mutant viruses, and the mutant viruses did not effectively inhibit wt gene expre

69 onotic potential; however, the wild-type and mutant viruses did not replicate to high titers in all i

70 Here we describe the creation of mutant viruses directly in the multicellular organism C.

71 ntly, compared with the wild-type virus, the mutant virus displayed a decreased capacity to infect an

72 In addition, these mutant viruses displayed an infection defect in monkey c

73 However, the drift mutant viruses displayed reduced stability, and we predi

74 This mutant virus does not require feces for stability at mos

75 re, we show that pro-necrotic murine CMV M45 mutant virus drives virus-induced necroptosis during non

76 the replication and pathogenesis of the DUB mutant virus (DUBmut) in cultured macrophages and in mic

77 We detected wild-type and single mutant viruses each possessing NA-F144C or NA-T342A in t

78 Viral growth of mutant virus encoding K229R, mimicking a non-acetylated

79 everely impaired compared to wildtype or the mutant viruses encoding K77R or K113R.

80 The HSV-1(F) gBDelta28syn mutant virus, encoding a carboxyl-terminal truncated gB,

81 TB reaction pharmacologically or by using a mutant virus enhanced or inhibited transmission, respect

82 In vitro, mutant viruses entered fibroblasts and epithelial cells

83 ere, we demonstrate that in U2OS cells, a B1 mutant virus escapes the block in DNA replication observ

84 its inoculated with either wtHTLV-2 or APH-2 mutant viruses established a persistent infection.

85 When transmitted, the mutant virus eventually reverted to the wild type in 2 o

86 HR mutant viruses exhibit impairments at several stages of

87 This mutant virus exhibited a delayed disease in cattle compa

88 In vivo, the NLR nonbinding F1L mutant virus exhibited an attenuated phenotype similar t

89 The mutant virus exhibited drastically reduced expression of

90 rus-infected controls, animals infected with mutant virus exhibited higher viral load in cerebrospina

91 Correspondingly, the ORF64 DUB active site mutant virus exhibited impaired ability to establish lat

92 The mutant virus exhibited two functional alterations as com

93 wer-fidelity W237I (W237I(LF)) and W237L(LF) mutant viruses exhibited lower ribavirin resistance.

94 These mutant viruses exhibited normal capsid morphology but we

95 erved in other cell types and, instead, this mutant virus exhibits impaired late protein accumulation

96 The DC480 mutant virus expressed full-size UL37 as detected by the

97 ble to produce infectious virus in DCs, this mutant virus expresses early and late genes.

98 A mutant virus expressing NCp15 shows greatly reduced infe

99 s or in the livers of infected mice, whereas mutant viruses expressing inactive VP3-CTD (H718A or H79

100 l of vIL-6 variants and utilization of HHV-8 mutant viruses expressing selected variants in phenotypi

101 However, unlike the wild-type virus, the mutant virus failed to enter into the axoplasm of gangli

102 Experimental infections with mutant viruses generated by using reverse genetics indic

103 mapping of the neutralizing mAbs via escape mutant virus generation revealed a shared binding epitop

104 Indeed, mutant virus genomes deficient for IE1 expression exhibi

105 In vaccinated animals, the GP85 mutant virus (GP85 DISC) induced an antibody response to

106 In both cell culture and mosquitoes, the mutant viruses grew equivalently and did not revert to w

107 The HA-K582I mutant virus had greater growth and virulence in DBA/2J

108 Patients infected with the H275Y mutant virus had higher day 28 mortality than others (80

109 Patients infected with the H275Y mutant virus had higher day-28 mortality than others (80

110 tinocytes infected with wild-type but not E7 mutant virus had perturbed transcriptional regulation of

111 In vitro, the mutant virus had reduced binding and infectivity in chol

112 Likewise, the RT-E138K plus IN-G140S/Q148H mutant virus had significantly greater fold increases in

113 Three of four escape mutant viruses had increased lethality in the DBA2/J mou

114 S/Q148H and the RT-E138K plus IN-G140S/Q148H mutant viruses had significantly greater fold increases

115 It reveals that the transmissible-mutant virus has a 200-fold preference for binding human

116 ximately 51-nucleotide contiguous subsegment mutant viruses having synonymous mutations revealed that

117 Consequently, the ratio of mutant virus in feces is reduced following additional cy

118 The same mutant virus in mice also enhanced virus replication and

119 s improved the fitness of the IN-G140S/Q148H mutant virus in the presence of raltegravir (RAL); the R

120 support spread of progeny virus was an HAdV3 mutant virus in which formation of PtDd was disabled (mu

121 e than WT viruses in vivo Replication of P50-mutant viruses in an APOBEC3-expressing stable cell line

122 that prevent reproduction and spread of the mutant viruses in human cells.

123 hout infection with either wild-type or ICP0 mutant viruses in human embryonic lung cells (HEL) or HE

124 n of viral siRNAs and rapid clearance of the mutant viruses in mice.

125 assessed the stability of the 18 recombinant mutant viruses in regard to their growth kinetics, antig

126 the HA stalk can lead to expansion of escape mutant viruses in study participants challenged with a 2

127 Our work reveals a defect of HR mutant viruses in the formation of viral replication cen

128 n gene expression elicited by the native and mutant viruses in the lungs of infected mice were determ

129 Co-culture of wild-type and mutant viruses in the presence of either a bNAb or human

130 Here, we constructed specific mutant viruses in which translation of D10 was prevented

131 Thus, the mutant virus incurs a fitness cost when environmental st

132 Point mutant viruses indicated that K90 is critical for the ne

133 On the other hand, the two mutant viruses induced lower STAT1 phosphorylation and g

134 The LR mutant virus induces higher levels of apoptotic neurons

135 However, E1B-55K mutant virus-infected cells became trapped in a mitotic-

136 the nucleus is severely compromised in UL92 mutant virus-infected cells, and mature virions are not

137 n the wild-type virus-infected cells and the mutant virus-infected cells.

138 reconstituted by plasmid transfection and in mutant virus-infected cells.

139 Immunofluorescence imaging of nsp15 mutant virus-infected macrophages revealed significant d

140 ages is dramatically increased during double-mutant virus infection and correlates with faster antivi

141 f UV treatment, lentivirus transduction, and mutant virus infection experiments, our results demonstr

142 ired to attenuate disease following PP1alpha-mutant virus infection.

143 e CTV, which correlated with invasion of the mutant virus into the immature xylem tracheid cells and

144 onstrate that the phenotype of an Ad5 L4-33K mutant virus is complex.

145 Even though the mutant virus is heat resistant, it is susceptible to ina

146 mice with WT or AM2 virus and found that the mutant virus is highly attenuated, yet it replicates suf

147 Although the mutant virus is no longer able to propagate by extracell

148 Analysis of temperature-sensitive (ts) mutant viruses is a classic method allowing researchers

149 can partially complement a growth-defective mutant virus lacking both UL21a and UL97, with significa

150 A mutant virus lacking the mu2 ITAM activates NF-kappaB le

151 es similar to those in cells infected with a mutant virus lacking the UL37x1 gene, subUL37x1.

152 a novel approach that employs HCMV deletion mutant viruses lacking HLA class I immunoevasins and all

153 Mutant viruses lacking hydrolase activity were unable to

154 deletions in the CT, we were able to rescue mutant viruses lacking two or four residues (rDelta2 and

155 3 inhibitor, GSK872, and infection with this mutant virus led to phosphorylation and aggregation of M

156 restore infectivity to maturation-defective mutant viruses led us to hypothesize that SP may play an

157 Mutant viruses locked in either state remain competent t

158 Additionally, most of the mutant viruses lost the capacity to escape MxA restricti

159 Surprisingly, the A77V mutant virus maintained the ability to replicate in mono

160 dilated cardiomyopathy, suggesting that such mutant viruses may be the forms responsible for persiste

161 asmid (McKbac) and utilized to construct the mutant virus McK(gKDelta31-68), carrying a 37-amino-acid

162 viruses, we found that APOBEC3 restricts the mutant viruses more than WT viruses in vivo Replication

163 Upon rescue of 21 mutant viruses, most substitutions in the receptor bindi

164 of mice with the macrodomain catalytic point mutant virus (N1347A) resulted in reductions in lethalit

165 A mutant virus, named Ban/AF, was developed in which the v

166 iii) that in cells infected with a DeltaICP0 mutant virus, Nectin-1 remained on the cell surface.

167 -KO Huh-7.5 cells supported infection by the mutant virus only when CLDN1, CLDN6, or CLDN9 was expres

168 Purified PA-X mutant virus particles displayed an increased ratio of h

169 The defects in assembly of gE(-) US9(-) mutant virus particles were novel because they were neur

170 Late-domain mutant virus particles were seen at the uropod in form o

171 In all cases, the mutant virus particles, as well as the antibody-bound wi

172 In vivo, both WT and F1/F2 mutant viruses persistently infected mice, although F1,

173 C terminus of the V gene in PIV5 results in mutant viruses (PIV5DeltaSH and PIV5VDeltaC) that enhanc

174 However, in cells infected with this mutant virus, PML formed novel track-like structures tha

175 A mutant virus possessing both the NA-F144C and NA-T342A m

176 protect mice against lethal challenge of the mutant viruses, possibly owing to its ability to mediate

177 veolar lavage fluid after infection with the mutant virus PR8 A/NS1-Y89F (PR8 Y89F) when compared wit

178 ar clone JFH-1, thereby producing a range of mutant viruses predicted to possess altered RNA secondar

179 Although the DeltaUS17 mutant virus produced numbers of infectious particles in

180 These mutant viruses produced smaller foci of infection in Ver

181 The L4-33K mutant virus produces only empty capsids, indicating a d

182 ing of this mutant confirmed the presence of mutant virus protein in the transfected BHK cell lysate.

183 Of the 14 single and double mutant viruses recovered in the backbone of pH1N1, four

184 he -3 position was found to be important for mutant virus recovery.

185 The mutant viruses remained susceptible to favipiravir.

186 The mutant viruses replicate poorly in the brains of infecte

187 The mutant virus replicated similarly to the wild type in vi

188 npermissive for VACV; however, wild-type and mutant viruses replicated in triple-KO cells in which RN

189 Although parental and mutant viruses replicated somewhat better in ducks than

190 The efficiency of mutant virus replication was similar to that of wild-typ

191 verexpressing P50 in this cell line enhanced mutant virus replication.

192 Infection with the mutant virus resulted in a significant decrease in viral

193 -resistant C57BL/6 mice with a CrmD deletion mutant virus resulted in uniform mortality due to excess

194 Interestingly, the mutant virus retained partial PF74 binding, and its repl

195 Further characterization of the mutant viruses revealed differences in particle morpholo

196 Analysis of revertant SL-1 mutant viruses revealed that a compensatory mutation in

197 isolate with a US17 deletion (the DeltaUS17 mutant virus) revealed blunted host innate and interfero

198 context of cells infected with wild-type or mutant virus, reversing the charge of these two residues

199 However, in the majority of the animals, the mutant virus reverted back to the wild-type sequence, he

200 Strikingly, glyco-Gag mutant virus reverted to glyco-Gag-containing virus only

201 ately twice as many upregulated genes in the mutant virus samples by 48 h postinfection, despite iden

202 dicating that cells infected with a UL97-L1m mutant virus show no defects in growth or E2F-responsive

203 to the wild-type virus, the ToV-PLP knockout mutant virus showed impaired growth and induced higher e

204 Although the mutant virus showed slightly decreased replication in mi

205 restingly, in mice the neutralization escape mutant viruses showed either attenuation (Urbani backgro

206 All mutant viruses showed reduced sensitivity to sCD4 and CD

207 Upon infection of guinea pigs, the RNase mutant viruses stimulate strong IFN responses, fail to r

208 The recombinant A/Puerto Rico/8/34 (rPR8) mutant virus strain was attenuated and caused reduced mo

209 uation to generate W7-791, a live attenuated mutant virus strain.

210 , and RFC5 mRNAs also enhanced spread of the mutant virus, strengthening the biological significance

211 , amantadine and rimantadine, while the S31N mutant viruses, such as the pandemic 2009 H1N1 (H1N1pdm0

212 ters in the brains of mice infected with the mutant virus suggest that the alphavirus TF protein is i

213 a clinically relevant dolutegravir resistant mutant virus suggesting potential clinical benefits for

214 escued the virulence of the PP1alpha-binding mutant virus, suggesting an IFN-independent role for eIF

215 lls infected with a newly isolated UL32-null mutant virus, suggesting that UL32 acts as a chaperone c

216 le in cells infected with E1B-55K or E4-ORF6 mutant viruses, suggesting that Ad regulates paralog-spe

217 teraction did not affect the HA titer of the mutant viruses, suggesting that the same amount of viral

218 The mutant virus tended to predominate over the WT in mouse

219 of the wild-type virus with all the p24(CA) mutant viruses tested.

220 We developed a FMDV mutant virus that could not bind DCTN3.

221 y as the wild-type virus; however, the smD1' mutant virus that does not express NS2 and NS4 underwent

222 Importantly, the smA1' mutant virus that does not express NS3 and NS4 replicate

223 ine expressing A30.5, we isolated a deletion mutant virus that exhibits a defect in morphogenesis in

224 g its performance in samples infected with a mutant virus that fails to block transcription terminati

225 Intriguingly, a TAg mutant virus that is unable to activate the DDR causes s

226 When exposed to CD11(+) DCs, the mutant virus that lacks the amino terminus of gamma134.5

227 ere, by using the previously described Q129H mutant virus that selectively lacks DNase activity but r

228 Although the G147R NA receptor-binding mutant virus that we characterize is a laboratory creati

229 Using mutant viruses that are defective for nuclear entry, we

230 become functionally exhausted or select for mutant viruses that escape T cell recognition.

231 In addition, we found that mutant viruses that express an unstable form of the UL10

232 mutant, wild-type, and HA-H241Q and HA-K582I mutant viruses that have HA activation pH values of 6.3,

233 We created mutant viruses that incorporate most of the approximatel

234 Growth analyses of mutant viruses that lack each individual miRNA revealed

235 h wild-type H18N11 leads to the emergence of mutant viruses that lack the N11 ectodomain and acquired

236 of action of these inhibitors, we generated mutant viruses that were resistant to the inhibitory eff

237 o AD-5 and neutralization activity toward gB mutant viruses that were similar to those of AD-5-specif

238 However, DC480 mutant virus titers increased nearly 20-fold when the vi

239 increases neutralization sensitivity of the mutant virus to CD4 binding site (CD4bs)-directed antibo

240 We generated and characterized an Ad5 L4-33K mutant virus to further explore its function(s) during i

241 V reverse genetics, we generated a series of mutant viruses to define the contributions of macrodomai

242 dergo continual antigenic evolution allowing mutant viruses to evade host immunity acquired to previo

243 stigate the potential threat of serum escape mutant viruses to humans and poultry, the impact of thes

244 MDC-mediated capture and transmission of MA mutant viruses to T cells were decreased, suggesting tha

245 antly, we show that the macrodomain and PLP2 mutant viruses trigger production of type I interferon i

246 t of WT virus revealed that the destabilized mutant virus triggered the upregulation of more host gen

247 Here, we characterize a UL93 stop mutant virus (UL93st-TB40/E-BAC) to demonstrate that the

248 These findings may explain why ORF75c mutant viruses unable to degrade PML had no demonstrable

249 We observed that each individual escape mutant virus was able to avoid neutralization by its res

250 MHV68 G50DblKo virus demonstrated that this mutant virus was able to establish latency in the spleen

251 AR1-sufficient CON(kd) cells, only the C(ko) mutant virus was an effective inducer and the IFN-beta R

252 A conditional lethal mutant virus was constructed by placing the A19 open rea

253 The mutant virus was debilitated in primary T cells and macr

254 DV1 was lethal, since no replication of the mutant virus was detected in human cells.

255 When the UL92 mutant virus was evaluated, function was fully complemen

256 nce of EFV, the RT-E138K plus IN-G140S/Q148H mutant virus was fitter than one with the RT-E138K mutat

257 2J mice than the wild type did, although the mutant virus was highly attenuated in ducks.

258 The HA-Y231H mutant virus was highly susceptible to acid inactivation

259 Moreover, the replication of the mutant virus was markedly impaired in activated primary

260 The higher-fidelity W237F (W237F(HF)) mutant virus was more resistant to the mutagenic nucleos

261 ependent on the viral protein NSs, as an NSs mutant virus was not found to induce the equivalent sign

262 Replication of the mutant virus was restored by pseudoreversion (A287V) or

263 An ns2 mutant virus was unable to replicate in the liver or ind

264 ingle-cycle (DISC) vaccine strategy, a GPCMV mutant virus was used that lacked the ability to express

265 at the membrane fusion step, and while this mutant virus was viable, it was significantly attenuated

266 n cytoplasmic virion envelopment, a cadre of mutant viruses was constructed and characterized.

267 istance mutations on the fitness of RT-Y181C mutant viruses was observed.

268 the replication of the S224A and S224A/T226A mutant viruses was reduced in cell culture and in vivo.

269 onoclonal antibody inhibition and a deletion mutant virus, we demonstrate that the KSHV virion glycop

270 Using a miR-H2-deficient mutant virus, we found no evidence that miR-H2 represses

271 By studying A6 mutant viruses, we found that A6 plays an essential role

272 verity and lethality caused by the different mutant viruses, we have identified specific residues loc

273 ncing of cyclophilin A (CypA), as well as CA mutant viruses, we implicated CypA in the SUN2-imposed b

274 By engineering mutant viruses, we showed caspase cleavage at this site

275 Levels of mutant virus were dramatically reduced upon amplificatio

276 rse transcription reactions of the glyco-Gag mutant virus were substantially inhibited compared with

277 als, whereas the NA-T342A and NA-F144C/T342A mutant viruses were detected in the nasal turbinates, in

278 of the F proteins expressed by the recovered mutant viruses were efficiently cleaved and transported

279 The resulting mutant viruses were evaluated in tissue culture and in m

280 While the UL15, UL32, and UL54 mutant viruses were fully susceptible to raltegravir, an

281 In the absence of drug, single-mutant viruses were less fit than the wild type; viruses

282 24)LL3D(YR) and double A(24)LL3B(PVKV)3D(YR) mutant viruses were markedly attenuated upon inoculation

283 although the fitness characteristics of the mutant viruses were not fully defined.

284 tly infected mice, although F1, F2 and F1/F2 mutant viruses were rapidly eliminated 1-7 days post-ino

285 Both P480A and R482A mutant viruses were rescued, grew similarly to wild-type

286 Both mutant viruses were significantly less dependent on SR-B

287 Instead, these mutant viruses were unable to expose VP2 upon arrival to

288 cine, based on a replication-defective HSV-2 mutant virus, which has been recently tested in clinical

289 address this question, we took advantage of mutant viruses whose viral entry into cells relies on th

290 A mutant virus with deletion of NS1 induced high levels of

291 An LR mutant virus with stop codons at the amino terminus of O

292 An LR mutant virus with stop codons at the amino terminus of t

293 Mutant viruses with increased frameshift efficiencies ha

294 cal for the induction of T-cell lymphomas as mutant viruses with precise deletions were significantly

295 We demonstrated that mutant viruses with RBS deletions are able to escape pol

296 NY99 or Eg101 strain (NY-WT or EgCME-WT) and mutant viruses with substitutions of amino acid 159 of t

297 Competitive growth of the escape mutant viruses with the wild-type virus revealed that so

298 in the viral polymerase (L protein) of most mutant viruses, with the vast majority of the amino acid

299 e the wild-type virus, it can also bind to a mutant virus without inhibiting fusion or attachment.

300 Surprisingly, ICP0-null mutant virus yields decreased upon TRIM27 depletion, arg