ライフサイエンスコーパス: neurovirulence

1 tures associated with HIV-1 neurotropism and neurovirulence.

2 ents leads to reversions that increase virus neurovirulence.

3 tructural coding regions contributed to AR86 neurovirulence.

4 e noncoding control region are necessary for neurovirulence.

5 the central nervous system and in increased neurovirulence.

6 the spike are also important in determining neurovirulence.

7 ibit OL differentiation, irrespective of MLV neurovirulence.

8 ), which were essential for AR86 adult mouse neurovirulence.

9 t Sindbis virus background confers increased neurovirulence.

10 aky-late (VP16) promoter exhibited wild-type neurovirulence.

11 ace of neural cells, contributing to greater neurovirulence.

12 res nPTB binding, translation initiation and neurovirulence.

13 s that has been selected in vivo for extreme neurovirulence.

14 f the Fr98 envelope gene are associated with neurovirulence.

15 s nonstructural protein genes in adult mouse neurovirulence.

16 TMEV) is divided into two subgroups based on neurovirulence.

17 l and sufficient for complete attenuation of neurovirulence.

18 tutions were engineered and tested for mouse neurovirulence.

19 ell-specific translational control and viral neurovirulence.

20 ficantly reduced virus neuroinvasion but not neurovirulence.

21 o directly address the role of the S gene in neurovirulence.

22 t these differences appear to correlate with neurovirulence.

23 plays an important role in conferring mouse neurovirulence.

24 sFrKP41 (KP41), which differ dramatically in neurovirulence.

25 macrophages in other tissues underlies HIV-1 neurovirulence.

26 he attenuation of vesicular stomatitis virus neurovirulence.

27 reatest effect on early viremia kinetics and neurovirulence.

28 identification of molecular determinants of neurovirulence.

29 ys, in DEN2 E as being responsible for mouse neurovirulence.

30 ucidating the molecular basis of mumps virus neurovirulence.

31 ection of neural cells, thereby facilitating neurovirulence.

32 replicative pathway contribute to increased neurovirulence.

33 ediated arrest of both viral replication and neurovirulence.

34 mbrane portion of envelope and/or nef confer neurovirulence.

35 al functional interactions influencing HSV-2 neurovirulence.

36 Oral poliovirus vaccine can mutate to regain neurovirulence.

37 E Env glycosylation features could influence neurovirulence.

38 the neurological signs observed during H5N1 neurovirulence.

39 ed host, which is required for full reovirus neurovirulence.

40 n processes involved in neuroattenuation and neurovirulence.

41 as the gE/gI interaction is critical for VZV neurovirulence.

42 innate immune responses and thereby enhance neurovirulence.

43 suggesting an immunopathogenic component to neurovirulence.

44 V can be classified into two groups based on neurovirulence: a highly virulent group, e.g., GDVII vir

45 in the RABV glycoprotein had greatly reduced neurovirulence after intracerebral inoculation in suckli

46 been used successfully in the past to reduce neurovirulence and abolish neuroinvasiveness of TBEV, na

47 SARS-CoV protein 6 increases MHV neurovirulence and accelerates MHV infection kinetics in

48 tor of IFN genes (STING) exhibit exacerbated neurovirulence and atypical lymphotropic dissemination o

49 tion, oral polio vaccine (OPV) can revert to neurovirulence and cause paralytic poliomyelitis.

50 p V of the 5'-non-coding region (NCR) reduce neurovirulence and cell-specific cap-independent transla

51 To study the role of these mutations in neurovirulence and demyelination, we prepared a recombin

52 f the rVSV genome, vectors that have reduced neurovirulence and enhanced immunogenicity can be made.

53 Thus, the RBD determined both neurovirulence and folding instability.

54 The levels of neurovirulence and immunogenicity of the chimeric viruse

55 lymphoblasts at a sequence essential for JCV neurovirulence and in cerebrospinal fluid of immunosuppr

56 In parallel with increased neurovirulence and increased viral replication, Sindbis

57 types were confirmed, another determinant of neurovirulence and its molecular basis was characterized

58 sal infection of two HPAI strains of varying neurovirulence and lethality.

59 y attenuated in the skin and yet retains its neurovirulence and may reactivate and damage sensory neu

60 39ns1, demonstrated significantly increased neurovirulence and morbidity, including weight loss and

61 tant of BHV-5 displayed a wild-type level of neurovirulence and neural spread in the olfactory pathwa

62 ecular basis for the observed differences in neurovirulence and neuroattenuation, the complete genome

63 R altered virus neuroinvasiveness, decreased neurovirulence and neuroinflammatory responses, and prev

64 9 deletion recombinant was generated and its neurovirulence and neuroinvasive properties were compare

65 ture and pathogenic properties, particularly neurovirulence and neuroinvasiveness for SCID mice, gene

66 e derivative, strain E5, exhibit significant neurovirulence and neuroinvasiveness in normal mice, alb

67 -5 Us9-deleted virus but conferred increased neurovirulence and neuroinvasiveness in our rabbit seizu

68 ells, with the E138K mutation abrogating the neurovirulence and neuroinvasiveness of Japanese encepha

69 pairs of Sindbis virus variants differing in neurovirulence and neuroinvasiveness were derived by lim

70 erent risk of the Sabin strains to revert to neurovirulence and reacquire greater transmissibility th

71 (HSV-1) ICP34.5 protein strongly influences neurovirulence and regulates several cellular antiviral

72 tion of the HIV envelope and viral clades to neurovirulence and residual virus replication in the CNS

73 strongly suggest that (i) the phenotypes of neurovirulence and spontaneous reactivation are separabl

74 These studies unveil determinants of neurovirulence and stability in Japanese encephalitis vi

75 attenuated recombinant viruses show reduced neurovirulence and that peripheral immunization blocks t

76 for the spike gene, differ in the extent of neurovirulence and the ability to induce demyelination.

77 1)Sabin were assessed, a correlation between neurovirulence and the ability to replicate in primary h

78 Further tests in mice demonstrated high neurovirulence and the age-dependent neuroinvasiveness o

79 Such derivative viruses often have increased neurovirulence and transmissibility, and in some cases t

80 gK 8mer treatment also increased viral neurovirulence and viral induced CS in ocularly infected

81 tural proteins are important contributors to neurovirulence and viral tissue tropism.

82 Here, we describe the attenuation, neurovirulence, and immunogenicity of rVSV vectors expre

83 of these amino acid changes in neurotropism, neurovirulence, and neuroattenuation is discussed.

84 tragenic suppressor mutation does not affect neurovirulence; and (iii) the attenuated gamma34.5 mutan

85 pe 1 (HSV-1) mutants that are attenuated for neurovirulence are being used for the treatment of cance

86 isms by which these amino acid changes alter neurovirulence are not known.

87 9 reversion caused a significant increase in neurovirulence as determined by the 50% lethal dose and

88 When tested in our rat neurovirulence assay against the respective parental str

89 vitro demonstrate a partial recovery of the neurovirulence associated with HSV-1; and (ii) vvD54-M00

90 e gene, MyD116, and the herpes simplex virus neurovirulence-associated gene, ICP34.5.

91 ghlighting a potential strategy to develop a neurovirulence-attenuated vaccine against chickenpox and

92 Recently, high levels of neurovirulence attenuation were achieved with geneticall

93 l nonstructural genes (except 3B) of the low-neurovirulence BeAn virus strain for cell death.

94 a mutation at residue 103(Lys) had decreased neurovirulence but did induce demyelination.

95 major role in determining organ tropism and neurovirulence but that other genes also play important

96 ropism and suggest that a strategy to reduce neurovirulence by deleting gI could prolong active infec

97 he genetic basis of MuV neuroattenuation and neurovirulence by generating a series of recombinant vir

98 s the first viral protein shown to influence neurovirulence by inhibiting CD8+ T cell protection.

99 CP34.5 (ICP, infected cell protein) enhances neurovirulence by negating antiviral functions of the IF

100 Neurovirulence can be attenuated by point mutations or b

101 In a standardized test for neurovirulence, ChimeriVax-JE and YF-Vax were compared i

102 lone, ps51, was significantly attenuated for neurovirulence compared to that derived from ps55.

103 The low-neurovirulence DA strain uses sialic acid as a corecepto

104 solution of the crystal structure of the low-neurovirulence DA virus in complex with the sialic acid

105 llustrate that (i) the protein synthesis and neurovirulence defects observed in gamma34.5 mutant viru

106 One neurovirulence determinant mapped to the N-terminal port

107 ama virus, four of which are predicted to be neurovirulence determinants based on various sequence co

108 em for investigating the molecular basis for neurovirulence determinants encoded within the JE E prot

109 estigate ZIKV-host interactions and identify neurovirulence determinants of ZIKV.

110 iral genome that correlate with the level of neurovirulence determined by the monkey neurovirulence t

111 es a potential mechanism for modulating TMEV neurovirulence during persistence in the mouse central n

112 nce of markers of virus neuroattenuation and neurovirulence, ensuring mumps vaccine safety has proven

113 of the MV genome which are required for full neurovirulence equivalent to CAM/RB.

114 Our data show that HSV-1 0DeltaNLS lacks neurovirulence even in highly immunocompromised mice lac

115 ta indicate that the MuV SH protein is not a neurovirulence factor and highlight the importance of di

116 mplex virus 1 (HSV-1) defective in the viral neurovirulence factor infected cell protein 34.5 (ICP34.

117 lence the expression of ICP34.5, a key viral neurovirulence factor, and that miR-III is able to silen

118 ression of lytic cycle genes (especially the neurovirulence factor, ICP34.5) and suggest a mechanism

119 utions lie outside the coding region for the neurovirulence factor, ICP34.5.

120 is blocked completely when viruses lack the neurovirulence factor, infected cell protein 34.5, or wh

121 90% of the ORF encoding ORF-34.5, a putative neurovirulence factor, which is transcribed from the opp

122 f the HSV gamma(1)34.5 gene, which encodes a neurovirulence factor.

123 neurotropism through ICP34.5, a major viral neurovirulence factor.

124 I reduces expression of ICP34.5, a key viral neurovirulence factor.

125 hat has a nearly 1 million-fold reduction in neurovirulence following intracerebral (i.c.) inoculatio

126 Even though LGT has low-level neurovirulence for humans, it, and its more attenuated e

127 sage of dengue and YF viruses have increased neurovirulence for mice but reduced viscerotropism for h

128 and 172 in the E2 glycoprotein determine the neurovirulence for mice of different ages and the effici

129 ve isolates of each lineage showed increased neurovirulence for PVR-Tg21 transgenic mice.

130 uroblastoma cells and reduced its peripheral neurovirulence for SCID mice.

131 ted herpes simplex virus lacking its ICP34.5 neurovirulence gene (HSVDelta34.5).

132 The herpes simplex virus type 1 (HSV-1) neurovirulence gene encoding ICP34.5 controls the autoph

133 ut this response is antagonized by the HSV-1 neurovirulence gene product, ICP34.5.

134 EV) consist of two groups, the high- and low-neurovirulence groups, based on lethality in intracerebr

135 afety test with which to measure mumps virus neurovirulence has also hindered analysis of the neuropa

136 del that mimics systemic DEN disease without neurovirulence has been an obstacle, but DENV-2 models t

137 of cluster-specific reversions could confer neurovirulence; however, residue 138 of the E protein (E

138 roteins of Sindbis virus have been linked to neurovirulence; however, the molecular mechanisms by whi

139 dies have mapped an important determinant of neurovirulence in adult mice to a single amino acid chan

140 protein 1 (nsP1) 538 that is associated with neurovirulence in adult mice.

141 oral poliovirus vaccine (OPV) is tested for neurovirulence in animals and also for the presence of n

142 els can serve as a host determinant of viral neurovirulence in C57BL/6 mice, reflecting the direct in

143 102/103 in an sPV1(M) background restored wt neurovirulence in CD155 transgenic (tg) mice and suppres

144 le genetically and phenotypically, including neurovirulence in CD155 transgenic mice, the large major

145 for poliovirus recombinants with attenuated neurovirulence in experimental animals that corroborate

146 ble molecular mechanisms of enhanced B virus neurovirulence in humans, which results in an 80% mortal

147 e virus, the ICP47- mutant expressed reduced neurovirulence in immunologically normal mice, and T cel

148 g1 vectors demonstrated dramatically reduced neurovirulence in mice following direct intracranial ino

149 However, the ICP47- mutant exhibited normal neurovirulence in mice that were acutely depleted of CD8

150 valuated for growth in cultured cells or for neurovirulence in mice.

151 s virus (SV) is a critical determinant of SV neurovirulence in mice.

152 ess, TBEV/DEN4Delta30 virus exhibited higher neurovirulence in monkeys than either LGTV or YF 17D, su

153 e primary target of MeV infection, abrogates neurovirulence in neonatal H-2(d) congenic C57BL/6 mice.

154 ited replication in C6/36 cells, and lack of neurovirulence in newborn ICR mice.

155 use of this vaccine candidate in humans, its neurovirulence in nonhuman primates needed to be evaluat

156 ed for clinical evaluation when assessed for neurovirulence in nonhuman primates.

157 rhinovirus type 2 resulted in attenuation of neurovirulence in primates.

158 is a determinant of Sindbis virus growth and neurovirulence in suckling mice as well as persistent in

159 ese results suggest that the determinants of neurovirulence in the envelope gene may influence the ef

160 ls that may not allow accurate prediction of neurovirulence in the human host.

161 phalitis virus/dengue virus) abolished virus neurovirulence in the mature mouse CNS.

162 dues as virus-specific determinants of mouse neurovirulence in this chimeric system.

163 beta in the brain represents a correlate of neurovirulence in this disease, whereas the TNF response

164 plays an important role in cell tropism and neurovirulence in vivo.

165 x virus type 1 (HSV-1) is required for viral neurovirulence in vivo.

166 an neuronal cells, exhibited increased mouse neurovirulence in vivo.

167 y for replication (neurotropism) and damage (neurovirulence) in the brain and an 88-1961 wild-type vi

168 -specific propagation deficit and eliminates neurovirulence inherent in poliovirus without affecting

169 any aspects of viral pathogenesis; promoting neurovirulence, inhibiting interferon-induced shutoff of

170 ike gene, we have previously shown that high neurovirulence is associated with the JHM spike protein,

171 Neurovirulence is determined by the sequence of the vira

172 Neurovirulence is determined by the sequence of the vira

173 heterokaryon analyses revealed that loss of neurovirulence is due to trans-dominant repression of PV

174 This difference in neurovirulence is not the complete explanation for the f

175 molecular and cellular basis of coronavirus neurovirulence is poorly understood.

176 tigate a possible role for HE in MHV-induced neurovirulence, isogenic recombinant MHV-A59 viruses wer

177 in primary neuronal cultures, the increased neurovirulence it conferred may be due in part to the in

178 L/ST-4BS was completely attenuated for neurovirulence (LD50 > 10(6) PFU) relative to wild-type

179 relationship between macrophage tropism and neurovirulence, macaques were inoculated with two recomb

180 nants of simian immunodeficiency virus (SIV) neurovirulence map to the env and nef genes.

181 alysis of the Cas-Br-E genome indicates that neurovirulence maps to the env gene, which encodes the s

182 Since neurovirulence may be determined at the early stages of

183 These findings suggest that coronavirus neurovirulence may depend on a novel discriminatory abil

184 nse silent transmission, whereas the reduced neurovirulence may have contributed to the absence of pa

185 oliovirus vaccine strain, known to attenuate neurovirulence, may further restrict tropism by eliminat

186 The increased neurovirulence mediated by the virus encoding glycine at

187 tified sites in the LGT genome that promoted neurovirulence/neuroinvasiveness.

188 However, when tested in a stringent NHP neurovirulence (NV) model, this vector was not adequatel

189 EV SA14-14-2 E protein, as shown by the high neurovirulence of an analogous YFV/JEV Nakayama chimera

190 n vivo relationship between hsp72 levels and neurovirulence of an hsp72-responsive virus using the mo

191 r-normal trigeminal ganglion replication and neurovirulence of an ICP34.5 mutant in IFN-alpha/betaR-/

192 , CD8+ T cell depletion did not increase the neurovirulence of an unrelated, attenuated HSV-1 glycopr

193 of the gE epitope significantly reduced the neurovirulence of BHV-5 in rabbits.

194 (HS) as an attachment receptor increases the neurovirulence of cell culture-adapted strains of Sindbi

195 We investigated the genetic basis of mouse neurovirulence of dengue virus because it might be direc

196 this interaction contributes to the extreme neurovirulence of EEEV.

197 eduction in viral replication and associated neurovirulence of HSV.

198 Here, we demonstrate that the high neurovirulence of JHM is associated with accelerated spr

199 oprotein GP2 has been shown to attenuate the neurovirulence of JUNV in suckling mice.

200 In contrast, the neurovirulence of LGTV exhibited the reverse profile, pr

201 is likely an important factor in the severe neurovirulence of MHV-JHM in wild-type mice.

202 n animal model that can reliably predict the neurovirulence of mumps virus vaccine candidates in huma

203 immune recognition because a decrease in the neurovirulence of mutant viruses was observed in neonata

204 We now show that attenuation of neurovirulence of PV/HRV2 chimeras is not confined to CD

205 Neurovirulence of several mumps virus strains was assess

206 s than for the parental GDVII virus, and the neurovirulence of the adapted virus in intracerebrally i

207 ne envelope residues were found to influence neurovirulence of the Friend murine polytropic retroviru

208 The reduced neurovirulence of the ICP47- mutant was due to a protect

209 Neurovirulence of the mutant virus was determined in a t

210 iated three amino acid changes with enhanced neurovirulence of the neuroadapted vaccine strain: one e

211 se and three amino acid changes with reduced neurovirulence of the neuroattenuated wild-type strain:

212 a significant (P = 0.031) difference in the neurovirulence of the two recombinants.

213 rvous system (CNS) enables alteration of the neurovirulence of the virus and control of the neuropath

214 We found that the level of neurovirulence of the virus correlates with its differen

215 anslation initiation, and attenuation of the neurovirulence of the virus without a marked effect on v

216 ese modifications also affected the residual neurovirulence of the virus, but it remained immunogenic

217 he capsid-specific mutations strongly affect neurovirulence of the virus.

218 The neurovirulence of these "spongiogenic retroviruses" is d

219 The relative human neurovirulence of these strains was proportional to the

220 ue sections indicated that the variations in neurovirulence of these viruses could not be explained b

221 The neurovirulence of these viruses has long been known to b

222 Deletion of gamma134.5 greatly decreases the neurovirulence of this mutant virus but also reduces its

223 ain, and may be a key reason for the greater neurovirulence of TSE prions relative to many other auto

224 The increased neurovirulence of vaccine derivatives has been known sin

225 These results suggest that the decreased neurovirulence of VarK may be due to its failure to effi

226 The neurovirulence of VSV in animal models requires the atte

227 nts of HRV2 and FMDV severely attenuated the neurovirulence of VSV without perturbing its oncolytic p

228 nize/evade immune responses, and the extreme neurovirulence of wild-type NA-EEEV may be a consequence

229 o determine those structures responsible for neurovirulence (or attenuation) of these chimeric viruse

230 infections may contribute to the adult mouse neurovirulence phenotype of S.A.AR86.

231 s responsible for the observed change of the neurovirulence phenotype.

232 dicate that the assay correctly assesses the neurovirulence potential of mumps viruses in humans and

233 rat model may prove useful in evaluating the neurovirulence potential of new live, attenuated vaccine

234 We describe here the neurovirulence properties of a herpes simplex virus type

235 Neurovirulence properties of these recombinant viruses w

236 We aimed to characterize antigenic and neurovirulence properties of WPV1-SOAS silently circulat

237 r of potentially causal genes, including the neurovirulence protein ICP34.5 (RL1).

238 virus 1 (HSV-1) encodes the multifunctional neurovirulence protein ICP34.5.

239 y is antagonized by the herpes simplex virus neurovirulence protein, ICP34.5.

240 ave indicated that sequences responsible for neurovirulence reside within the env gene.

241 sociated with persistent virus and increased neurovirulence, RJHM(N514S) was not more virulent than t

242 ines have neurovirulent properties, a monkey neurovirulence safety test (MNVT) is performed.

243 tates, to test a novel rat-based mumps virus neurovirulence safety test.

244 A trend of higher neurovirulence scores was observed in monkeys inoculated

245 Low- but not high-neurovirulence strains use sialic acid as an attachment

246 gy data from an exploratory nonhuman primate neurovirulence study indicated that some of these attenu

247 irus strains was assessed in a prototype rat neurovirulence test and compared to results obtained in

248 SH protein (rMuVDeltaSH) are attenuated in a neurovirulence test using newborn rat brains and may be

249 nt DEN virus tetravalent vaccine in a formal neurovirulence test, as well as its protective efficacy

250 ompared to that of YF-VAX in a formal monkey neurovirulence test.

251 d compared to results obtained in the monkey neurovirulence test.

252 l of neurovirulence determined by the monkey neurovirulence test.

253 st national regulatory organizations require neurovirulence testing of virus seeds used in the produc

254 , NB15a did not differ from YF5.2iv in mouse neurovirulence testing, based on mortality rates and ave

255 s and CD155 receptor-specific antibodies and neurovirulence tests in CD155 transgenic mice confirmed

256 etic elements that contribute to adult mouse neurovirulence, the neurovirulent Sindbis virus strain A

257 The high-neurovirulence Theiler's murine encephalomyelitis virus

258 Infection of susceptible mice with the low-neurovirulence Theiler's murine encephalomyelitis virus

259 The low-neurovirulence Theiler's murine encephalomyelitis viruse

260 the sequence of the envelope gene determines neurovirulence, this effect appears to operate through a

261 that M1-D macrophages infected with the low-neurovirulence TMEV BeAn virus became apoptotic through

262 In this study, we demonstrate that the high-neurovirulence TMEV GDVII virus uses the glycosaminoglyc

263 Low-neurovirulence TMEV result in a persistent central nervo

264 5 mutation in the suppressor mutant restores neurovirulence to wild-type levels.

265 stinct clusters were required to restore the neurovirulence typical of the YFV/JEV Nakayama virus.

266 Neurovirulence was assayed in a mouse model for MV encep

267 surveillance isolates were sequenced, their neurovirulence was determined using transgenic mouse exp

268 fectious particles yielded virus whose mouse neurovirulence was highly attenuated.

269 the contribution of nsP1 Thr 538 to S.A.AR86 neurovirulence was provided by experiments in which a th

270 enetic basis of mumps virus neurotropism and neurovirulence was until recently not understood, largel

271 e only feature that correlated with relative neurovirulence was viral burden as measured by both vira

272 s system (CNS) infection that correlate with neurovirulence, we compared two neurovirulent MuLV, Fr98

273 To identify the molecular determinants of neurovirulence, we constructed an infectious simian immu

274 this hyperactive membrane fusion activity in neurovirulence, we discovered that the growth of JHM in

275 To investigate how histidine confers neurovirulence, we examined the various stages of the vi

276 better understand the determinants of HIV-1 neurovirulence, we isolated viruses from brain tissue sa

277 andidate host genes that modulate alphavirus neurovirulence, we utilized GeneChip Expression analysis

278 No differences in neurovirulence were seen between the wild-type and the S

279 ruses passaged in vivo demonstrate decreased neurovirulence, whereas those passaged in vitro demonstr

280 aviruses attenuates S.A.AR86 for adult mouse neurovirulence, while introduction of Thr at position 53

281 viruses (mouse hepatitis virus) of different neurovirulences with primary cell cultures of brain immu

282 is important for efficient neural spread and neurovirulence within the CNS and could not be replaced