ライフサイエンスコーパス: virus spread

1 However, this alone does not promote virus spread.

2 alternate MT organizing center to facilitate virus spread.

3 t alter the integrity of the cell and enable virus spread.

4 BM) contact network and the implications for virus spread.

5 ssing, virus incorporation, virus entry, and virus spread.

6 mphocyte survival factor IL-2 and to enhance virus spread.

7 macrophages affected the sites or timing of virus spread.

8 enes and so cannot cause cell-cell fusion or virus spread.

9 fection, which is essential to curb systemic virus spread.

10 use lethal disease or exhibit extrapulmonary virus spread.

11 ponse to HCMV-infected cells and can prevent virus spread.

12 a balance between host immune responses and virus spread.

13 n accumulation, infectious-center titer, and virus spread.

14 influence their subcellular localization and virus spread.

15 vitro that was associated with cell-to-cell virus spread.

16 responses to contain replication and inhibit virus spread.

17 axonal degeneration in Wld mice could favor virus spread.

18 ign of effective tools and vaccines to block virus spread.

19 tope of the gH2/gL2 complex, and all blocked virus spread.

20 n to the TGN, but this is not sufficient for virus spread.

21 to cell junctions at late times and mediated virus spread.

22 calize to cell junctions and did not mediate virus spread.

23 f magnitude, and, most importantly, promotes virus spread.

24 sols also might be exploited for intentional virus spread.

25 nstrain WNV infection and limit cell-to-cell virus spread.

26 ceptor at junctions where it can be used for virus spread.

27 stablishment of virus reservoirs and prevent virus spread.

28 1 (HTLV-1) envelope protein is required for virus spread.

29 (IgG) Fc binding protein and is involved in virus spread.

30 the initial exposure, thus blocking systemic virus spread.

31 re plaque formation depended on cell-to-cell virus spread.

32 acellular virus penetration or intercellular virus spread.

33 rt activity is required for SPCA1 to promote virus spread.

34 hitefly population size and thereby decrease virus spread.

35 of inoculation and at early sites of distal virus spread.

36 as an alternative reservoir and mechanism of virus spread.

37 equent infection of T cells and hematogenous virus spread.

38 n virus-infected plants therefore subsequent virus spread.

39 of autophagy leads to a marked reduction in virus spread.

40 understanding of the parameters involved in virus spread.

41 l junctions which form a physical barrier to virus spread.

42 ea pigs and determined the mechanisms behind virus spread.

43 fection, resulted in effective inhibition of virus spread.

44 e approach to vaccination for the control of virus spread.

45 an innate immune response and inhibition of virus spread.

46 on of infected hepatocytes in the absence of virus spread.

47 potent reduction of progeny infectivity and virus spread.

48 study the complete HBV life cycle, including virus spread.

49 tissues, reduced viremia, and less efficient virus spread.

50 embrane fusion events during virus entry and virus spread.

51 trigger apoptosis as a mechanism to increase virus spreading.

52 ET domain was necessary for gE/gI to promote virus spread, a panel of gE mutants with small insertion

53 Zika virus spread across Africa and Asia in part owing to uni

54 logs of gE have analogous roles in promoting virus spread across lateral membranes of polarized epith

55 ver, the human immune system interfered with virus spread across lung grafts, responded to infection

56 Here, we show that vaccinia virus spreads across one cell every 75 minutes, fourfold

57 n parenchyma infected with LCMV and that the virus spreads across the brain principally via contiguou

58 which has been found to occur in many plant viruses spread across numerous genera.

59 lamus would affect the timing and pattern of virus spread after AC inoculation.

60 ses to confer long-term protection and limit virus spread after infection.

61 E/gI is a glycoprotein that facilitates this virus spread, although by poorly understood mechanisms.

62 presence in poultry houses, could facilitate virus spread among poultry and wild birds in the face of

63 The mechanisms by which this virus spreads among permissive target cells locally duri

64 Tracing viruses spread among synaptically connected neurons and,

65 power of the immune system to maximize both virus spread and anticancer immunity, to develop more me

66 y to lytic replication is key to controlling virus spread and can affect the development of intervent

67 the involvement of gD remained essential for virus spread and cell fusion, we propose that gH:KV mimi

68 he swine-adapted H5N2 virus could facilitate virus spread and could be a potential model for pandemic

69 ity of antiviral Abs, resulting in augmented virus spread and disease induction.

70 r antireceptor antibodies in protection from virus spread and disease progression.

71 cell junctions would be expected to enhance virus spread and enable viruses to avoid host immune def

72 onditional-lethal phenotype, as cell-to-cell virus spread and formation of infectious progeny were de

73 n the in vitro assays, HF5 and CD6 inhibited virus spread and growth more effectively than 4E9 and 1H

74 cover an unexpected role for clathrin during virus spread and have important implications for the reg

75 rions secreted by infected cells, preventing virus spread and hence the formation of mammary tumors.

76 that virally modified exosomes contribute to virus spread and immune evasion.

77 le-knockout mice showed a remarkably reduced virus spread and lung pathology, in addition to reduced

78 e importance of the SLAM-MV interactions for virus spread and pathogenesis, we generated a wild-type

79 o increase vascular permeability and promote virus spread and pathogenesis.

80 hat has the potential to dramatically affect virus spread and pathogenesis.

81 w fluorescence, reflecting reduced levels of virus spread and reduced accumulation of both CP:GFP and

82 responsible for cleaving sialic acid to aid virus spread and release.

83 RV will be a useful tool not only to monitor virus spread and screen for antiviral compounds, but als

84 d disease severity correlated with extensive virus spread and severe pulmonary pathology, stronger an

85 -needed insights into the modes of influenza virus spread and strain-specific differences in the effi

86 transiently trigger IRF-3 activation during virus spread and that in chronic HCV, IRF-3 activation w

87 during the early stages of infection, where virus spread and the need for biosafety level 3 containm

88 This is done in the context of both free virus spread and transmission of the virus through virol

89 ypes and therefore be important in efficient virus spread and transmission.

90 ies of mutation and recombination are key to virus spread and virulence in infected animals.

91 ral patient tissues, which is a key step for virus spreading and pathogenesis.

92 proteins is essential to understand how the virus spreads and causes disease.

93 Becker into late-stage chicken embryos, the virus spreads and replicates in the brain, where severe

94 etrovirus data can be used to understand how viruses spread and adapt on evolutionary timescales by c

95 d the absence of clinical symptoms, systemic virus spread, and organ pathology.

96 fection of CAST mice only after considerable virus spread, and the absolute cell numbers remained low

97 acilitate the phloem-dependent long-distance virus spread, and/or intensify disease symptoms in syste

98 The mechanisms underlying influenza virus spread are poorly understood, in part because of t

99 ripheral site presented a similar barrier to virus spread as the gut.

100 Virus spread at late times in infection determines wheth

101 Virus spread at the same rate in wild-type and Ro knocko

102 r, interleukin-4 is not required for in vivo virus spread, because mice lacking interleukin-4 or the

103 t responses in all cells intended to contain virus spread before intervention by the adaptive immune

104 rkably, gH:KV uniquely facilitated secondary virus spread between cells that lacked canonical entry r

105 ved in part from a specialized mechanism for virus spread between cells.

106 In an analogous fashion, gE/gI promotes virus spread between certain cell types in culture, e.g.

107 r importance as reactivation is critical for virus spread between susceptible individuals and is nece

108 The virus spreads between people by different routes, includ

109 is critical for cell-to-cell and long-range virus spread both in vitro and in vivo.

110 nonimmunological mechanisms to prevent early virus spread, but it does not completely block infection

111 RIPK3 and RIPK1 limit virus spread by executing either apoptotic or necroptoti

112 tom expression increasing the probability of virus spread by insects.

113 may play a substantial role in regulation of virus spread by reducing the damage caused by the MP on

114 R3616 was at the site of injection, (ii) the virus spread by retrograde transport from the site of in

115 The factors that determine whether a virus spreads by either pathway are poorly understood.

116 e of another arthropod-borne flavivirus-Zika virus-spread by the same vector, the Aedes aegypti mosqu

117 EBOV attenuation in vivo, explained by lower virus spread caused by the higher virus cytotoxicity and

118 of GLUT1 enhanced HTLV-I transfer, efficient virus spread correlated largely with heparan sulfate pro

119 icient mice also exhibited accelerated early virus spread, demonstrating that this response inhibits

120 , the ability of LIR1(+) NK cells to control virus spread differed between HCMV viral strains, and th

121 otein; and (iii) after initial infection, by virus spread directly across lateral membranes to adjace

122 endothelial cells appears to be important in virus spread, disease, and persistence.

123 wo innate immune cell subsets in controlling virus spread early during infection.

124 Whereas the NL602 virus spread efficiently, the PR8 virus did not transmit

125 production that reduces ECTV replication and virus spread, facilitating survival following infection.

126 The virus spreads faster than MV-Edm and is highly fusogenic

127 However, SAg was absolutely required for virus spread following completion of this proliferative

128 hroughout lymphoid tissues leads to systemic virus spread following infection.

129 en proposed, all involving opportunities for virus spread (for example, agricultural practices, clima

130 frica Ebola virus unique and details how the virus spread from Guinea to Sierra Leone.

131 se results suggest a key role for sigma1s in virus spread from intestinal lymphatics to the bloodstre

132 ction to control viral replication, reducing virus spread from the peripheral site.

133 Virus spread from the RPE and the photoreceptor layer to

134 Lassa virus spreads from a rodent to humans and can lead to le

135 Both PLAP- and GFP-expressing viruses spread from cell to cell and allowed analysis of

136 Nevertheless, because this virus spreads globally, some scientists predict that mut

137 leavage site (S328Y) that appears to control virus spread in a plasmin-dependent manner.

138 Titration and plaque assays showed no virus spread in ac92-knockout bacmid DNA-transfected ins

139 Kinetic studies of virus spread in adult mice following s.c. inoculation sh

140 on, virus-induced cytopathogenic effects and virus spread in cell culture without inducing cytotoxici

141 and more severe pathology and extrapulmonary virus spread in chickens.

142 the G1-like M gene conferred extrapulmonary virus spread in chickens.

143 A and Dryvax were neutralizing and inhibited virus spread in cultured cells.

144 coprotein heterodimer gE/gI is necessary for virus spread in epithelial and neuronal tissues.

145 uld be considered as a factor limiting swine virus spread in humans.

146 rties of the isolates, possibly facilitating virus spread in immunized populations.

147 ing the importance of cell-to-cell fusion in virus spread in infected tissues.

148 ally, comparative source-to-sink analysis of virus spread in leaves of N. benthamiana and N. clevelan

149 lymorphisms constitute major determinants of virus spread in mice and also dictate previously recogni

150 the injected eye may play a role in delaying virus spread in mice infected with H129wt and the IL-16-

151 SH2bm within the A/NS1 results in restricted virus spread in mouse lung and strongly reduced virulenc

152 tudying the viral life cycle and dynamics of virus spread in native tissue and also allows one to eva

153 y lethal strain of virus, (ii) resistance to virus spread in newborns inoculated with either tumorige

154 three mutants were compromised for systemic virus spread in P19-dependent hosts but had differential

155 Live-cell imaging was used to follow virus spread in real time.

156 c understanding of the principles underlying virus spread in spatially structured target cell populat

157 Reduced virus spread in SPBN-TNF-alpha+-infected mouse brains wa

158 lls, which in turn likely promotes efficient virus spread in T cell cultures.

159 ated less efficiently, and exhibited reduced virus spread in the brain at 5 days postinfection (peak

160 at we identify the immune factors that limit virus spread in the heart and other organs.

161 s in virus titers or the route and timing of virus spread in the injected eyes or in the suprachiasma

162 ls (mu-chain knockouts) showed no detectable virus spread in the mammary glands or lymphoid tissues.

163 the molecular machinery required for rabies virus spread in the nervous system.

164 is internalized, might be important to block virus spread in the organism.

165 hough expression of glycosylated Gag affects virus spread in the spleen, it appears not to affect vir

166 lated with enhanced transgene expression and virus spread in the tumors.

167 e, are resistant to MMTV, and show a lack of virus spread in their lymphoid compartments but not thei

168 h observation period, documenting continuing virus spread in this community.

169 In the United Kingdom, the novel virus spread in three temporally distinct waves between

170 VP22 in the tegument is needed for efficient virus spread in Vero cell monolayers.

171 generated an antibody response that reduced virus spread in vitro and conferred protection from chal

172 VZV, but the AYRV mutation resulted in rapid virus spread in vitro and the SSTT mutation resulted in

173 read in the spleen, it appears not to affect virus spread in vitro in fibroblast cell lines.

174 that CD81 is required for HCV infection and virus spread in vivo, and that anti-CD81 antibodies such

175 nsitive pathological assessment of routes of virus spread in vivo.

176 sent study was to test how specifically this virus spreads in the visual system, a system with well-d

177 How viruses spread in new host and geographic environments i

178 formation of satellite plaques, and delayed virus spread, indicating an important role for receptor-

179 functions, including its ability to restrict virus spread into the brain and to clear chronic viral i

180 ovel model system to study the mechanisms of virus spread into the CSF and the pathogenesis of acute

181 choroid plexus is not a significant route of virus spread into the CSF.

182 immune response and subsequent inhibition of virus spread into the optic nerve and retina.

183 spread likely continue to occur and (ii) the virus spread is apparently inefficient, which is consist

184 Virus spread is increased with longer contact times with

185 parate gag-pol or env genomes, and therefore virus spread is limited to cells that are infected with

186 spect of HSV-1 corneal infection is that the virus spread is normally restricted to only a small frac

187 However, cell-free virus spread is often very inefficient.

188 in does indeed dramatically reduce cell-free virus spreading, it has little to no effect on direct ce

189 Furthermore, virus spread more readily to the skin and brains of MAb

190 which lack parasympathetic innervation, the viruses spread more efficiently to DRG than to SC.

191 The limitations of the cell-to-cell virus spread most likely are mediated at the level of th

192 ng antiviral cell response aimed at blocking virus spread on an organismal level.

193 Virions of mouse leukemia virus spread on glass substrates were visualized by atom

194 These viruses spread only in cells secreting MMP.

195 Design of vaccines to limit the virus spread or diagnostic tests to track newly emerging

196 merely 4 d postinfection, before significant virus spread or the appearance of RABV-specific immune m

197 instead of moderating infection and reducing virus spread, overexpression of TNF-alpha has deleteriou

198 nefited nonmyocarditic more than myocarditic virus spread (P < 0.001), and this benefit was associate

199 ibody, and the concept underpins analysis of virus spread, plaque size, viral and host functions, and

200 ma membrane proteins, some of which modulate virus spread positively or negatively, and suggests a po

201 rrant vascular permeability could facilitate virus spread, promote inflammation and angiogenesis, and

202 on of a steel mesh was effective at stopping virus spread, provided that infectious animal bedding wa

203 Measles virus spreads rapidly and efficiently in human airway ep

204 Clade 2.3.2.1c viruses spread rapidly during 2012 and were detected in

205 ver, the human immune system interfered with virus spread, responded to infection by leukocyte infilt

206 Theory suggests that a fast rate of virus spread results in high degrees of helper cell impa

207 administration to bypass the gut barrier to virus spread, RRV and SA11-Cl4 both were recovered in th

208 In situ analysis of virus spread shows that the inability to disrupt Aux/IAA

209 Treatment with dsnsP3 inhibited virus spread significantly, as determined by eGFP expres

210 eutralizing antibody which appeared to limit virus spread sufficiently to protect even in the absence

211 y, an H7N7 virus, as well as some avian H5N1 viruses, spread systemically following ocular inoculatio

212 t also the sites where a major fight against virus spread takes place.

213 th SPBN-TNF-alpha+ showed significantly less virus spread than did mouse brains after SPBN-TNF-alpha-

214 that depending on our assumptions about the virus spread, there can be two distinct types of dynamic

215 The rate of MCF virus spread through a population of permissive human ce

216 Mathematical descriptions of virus spread through cell populations are well establish

217 However, as the virus spread through the fields, the cucumber beetles be

218 The dynamics of virus spread through tumor cell populations has been stu

219 ations for the initial dynamics of oncolytic virus spread through tumors are discussed.

220 roduction of virus particles is very low and virus spread throughout the culture requires several wee

221 ficantly enhanced transduction and increased virus spread throughout the tumor when compared with non

222 From here, the virus spread to Brazil with the first report of autochth

223 Rarely, zoonotic strains of influenza virus spread to humans, where they have the potential to

224 the motile actin tails enhance extracellular virus spread to neighboring cells.

225 anged in a two-dimensional setting and allow virus spread to occur only to target cells within the lo

226 depopulation measures is essential to limit virus spread to other farms.

227 after intranasal administration and reduces virus spread to other organs.

228 Within a few months, this virus spread to seals of the coastal waters of Germany a

229 n virus replication in the liver followed by virus spread to the brain.

230 uent alveolar involvement and extrapulmonary virus spread to the brain.

231 he olfactory mucosa and prevented subsequent virus spread to the CNS.

232 ted immunity during pregnancy could increase virus spread to the fetus.

233 H129wt and H129/IL-16 resulted in a delay of virus spread to the hypothalamus and the contralateral r

234 rsensitive response (HR) to TMV and restrict virus spread to the inoculated site.

235 Subsequently, virus spread to the spinal cord and the brain at virtual

236 e by several orders of magnitude, indicating virus spread to the thymic lymphoid cells.

237 Despite the failure of virus spread to the tumor, infection resulted in signifi

238 he lethal effects of HSV infection, with the virus spreading to the brain causing encephalitis.

239 persistence and the mechanisms by which the virus spreads to the CNS to cause disease.

240 In subsequent weeks, the virus spreads to the thymocytes.

241 These neurotropic viruses spread to CNS tissues trans-axonally, where they

242 Occasionally, however, these viruses spread to the central nervous system (CNS), wher

243 phalitis, and (iii) that upon infection, the virus spreads transneuronally.

244 Analysis of virus spread using co-expressed reporter proteins has pr

245 Inhibition of virus spread was accompanied by the appearance in the se

246 dicating that infection was established, but virus spread was blocked, by the anti-CD81 mAb.

247 more susceptible to MMTV infection, because virus spread was more rapid and extensive than in their

248 rd genetic selection for variants capable of virus spread, we identified second-site mutations in E1,

249 To evaluate the kinetics of virus spread, we inoculated macaques intravaginally and

250 For the initial months in which the Ebola virus spreads, we find that the arrival times of the dis

251 ht be a beneficial mechanism that limits the virus spread, whereas slow axonal degeneration in Wld mi

252 nsport represents an alternative pathway for virus spread, which is resistant to the host humoral imm

253 nvelope gene may influence the efficiency of virus spread within the brain and that a critical number

254 n be transported axonally, thereby enhancing virus spread within the brain.

255 stablishment of HIV infection also decreased virus spread within the culture.

256 ng adaptive immune response, suggesting that virus spread within the heart may be tightly constrained

257 eutralizing antibodies and probably promotes virus spread within the liver, anti-capsid antibodies re

258 s dependent on SAg activity and required for virus spread within the mammary gland, we performed mamm

259 itial steps of viral infection, but also for virus spread within the mammary gland.

260 release from infected cells and facilitates virus spread within the respiratory tract.

261 butes to the arrest of virion production and virus spread without cellular elimination.

262 s in order to determine whether blocking the virus spread would facilitate the suppression of chronic