ライフサイエンスコーパス: virus spread

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

2 ced by HCMV infection that leads to enhanced virus spread.

3 potent reduction of progeny infectivity and virus spread.

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

5 embrane fusion events during virus entry and virus spread.

6 alternate MT organizing center to facilitate virus spread.

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

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

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

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

11 macrophages affected the sites or timing of virus spread.

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

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

14 use lethal disease or exhibit extrapulmonary virus spread.

15 a balance between host immune responses and virus spread.

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

17 influence their subcellular localization and virus spread.

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

19 responses to contain replication and inhibit virus spread.

20 axonal degeneration in Wld mice could favor virus spread.

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

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

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

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

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

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

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

28 stablishment of virus reservoirs and prevent virus spread.

29 1 (HTLV-1) envelope protein is required for virus spread.

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

31 the initial exposure, thus blocking systemic virus spread.

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

33 acellular virus penetration or intercellular virus spread.

34 cur during infection and their importance to virus spread.

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

36 s purified from HCMV-infected cells enhanced virus spread.

37 an innate immune response and inhibition of virus spread.

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

39 However, this alone does not promote virus spread.

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

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

42 sols also might be exploited for intentional virus spread.

43 hitefly population size and thereby decrease virus spread.

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

45 as an alternative reservoir and mechanism of virus spread.

46 equent infection of T cells and hematogenous virus spread.

47 n virus-infected plants therefore subsequent virus spread.

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

49 understanding of the parameters involved in virus spread.

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

51 ea pigs and determined the mechanisms behind virus spread.

52 fection, resulted in effective inhibition of virus spread.

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

54 trigger apoptosis as a mechanism to increase virus spreading.

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

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

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

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

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

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

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

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

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

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

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

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

67 Tracing viruses spread among synaptically connected neurons and,

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

69 irus provides a safe and pivotal channel for virus spread and biparental transmission to progeny.IMPO

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

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

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

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

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

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

76 o recruit effector CD8(+) T-cells to prevent virus spread and establish immune surveillance at barrie

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

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

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

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

81 data yields i) more realistic hypotheses of virus spread and ii) higher posterior predictive accurac

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

83 Furthermore, intravital imaging showed that virus spread and lesion formation are attenuated in the

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

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

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

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

88 athways of spread to elucidate mechanisms of virus spread and pathogenesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 fore, it is important to understand how this virus spreads, as well as the resulting pathogenesis in

109 Virus spread at late times in infection determines wheth

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

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

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

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

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

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

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

117 The virus spreads between people by different routes, includ

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

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

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

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

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

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

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

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

126 ence virion stability and fitness.IMPORTANCE Viruses spread by the fecal-oral route need to maintain

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

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

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

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

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

132 However, whether the virus spread directly to humans or through an intermedia

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

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

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

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

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

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

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

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

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

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

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

144 Virus spread from the RPE and the photoreceptor layer to

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

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

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

148 ming infection and enhance the efficiency of virus spread.IMPORTANCE Human cytomegalovirus (HCMV) is

149 early innate immune responses at inhibiting virus spread.IMPORTANCE Influenza A virus (IAV) is a res

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

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

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

153 Increased virus spread in CaMKIIcre:IFNAR(fl/fl) mice compared to

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

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

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

157 zero-COVID policy has effectively controlled virus spread in China, China has to face challenges in b

158 and in clarifying the primary means of Zika virus spread in clinically relevant target cells.

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

160 ive bifurcation model for analyzing COVID-19 virus spread in different countries.

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

162 -independent pathways are also beneficial to virus spread in fibroblasts, as treatment with the EV in

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

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

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

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

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

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

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

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

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

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

173 cal studies to understand the true extent of virus spread in populations.

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

175 ctive infection has the potential to promote virus spread in reproductive tissue and induce reproduct

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

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

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

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

180 In addition, we modeled how the virus spread in the country.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 How viruses spread in new host and geographic environments i

199 not affect virus assembly, but does prevent virus spread, in feline kidney cells.

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

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

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

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

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

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

206 Early forecasting of COVID-19 virus spread is crucial to decision making on lockdown o

207 Virus spread is increased with longer contact times with

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

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

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

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

212 pecialized environment of the BM can promote virus spread locally and to distant lymphoid tissues.

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

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

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

216 at the decreased survival time and increased virus spread observed in IL-36gamma(-/-) mice are not ne

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

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

219 These viruses spread only in cells secreting MMP.

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

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

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

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

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

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

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

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

228 Measles virus spreads rapidly and efficiently in human airway ep

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

230 (IFNAR1) specifically in neurons to control virus spread, regulate IFN-gamma signaling, and prevent

231 npharmaceutical interventions (NPIs) on this virus spread remain challenging.

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

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

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

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

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

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

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

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

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

241 l cultures and attenuated virus replication, virus spread, the severity of infection, and cellular in

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

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

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

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

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

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

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

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

250 Democratic Republic of the Congo (DRC), the virus spread to an urban center by early May.

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

252 more resistant to virus infection, limiting virus spread to different degrees.

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

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

255 hogenic avian influenza (HPAI) clade 2.3.4.4 virus spread to North America by wild birds and reassort

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

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

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

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

260 le mice was due predominantly to compromised virus spread to the B-2 cell population.

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

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

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

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

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

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

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

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

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

270 surrounding cellular environment to promote virus spread to uninfected cells.

271 s this pathway to increase the efficiency of virus spread to uninfected cells.

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

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

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

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

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

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

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

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

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

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

282 rential response of enhanced replication and virus spread was observed for GII.3, but not the globall

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

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

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

286 Additionally, H84T BanLec arrested virus spread when treatment was delayed.

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

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

289 Host survival would facilitate virus spread, which would also provide an advantage to t

290 f MuV and its influence on the mechanisms of virus spread within infected tissues.

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

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

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

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

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

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

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

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

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

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