ライフサイエンスコーパス: (viral|virus) infection(|s)

1 Viral infection induced the expression of Lck/Hck/Fgr th

2 Viral infection is one contributing factor for the devel

3 Viral infection led to mass cell lysis of the O. tauri c

4 Viral infection of the central nervous system (CNS) is c

5 Viral infections are closely linked to wheezing illnesse

6 Viral infections are thought to be a significant factor

7 Viral infections have been proposed to elicit pathologic

8 Viral infections have been reported with dasatinib use,

9 Viral infections kill millions yearly.

10 Viral infections typically used in other lab animals to

11 Virus infection of humans and livestock can be devastati

12 that significantly amplified after Dengue-2 virus infection.

13 ytes sequentially throughout the course of a viral infection in vivo.

14 cytidylic acid (Poly I:C), which simulates a viral infection, on gestational day 12.5 according to an

15 vonorgestrel, impacts sequential influenza A virus infection by modulating antibody responses and dec

16 ough it is well established that Influenza A virus infection is initiated in the respiratory tract, t

17 Susceptibility to colitis and influenza A virus infection occurring upon commensal bacteria eradic

18 ect adaptive immune responses to influenza A virus infection, with their effect on the outcome of inf

19 that develop in the lung during influenza A virus infection.

20 present a novel animal model for influenza A virus infection.

21 ipig as a novel animal model for influenza A virus infection.

22 important and unexpected role in influenza A virus infection.

23 rging evidence from vaccinia and influenza A virus infections indicates that subsets of cellular prot

24 pproach offers a method for screening active viral infections and develops links between viruses and

25 and antibody responses that accompany acute viral infection.

26 B cell and CD4 T cell responses during acute viral infection and that rapamycin treatment alters the

27 ctor limiting neuroinflammation during acute viral infection.

28 Herein, acute viral infection of murine liver with adenovirus, a model

29 In a murine model of acute viral infection, TET2 loss promotes early acquisition of

30 ion is essential for innate control of acute viral infection; however, prolonged high-level IFN produ

31 This can occur after acute viral infections, such as infections with lymphocytic ch

32 e Tfh response that is generated after acute virus infection.

33 diverse mammalian viruses and, additionally, viral infection was found to be modulated by the abundan

34 increased expression of NKG2D ligands after virus infection depends on interferon response factors a

35 IFN axis during host innate immunity against viral infection.

36 iants that provide enhanced immunity against viral infection.

37 mmunity genes and confers protection against viral infection.

38 IFN-mediated innate immune responses against viral infection.

39 The first line of defense against viral infections is the innate immune response.

40 a central role in the immune defense against viral infections.

41 the ribosome plays an essential role in all viral infections.

42 ogenous retroviruses are relics of ancestral virus infections in the human genome.

43 that contribute to congenital disorders and viral infection, we discuss the varied roles of Notch in

44 tion patterns regulating innate immunity and viral infection.

45 lichen planus, a drug-related reaction, and viral infection.

46 females to parasitic, fungal, bacterial, and viral infections.

47 d in the mucosal system during parasitic and viral infections.

48 ein homeostasis, cell cycle, DNA repair, and viral infections.

49 including cancers, autoimmune diseases, and virus infections.

50 ireplicon systems, virus-like particles, and virus infections, we determined the antiviral potential

51 tional analysis of prevalence of hepatitis B virus infection (HBV) among rural couples was conducted

52 r cells and serves as an innate link between viral infection and B cell immunity.

53 at allows the bacterium to spread, and block viral infections.

54 f these pathways and their relevance in both viral infections and cancer.

55 Respiratory illness caused by viral infection is associated with the development and e

56 H) cells, but not TH1 effectors, elicited by viral infection.

57 ces of DNA damage, which can be triggered by viral infection.

58 vascular disease, hepatitis B or hepatitis C viral infection, and a known bleeding disorder.

59 arcinoma and concomitant chronic hepatitis C viral infection.

60 minant Gag CD4(+) T cell epitopes in clade C virus infection, constructed MHC class II tetramers, and

61 cryoglobulinemia and is seen in hepatitis C virus infection and systemic diseases such as B-cell lin

62 ugs for the treatment of chronic hepatitis C virus infection have reduced mortality and the number of

63 Chronic hepatitis C virus infection is associated with significant morbidity

64 age, race or ethnicity, smoking, hepatitis C virus infection, alcohol use disorders, drug use disorde

65 ron-based treatments for chronic hepatitis C virus infection, whereas Asian race was associated with

66 e, are also less likely to clear hepatitis C virus infection.

67 third of prevalent chronic hepatitis B (CHB) virus infection (HBV) occurred in China.

68 In chronic lymphocytic choriomeningitis virus infection, blockade of type I IFN signaling partia

69 immunosuppressive role in cancer and chronic viral infection, and have been effectively targeted in c

70 ory origins of T cell dysfunction in chronic viral infection.

71 on of type I IFN, at doses mimicking chronic viral infection, induced immunosuppression.

72 ory responses and is associated with chronic viral infection.

73 Chronic viral infections and cancer often lead to the emergence

74 Chronic viral infections are difficult to treat, and new approac

75 hed studies on the compound in other chronic viral infections show that it can effectively induce imm

76 an cytomegalovirus (HCMV) is the most common viral infection acquired by the developing human fetus a

77 alovirus (HCMV) infection is the most common viral infection of the developing human fetus and can re

78 ilure presenting as AM, notably after common viral infections in children.

79 ANCE HCMV is the leading cause of congenital viral infection, and development of a preventive vaccine

80 Rapid induction is key to control virus infection, whereas proper limitation of signaling

81 effective at protecting mice from cutaneous viral infection, and lung Fabp4/Fabp5 double-knockout CD

82 ticular of those that carry gp120, decreases viral infection of human lymphoid tissue ex vivo.

83 that both cell lines that support DeltaICP0 virus infection have defects in the STING DNA-sensing pa

84 Dengue virus infection typically causes mild dengue fever, but,

85 provide long-term protection against dengue virus infection is needed.

86 uch as tuberculosis, melioidosis, and dengue virus infection.

87 spite the clear medical importance of dengue virus infection, the mechanism of viral replication, a p

88 sample each was confirmed for ZIKV or dengue virus infection.

89 ters in cases were unrelated to prior dengue virus infection.

90 ding of the innate immune response to dengue virus infection.

91 Secondary dengue virus infections were also shown to influence disease ou

92 cytopathic effect seen during many different viral infections.

93 year's Advances in Asthma review, we discuss viral infections in asthmatic patients and potential the

94 oncentrations of IFNalpha in healthy donors, viral infection, and complex and monogenic interferonopa

95 During viral infection and growth limitation of the picoeukaryo

96 hibited the highest rate of autophagy during viral infection.

97 Classically, during viral infection, the presence of foreign DNA in the cyto

98 e blocks p53-mediated adverse effects during viral infection and transformation.

99 IFNs are produced at high levels during viral infection and have convergent signaling through ST

100 ough activating the ER stress pathway during viral infection.

101 s and their differentiation potential during viral infection.

102 r of cytokine-producing ILC responses during viral infection via ILC-extrinsic regulation of IL-33 an

103 FN-gamma are coexpressed by Tfh cells during viral infections, but transcriptional regulation of thes

104 mory T cells have mainly been studied during viral infections, whereas their existence and functions

105 oviruses and expressed at high levels during virus infection.

106 plify proinflammatory signaling during Ebola virus infection, potentially contributing to the dysregu

107 ficacy in a non-human primate model of Ebola virus infection.

108 irus-positive woman was diagnosed with Ebola virus infection on her first day of life.

109 erienced an unanticipated explosion of Ebola virus infections.

110 n KSHV infection of cells, allowing enhanced viral infection of cells.

111 Cs in IFN-lambda-mediated control of enteric viral infection, and these findings provide insight into

112 ambda-responsive cells in control of enteric virus infection in vivo Upon murine norovirus or reoviru

113 m antiviral compound that inhibits enveloped virus infections by specifically targeting phospholipids

114 ing suggested the possibility that exogenous viral infections could likewise increase pathogenicity,

115 to infer the district-specific yellow fever virus infection risk during the course of the epidemic i

116 vents were similar in the 2 arms, with fewer viral infections in the inolimomab arm compared with the

117 Following viral infection of the myocardium, cDCs accumulated in t

118 oduction of interferon (IFN)-gamma following viral infection.

119 emonstrate that neuro-inflammation following viral infection increases expression of activating Fcgam

120 cell death pathways are regulated following viral infection may reveal strategies to limit tissue de

121 Cell death following virus infection can occur by apoptosis or a regulated fo

122 to avoid the generation of target cells for viral infection.

123 r, it may be associated with a high risk for viral infections due to combined T cell and B cell deple

124 ransplant and were older with lower risk for viral infections due to serostatus.

125 ry have long been an effective treatment for viral infections because of the strong D-stereoselectivi

126 lock house virus (FHV) as a model system for virus infection in bees and revealed an important role f

127 ded Cas9 endonucleases protect bacteria from viral infection and have been creatively repurposed as p

128 ver failure from any number of sources (e.g. viral infection, overnutrition, or oncologic burden) is

129 of highly pathogenic avian influenza A(H5N1) virus infection, detected through population-based activ

130 can be a powerful resource for studying how viral infection can cause different neurological outcome

131 d deficiency [n = 1], human immunodeficiency virus infection [n = 4]).

132 .21) or patients with human immunodeficiency virus infection or AIDS (P = 0.60).

133 Human immunodeficiency virus infection was independently associated with renal

134 Human immunodeficiency virus infection.

135 major infections like human immunodeficiency virus infection.

136 ver, the function and regulation of IL-22 in viral infection remain largely unknown.

137 structures that play a conserved function in viral infection cycles.

138 The loss in viral infection was associated with reduced viral fusion

139 e "empty" capsids (ECs) normally produced in viral infection.

140 enomes of RNA viruses play critical roles in viral infection, yet their importance in the bipartite g

141 ogen spread, but in some settings, including viral infection, this response can contribute to cell de

142 Influenza viral infections often lead to increased mortality in ol

143 ate more potent protection against influenza virus infection in animal models.

144 e essential for protection against influenza virus infection.

145 (RT-PCR) for laboratory-confirmed influenza virus infection (LCI).

146 to promote the host defense during influenza virus infection.

147 ositive protective effect of early influenza virus infection later in life continues to be observed.

148 timal antiviral response following influenza virus infection or immunization.Broadly reactive antibod

149 of memory CD8(+) T cells following influenza virus infection or vaccination, they failed to support a

150 n protection of the lung following influenza virus infection.

151 spitalized infants were tested for influenza virus infection and 1 tested positive.

152 tends beyond its classical role in influenza virus infection and that antineuraminidase antibodies of

153 used animal model for the study of influenza virus infection and vaccination.

154 Innate sensing of influenza virus infection induces activation of programmed cell de

155 de better protection from seasonal influenza virus infection and improve pandemic preparedness.

156 or studying the immune response to influenza virus infection and vaccination in the ferret model.

157 Influenza virus infections are associated with a wide spectrum of

158 enicity and low incidence of avian influenza virus infections in humans, the immune correlates of pro

159 Studies in preclinical models of influenza virus infections have shown that antibodies alone are su

160 ost protein that is neutralized during Junin virus infection.

161 A nurse who acquired Lassa virus infection in Togo in the spring of 2016 was repatr

162 nd reduce the rate of reactivation of latent virus infection.

163 irect causative link was established linking viral infection to herbicide resistance, transcriptome s

164 improved NK-cell number and function, lower viral infections, and low relapse rate posttransplant.

165 Many viral infections cause host shutoff, a state in which ho

166 orn has yet to be determined, other maternal viral infections resulting in transmission to the fetus

167 complex than treatment for bacterial or most viral infections, and drug interactions are particularly

168 dramatically increased during double-mutant virus infection and correlates with faster antiviral res

169 blood-brain barrier (BBB) during neurotropic viral infection.

170 ay have broad potential for discovery of new viral infections of possible medical importance, such as

171 ng showed decreased survival after West Nile virus infection.

172 me-localized protein that restricts numerous virus infections.

173 lular carcinoma (HCC) involves components of viral infection, inflammation and time.

174 and contributes to cell-intrinsic control of viral infection.

175 own to regulate T cell function in models of viral infection and autoimmunity.

176 y diversification/maturation, restriction of viral infection, and generation of somatic mutations.

177 ral surface proteins can blunt the spread of viral infection by coating viral particles, mediating up

178 The spread of viral infection from conducting airways to the alveolar

179 tein 1 (NPC1) arising during early stages of viral infection.

180 lication.IMPORTANCE One intriguing aspect of viral infections is their dependence on efficient subcel

181 se intricate relationships in the context of viral infections.

182 c approach in relevant preclinical models of viral infections.

183 The prevalence of viral infections in any given host is determined by vari

184 prevention and treatment of a broad range of viral infections including BK virus, cytomegalovirus, ad

185 ghlighting the importance of surveillance of viral infections.

186 utic, and a tool for exploring mechanisms of virus infection inhibition by antibodies.

187 We demonstrate that increased prevalence of virus infection in individual bees is associated with hi

188 ation, suggesting that SGs have an impact on virus infection.

189 Immunodeficiency and (chronic/oncogenic) viral infections together constitute a major risk.

190 d were unable to control tumor metastasis or viral infection.

191 s, brain and cardiac ischemia, pancreatitis, viral infection and inflammatory diseases).

192 ospitalization in patients with A(H1N1)pdm09 virus infection.

193 logous immunity in the context of persistent viral infection.

194 Persistent viral infections result from evasion or avoidance of ste

195 In acute and persistent viral infections, IL-22 deficiency resulted in thymic an

196 lymphoid organs during acute and persistent viral infections.

197 te how a history of an acute or a persistent virus infection can substantially influence the immune r

198 o brain atrophy in a system where persistent virus infection and demyelination are not factors in lon

199 l receptor profiles (BCR/TCR), and potential viral infections.

200 itis media, pharyngitis, sinusitis, presumed viral infection) after adjusting for patient age and enc

201 the mice that were protected against primary viral infection as a result of heat-killed DK128 pretrea

202 virus-infected cells that permits productive virus infection.

203 isms by which either protein acts to promote virus infection is missing.

204 le for these effects, and mutant CrPV(R146A) virus infection is attenuated in Drosophila melanogaster

205 However, for unknown reasons, viral infections rarely cause clinical symptoms in bats.

206 which is present in a patient with recurrent viral infection, granuloproliferation, and intracerebral

207 eficiency can result in severe or refractory viral infections.

208 Respiratory viral infection in early childhood, including that from

209 Early-life respiratory viral infection is a risk factor for asthma development.

210 Respiratory viral infections represent the most common cause of alle

211 between asthma exacerbations and respiratory viral infections, and interaction between viruses and al

212 ave become available to diagnose respiratory viral infections.

213 Interestingly, upper-respiratory viral infections increase the risk for relapse.

214 Respiratory virus infection is a common cause of hospitalisation in

215 Respiratory virus infection without illness is not innocuous but may

216 eneic stem cell transplantation, respiratory virus infection, and Aspergillus PCR positivity were all

217 Rapid diagnosis of respiratory virus infections contributes to patient care.

218 For reasons unknown, respiratory virus infections have a prolonged duration in CF.

219 The host response to RNA virus infection consists of an intrinsic innate immune r

220 associated with many factors, including RNA virus infections.

221 y triggers of antiviral immunity in many RNA virus infections.

222 nt heterosubtypic immunity against secondary virus infection.

223 We find that during Sendai virus infection this phenotype results from DVGs stimula

224 wn of La in HEK 293 T cells increased Sendai virus infection efficiency, decreased IFN-beta, IFN-lamb

225 During severe viral infection and chronic inflammation, the submucosa

226 ease treatment-related mortality from severe viral infections.

227 1, HIV-2, Influenza virus and herpes simplex virus infection, and enhances the potential of reactive

228 nhibitor for the treatment of herpes simplex virus infections, was prepared.

229 positive-sense single-stranded RNA (+ssRNA) viral infection, especially since RNA is not known to ac

230 3 (TLR3) agonist used as a mimetic to study viral infection, has been shown to elicit inflammatory r

231 To treat patients suffering from such viral infections, broadly reactive and highly sensitive

232 that during Sendai and respiratory syncytial virus infections DVGs selectively protect a subpopulatio

233 up B streptococcus and respiratory syncytial virus infections, among others.

234 nts undergoing transplantation with systemic viral infections had poor survival in comparison with th

235 ations, this study evaluated the impact that viral infection had on human FM innate immune responses.

236 Here, we report that viral infection triggered early IL-22 production from th

237 Here, To et al. show that virus infection activates endosomal NOX2 oxidase and res

238 Here, we show for the first time that virus infection of human airway epithelia can also induc

239 the result of complex interactions among the viral infection, host factors, traditional risk factors,

240 cells in the lytic cycle and to control the viral infection involving IFN-gamma secretion.

241 ion of liver diseases, they fail to cure the viral infection.

242 but a minority are nonpermissive because the virus infection aborts before its completion.

243 M symptoms arise as a consequence not of the virus infection per se but of the hyperactivated immune

244 s more likely associated with aging than the virus infection and could be compensated by applying a 5

245 This viral infection-induced PTEN overexpression appears resp

246 y cerebellar astrocytes as key responders to viral infection and highlight the existence of distinct

247 t that an exaggerated interferon response to viral infection by airway epithelial cells may be a mech

248 w La regulates IFN production in response to viral infection.

249 vered indicating a host systemic response to viral infection.

250 ponent of the host innate immune response to viral infection.

251 +) T cell cytokine production in response to viral infection.

252 i), suggesting a unique neuronal response to viral infection.

253 ta2(neg) T cells, implicated in responses to viral infection and cancer.

254 Protective immune responses to viral infection are initiated by innate immune sensors t

255 lter innate and adaptive immune responses to viral infection.

256 ing of CD8(+) and CD4(+) T cell responses to viral infection.

257 ls molecular pathways linking RNA biology to viral infections.

258 TANCE Understanding how the host responds to viral infections informs the development of therapeutics

259 of metabolic activity changes in response to viral infections and identify key time points and locati

260 t protein with dual functions in response to viral infections: it traps newly assembled enveloped vir

261 virus replication or enhancing resistance to virus infection.

262 al for the induction of B cell immunity upon viral infection.

263 and type III (lambda) IFNs are induced upon viral infection through host sensory pathways that activ

264 with either virus, after a cleared vaccinia virus infection, and during a persistent/latent murine C

265 ve phosphorylation increased during vaccinia virus infection, while inhibition of the cellular oxidat

266 ove of double-stranded DNA, inhibit vaccinia virus infection by blocking viral DNA replication and ab

267 yzed the responses of host cells to vaccinia virus infection at both the transcriptional and translat

268 the host transcriptional response to various viral infections provides a wealth of data but utilizati

269 reveal a progressive expansion of vertebrate viral infections over time following HSCT, and they sugg

270 Zika virus infection could also cause Guillain-Barre syndrome

271 Zika virus infection during pregnancy can cause congenital ab

272 Zika virus infection induced detectable Dengue cross-reactive

273 oth for appraisal of the evidence about Zika virus infection and for the next public health threats t

274 CI 13.0-infinity) for microcephaly and Zika virus infection after adjustments.

275 he association between microcephaly and Zika virus infection.

276 d systematic review about links between Zika virus infection and (a) congenital brain abnormalities,

277 uestions about the relationship between Zika virus infection and each of the two clinical outcomes in

278 adverse reproductive outcomes caused by Zika virus infection is not yet determined, a distinctive phe

279 th microcephaly or laboratory-confirmed Zika virus infection but not for all infants potentially expo

280 ith polymerase chain reaction-confirmed Zika virus infection in maternal specimens, 24 infants (21.4%

281 Congenital Zika virus infection has stimulated great international conce

282 ion between microcephaly and congenital Zika virus infection was confirmed.

283 tial causes of microcephaly: congenital Zika virus infection, vaccines, and larvicides.

284 the only initial finding in congenital Zika virus infection.

285 ing findings associated with congenital Zika virus infection.

286 s-reactive antibodies induced following Zika virus infection might enhance subsequent Dengue infectio

287 ZIKV-3'UTR-LAV is warranted for humans.Zika virus infection can result in congenital disorders and c

288 evidence to conclude that intrauterine Zika virus infection is a cause of microcephaly and serious b

289 fants with birth defects after maternal Zika virus infection by trimester of infection and maternal s

290 of available evidence from outbreaks of Zika virus infection and clusters of microcephaly is that Zik

291 of available evidence from outbreaks of Zika virus infection and GBS is that Zika virus infection is

292 e ocular manifestations and sequelae of Zika virus infection are not well known.

293 om individuals with a typical course of Zika virus infection is low.Zika virus (ZIKV) is present in b

294 laboratory evidence of possible recent Zika virus infection and outcomes reported in the continental

295 o, Brazil, who presented with suspected Zika virus infection during pregnancy were referred to our in

296 on and clusters of microcephaly is that Zika virus infection during pregnancy is a cause of congenita

297 of Zika virus infection and GBS is that Zika virus infection is a trigger of GBS.

298 es or infants with prenatal exposure to Zika virus infection only in the second or third trimesters.

299 e risk of birth defects associated with Zika virus infection during pregnancy may help guide communic

300 e, and durable protection against human Zika virus infections or syndromes.