ライフサイエンスコーパス: viral infection

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

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

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

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

5 arcinoma and concomitant chronic hepatitis C viral infection.

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

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

8 IFN-mediated innate immune responses against viral infection.

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

10 s and their differentiation potential during viral infection.

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

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

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

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

15 er host immune and inflammatory responses to viral infection.

16 wn when spacer sequences are acquired during viral infection.

17 ns involved in the innate immune response to viral infection.

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

19 light direct targets and treatments against viral infection.

20 mportant role during the initial stages of a viral infection.

21 a nucleus-like structure in bacteria during viral infection.

22 in cells is prevented from aggregation until viral infection.

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

24 a-thalassemia, myelodysplastic syndrome, and viral infection.

25 ough activating the ER stress pathway during viral infection.

26 is also monopartite and is indispensable for viral infection.

27 MDA5) mediates the innate immune response to viral infection.

28 om defensin neutralization or enhancement of viral infection.

29 ion, potentially favoring the progression of viral infection.

30 ly expressed ISGs protect stem cells against viral infection.

31 tease regulation and stability as well as in viral infection.

32 1 expression and thereby enhanced control of viral infection.

33 ariety of diseases ranging from neoplasms to viral infection.

34 athways involved in the cellular response to viral infection.

35 pite chronic stimulation during a persistent viral infection.

36 mmune responses are necessary for persistent viral infection.

37 nate defense molecules against bacterial and viral infection.

38 eral host systemic response to many types of viral infection.

39 beta-cells of pancreatic islets, may involve viral infection.

40 g the gene expression cascade which controls viral infection.

41 esponse, also represent the target cells for viral infection.

42 defense mechanisms designed to eradicate the viral infection.

43 fusion is an important step for a successful viral infection.

44 dentified five novel host factors regulating viral infection.

45 deformities, and a history of bacterial and viral infection.

46 al T cells and immunopathology in persistent viral infection.

47 arcinoma and concomitant chronic hepatitis C viral infection.

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

49 and antibody responses that accompany acute viral infection.

50 tion patterns regulating innate immunity and viral infection.

51 ory responses and is associated with chronic viral infection.

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

53 iants that provide enhanced immunity against viral infection.

54 hibited the highest rate of autophagy during viral infection.

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

56 logous immunity in the context of persistent viral infection.

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

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

59 IFN axis during host innate immunity against viral infection.

60 lter innate and adaptive immune responses to viral infection.

61 ctor limiting neuroinflammation during acute viral infection.

62 vered indicating a host systemic response to viral infection.

63 mmunity genes and confers protection against viral infection.

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

65 c approach in relevant preclinical models of viral infections.

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

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

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

69 of the heart muscle that can follow various viral infections.

70 veloping countermeasures to prevent or treat viral infections.

71 e bacteria but remains poorly documented for viral infections.

72 ences in patients with tuberculosis and some viral infections.

73 by autoreactive T cells and associated with viral infections.

74 responses following antigen immunization and viral infections.

75 a broad spectrum of established and emerging viral infections.

76 eficiency can result in severe or refractory viral infections.

77 hat helps protect humans and animals against viral infections.

78 n cardiovascular diseases, inflammation, and viral infections.

79 n important defense mechanism in response to viral infections.

80 at the time of non-HLAabs development, 4 had viral infections.

81 s and/or their impact on chronic (oncogenic) viral infections.

82 a realistic model to study human respiratory viral infections.

83 potential of IFN-lambda for treating mucosal viral infections.

84 ly thought to occur during bacterial and DNA viral infections.

85 therapeutic strategy to prevent and control viral infections.

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

87 ls molecular pathways linking RNA biology to viral infections.

88 ease treatment-related mortality from severe viral infections.

89 lymphoid organs during acute and persistent viral infections.

90 ave become available to diagnose respiratory viral infections.

91 ghlighting the importance of surveillance of viral infections.

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

93 se intricate relationships in the context of viral infections.

94 cytopathic effect seen during many different viral infections.

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

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

97 In response to acute viral infection, activated naive T cells give rise to ef

98 ous pathophysiological conditions, including viral infection, acute kidney injury, and cardiac ischem

99 ever is the most common mosquito transmitted viral infection afflicting humans, estimated to generate

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

101 We demonstrate that LPS, TNF-alpha, and viral infection, all of which induce robust inflammatory

102 We also show that viral infection alters the nature of nitrogen compound u

103 re often elevated in both carcinogenesis and viral infection and are associated with DNA mutations.

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

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

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

107 During severe viral infection and chronic inflammation, the submucosa

108 tal factor in determining cell fate during a viral infection and delineate a MAVS/TNFR2-mediated mech

109 quely up-regulated SR-AI during hepatotropic viral infection and displayed increased expression of al

110 During viral infection and growth limitation of the picoeukaryo

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

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

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

114 ays an important role in host restriction to viral infection and inflammation.

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

116 or infected with Sendai virus to model acute viral infection and subsequently validated our findings

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

118 inantly inhibited GC B cell responses during viral infection and that this led to biased helper CD4 T

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

120 at the tumor site allowed for the imaging of viral infection and tumor regression.

121 have identified ZBP1 as an innate sensor of viral infections and a target of viral evasion strategie

122 randed RNA (dsRNA) is a common by-product of viral infections and acts as a potent trigger of antivir

123 Chronic viral infections and cancer often lead to the emergence

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

125 orted that some pathological states, such as viral infections and certain cancers, coincide with ERV

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

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

128 hemorrhagic fever is one of the most lethal viral infections and lacks a licensed vaccine.

129 O metabolism in healthy infants before first viral infections and sensitization is related to mechani

130 ve useful for the prevention or treatment of viral infections and tumors that express viral antigens.

131 nesthetized ferrets in vivo using a combined viral-infection and optogenetics approach to drive expre

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

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

134 us (HCMV) is the leading cause of congenital viral infection, and developing a prophylactic vaccine i

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

136 s and innate immunity in clearing persistent viral infection, and discussing the broader implications

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

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

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

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

141 adaptive immune systems for protection from viral infection, and viruses have evolved diverse anti-C

142 ibosylation to stress responses, metabolism, viral infections, and cancer.

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

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

145 ious stimuli, including bacterial pathogens, viral infections, and light.

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

147 r, when the same antigen is presented during viral infection, antigen-specific T cells access the ret

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

149 Persistent hepatotropic viral infections are a common etiologic agent of chronic

150 Respiratory and arthropod-borne viral infections are a global threat due to the lack of

151 Viral infections are closely linked to wheezing illnesse

152 ral myocarditis (AVM), given that the causal viral infections are common, is unknown.

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

154 Viral infections are thought to be a significant factor

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

156 on in rapid diagnosis of acute bacterial and viral infections as well as chronic disease management.

157 s essential HCV co-factors, thus restricting viral infection at multiple stages.

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

159 -kappa imparted cellular protections against viral infections both in vitro and ex vivo.

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

161 r exhausted T cells during acute and chronic viral infection, but these are not well studied in human

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

163 lls with global DNA hypomethylation mimics a viral infection by activating cytoplasmic DNA sensors.

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

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

166 Vertebrates respond to viral infection by inducing IFNs, which trigger antivira

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

168 o test the hypothesis that upper-respiratory viral infection can cause glial activation, promote immu

169 cation during a host shutoff.IMPORTANCE Many viral infections cause global host protein synthesis shu

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

171 Long-term persistent viral infections cause substantial morbidity and associa

172 two genes known to be highly upregulated in viral infections (CCL8/CXCL11), we screened 92 asthmatic

173 ons) and/or limiting cytoplasmic PABP (e.g., viral infection, cell stress).

174 Stem cells are highly resistant to viral infection compared to their differentiated progeny

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

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

177 alemtuzumab were older and at lower risk of viral infection due to serostatus.

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

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

180 Viral infection during pregnancy is correlated with incr

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

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

183 with IAV markedly accelerated the spread of viral infection from the airways to alveoli compared wit

184 unization, IgM levels were reduced and, upon viral infection, germinal center responses were defectiv

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

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

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

188 NCE Sex bias in severe sequelae from enteric viral infections has been observed.

189 3 (TLR3) agonist used as a mimetic to study viral infection, has been shown to elicit inflammatory r

190 rvations: Immune evasion mechanisms of these viral infections have an important role in carcinogenesi

191 Viral infections have been proposed to elicit pathologic

192 Viral infections have been reported with dasatinib use,

193 Viral infections have long been suspected to be involved

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

195 family plays a role in host defense against viral infection, however its role in HCV infection is st

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

197 n the face of chronic cancers and protracted viral infections, human immune cells are known to adopt

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

199 Respiratory viral infection in early childhood, including that from

200 esponsible for this ILC dysregulation during viral infection in STAT1-deficient mice.

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

202 e expression in CD8(+) T cells responding to viral infection in vivo.

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

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

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

206 microscopy studies have produced evidence of viral infections in Symbiodinium, the endosymbiotic alga

207 le is known about the effects of respiratory viral infections in the absence of illness.

208 Despite the prevalence of viral infections in the American population, we still ha

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

210 ugh understanding of the processes governing viral infection includes knowledge of how viruses manipu

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

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

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

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

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

216 rther, the inflammatory mechanisms mediating viral infection-induced bone loss depend on the specific

217 This viral infection-induced PTEN overexpression appears resp

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

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

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

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

222 Viral infection is an exacerbating factor contributing t

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

224 In AHB, viral infection is detected and restrained by the innate

225 l killer (NK) cell activation in response to viral infection is known, but the underlying mechanism r

226 Viral infection is one contributing factor for the devel

227 This stable intermediate of viral infection is persistently maintained in reservoirs

228 Immune control of viral infections is heavily dependent on helper CD4(+) T

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

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

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

232 Viral infections kill millions yearly.

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

234 Thus, viral infections likely represent a significant risk fac

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

236 iated conditions, including autoimmunity and viral infections, may have an increased risk of RBC allo

237 critical for T cell function and survival in viral infection models.

238 differences in the susceptibility of mice to viral infection, morbidity, viral organ titers, recovery

239 an blunt some of the perilous impact of this viral infection, new treatments are needed due to the co

240 Eczema herpeticum (EH) is characterized by viral infection of a preexisting inflammatory dermatosis

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

242 This study shows that a herpes viral infection of FMs sensitizes the tissue to low leve

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

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

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

246 in innate immune responses of the BBB during viral infection of the CNS remains to be fully elucidate

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

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

249 how that mouse CD8(+) TRM cells generated by viral infection of the skin differentially express high

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

251 Productive viral infection often depends on the manipulation of the

252 Influenza viral infections often lead to increased mortality in ol

253 ossible to distinguish LCI from noninfluenza viral infections on clinical evaluations alone in this p

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

255 Antigens derived from viral infection or vaccination can persist within a host

256 ate protection against reinfection following viral infection or vaccination.

257 rial (RR = 0.46; 95% CI: 0.34-0.62), but not viral infections or ILI.

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

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

260 t just on drug efficacy, but also on several viral infection parameters, such as infection and produc

261 cible T cell kinase (ITK) are susceptible to viral infections, particularly EBV, suggesting that thes

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

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

264 IL-1 elements in host immunity to cutaneous viral infection remain elusive.

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

266 how these networks control host immunity and viral infection remain to be elucidated.

267 first observed in 1969, but its role during viral infection remains unclear.

268 of circulating viruses.IMPORTANCE Influenza viral infections represent a serious public health probl

269 Respiratory viral infections represent the most common cause of alle

270 Persistent viral infections result from evasion or avoidance of ste

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

272 n in naive, MP, and TE CD8(+) T cells during viral infection revealed increased H3K27me3 deposition a

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

274 Viral infection spread to tumor cells, where tumor cell

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

276 such as atherosclerosis and diabetes, and in viral infections, such as influenza infection.

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

278 iodinium cells may host latent or persistent viral infections that are induced via stress.

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

280 Following viral infection, the ubiquitin-binding domain in WHIP br

281 8(+) T cells provide protection against many viral infections, their role in Zika virus (ZIKV) immuni

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

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

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

285 ms of the immune response is critical during viral infection to promote efficient viral clearance whi

286 examined pDC spatiotemporal dynamics during viral infection to uncover when, where, and how they exe

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

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

289 he generality of these signatures across all viral infection types has not been established.

290 Viral infections typically used in other lab animals to

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

292 Select humans and animals control persistent viral infections via adaptive immune responses that incl

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

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

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

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

297 cterial infections can induce sensitivity to viral infections, which may have important implications

298 peutic for aquaculture settings that include viral infections with lower virus-shedding rates than IH

299 expressed with Bcl6 in Tfh cells after acute viral infection, with a temporal decline in T-bet in the

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