ライフサイエンスコーパス: antiviral response

1 ased IFN-gamma expression (which is a mature antiviral response).

2 t may have roles during the RNase L-mediated antiviral response.

3 thereby promotes IFN-beta induction and the antiviral response.

4 properties and is a component of host innate antiviral response.

5 ction and are important in the host's innate antiviral response.

6 at plays a multifaceted role in the cellular antiviral response.

7 of p53 activity and notably the p53-mediated antiviral response.

8 s have distinct biological activities in the antiviral response.

9 ear less sensitive to the interferon-induced antiviral response.

10 attern recognition sensing to mount a potent antiviral response.

11 their main function is to participate in the antiviral response.

12 and viral RNA during the type VI CRISPR-Cas antiviral response.

13 the ability of these viruses to counter the antiviral response.

14 uction and highlighted the complexity of the antiviral response.

15 s as well as other cytokines, to generate an antiviral response.

16 itude of virus antagonism of the host innate antiviral response.

17 t, BKV infection of leukocytes did elicit an antiviral response.

18 ocytes and the induction of the early innate antiviral response.

19 detect pathogenic RNA and induce a systemic antiviral response.

20 ression, indicating BKV did not modulate the antiviral response.

21 nting inappropriate activation of the innate antiviral response.

22 d highlights the breadth of the cGAS-induced antiviral response.

23 rous tubules, is robust and induces a strong antiviral response.

24 reveal a new strategy for EV71 to evade the antiviral response.

25 g pathway important for both mitosis and the antiviral response.

26 echanism employed by viruses to counter this antiviral response.

27 ancy of these enzymes in the IFITM3-mediated antiviral response.

28 ) by the STING pathway potently triggers the antiviral response.

29 y a role in transcription, neurogenesis, and antiviral response.

30 sity to escape the bottlenecks of the host's antiviral response.

31 the main viral factor counteracting the host antiviral response.

32 f of YAP-mediated inhibition of the cellular antiviral response.

33 tein translation, energy conversion, and the antiviral response.

34 m2, which cripples the cellular p53-mediated antiviral response.

35 e is associated with suppression of the host antiviral response.

36 with RV1B to determine lung inflammation and antiviral response.

37 ine/threonine kinases play a central role in antiviral response.

38 tent mice and mice lacking components of the antiviral response.

39 te immune receptors to promote an integrated antiviral response.

40 ignaling and promote fly survival during the antiviral response.

41 MDA5), to further amplify IFN production and antiviral response.

42 place of the IFN system within the concerted antiviral response.

43 y broad spectrum of cellular pathways in the antiviral response.

44 s that are considered central players in the antiviral response.

45 n 1 (NS1) is to antagonize the host cellular antiviral response.

46 h respect to the skin, inflammation, and the antiviral response.

47 ntial factor involved in this TRIM6-mediated antiviral response.

48 C's effects on IAV growth and the macrophage antiviral response.

49 it enables viral gene expression and blocks antiviral responses.

50 pathways that promoted specific T helper and antiviral responses.

51 Rylating) PARPs are associated with cellular antiviral responses.

52 This study links glucose metabolism to antiviral responses.

53 h chromatin remodeling and potentiate robust antiviral responses.

54 innate immunity by participation in cellular antiviral responses.

55 ute to the dysregulation of inflammatory and antiviral responses.

56 located to the nucleus and further augmented antiviral responses.

57 l proliferation, DNA repair, metabolism, and antiviral responses.

58 a key role in viral detection and generating antiviral responses.

59 imulate the immune system via cell-intrinsic antiviral responses.

60 d-type VSV that is more effective at evading antiviral responses.

61 ved multiple strategies to suppress the host antiviral responses.

62 t that activates pathogen sensors and innate antiviral responses.

63 ies at the intersection of antibacterial and antiviral responses.

64 ase activity on its surface that antagonizes antiviral responses.

65 on occurred independently of the plant siRNA antiviral responses.

66 as also found to regulate cell-type-specific antiviral responses.

67 nterferons (IFNs) are essential mediators of antiviral responses.

68 s proteins that are dedicated to combat host antiviral responses.

69 greater insight into viral pathogenicity and antiviral responses.

70 M36) and RIP3 signaling (M45) suppress these antiviral responses.

71 sitive regulatory role for NLRX1 in inducing antiviral responses.

72 cell as a potential mechanism to escape host antiviral responses.

73 e of type I IFN signaling partially restores antiviral responses.

74 CD4(+) T cells yet limited CD8(+) T cell and antiviral responses.

75 on and affect processes including immune and antiviral responses.

76 toimmune diabetes and, conversely, restrains antiviral responses.

77 favorable cell conditions and overcome cell antiviral responses.

78 wheezing but not increased atopy or reduced antiviral responses.

79 ge in macrophages to promote interferons and antiviral responses.

80 ruses accomplish this by repressing specific antiviral responses.

81 ncoded immune evasion molecules that inhibit antiviral responses.

82 stioned whether BKV suppresses and/or evades antiviral responses.

83 initiation of host interferon (IFN)-mediated antiviral responses.

84 tly related to aeroallergen sensitization or antiviral responses.

85 rupting the TBK1-DRP1 connection compromised antiviral responses.

86 scription factor IRF3 is a key event in host antiviral responses.

87 that activates NOD2, on HCMV replication and antiviral responses.

88 erstand the role of adaptive immunity in bat antiviral responses.

89 gnaling, possibly inappropriately throttling antiviral responses.

90 differential effects on HCMV replication and antiviral responses.

91 ulation that inhibition of AXL would promote antiviral responses.

92 efects in the initiation of optimal adaptive antiviral responses.

93 A (dsRNA), as has been observed in mammalian antiviral responses.

94 ntiation-associated protein 5 (MDA5) mediate antiviral responses.

95 here it functions to stimulate cell-mediated antiviral responses.

96 n eliminates several innate and inflammatory antiviral responses.

97 involved in cytoplasmic RNA recognition and antiviral responses.

98 viral-induced glycolysis and enhanced innate antiviral responses.

99 nd CD4(+) T cell responses, including type 1 antiviral responses.

100 al multifunctional NS1 protein inhibits host antiviral responses.

101 macrophage polarization, tumour immunity and antiviral responses.

102 ossmann fold domain(6), sculpting a powerful antiviral response(7-10) that can drive viruses to extin

103 ovide evidence that TRIM6 contributes to the antiviral response against WNV and identify VAMP8 as a n

104 e I interferon is essential for promoting an antiviral response against WNV infection; however, it is

105 butes to the establishment of an IFN-induced antiviral response against WNV.

106 both type I and type III IFN-mediated innate antiviral responses against human coronaviruses and disc

107 epletion of HDAC6 expression led to impaired antiviral responses against RNA viruses, but not against

108 train T1L, but not strain T3D, represses one antiviral response: alpha/beta interferon signaling.

109 ave been implicated in viral evasion of host antiviral responses, although the mechanisms are still u

110 we establish a direct interplay between this antiviral response and cell-cell interactions, indicatin

111 t1 depletion or ablation enabled an enhanced antiviral response and defense in cells and mice.

112 us, a small group fail to mount an effective antiviral response and develop chronic infections that t

113 aternal exposure to PolyI:C induced a potent antiviral response and hypoxia in the early pregnant ute

114 lymphocyte populations that are key for the antiviral response and immune reconstitution.FUNDINGNIH

115 ival that is associated with pronounced host antiviral response and inflammasome activation together

116 rrectly identifies cells precocious in their antiviral response and links uncertainty in the ordering

117 ected by influenza virus mount a large-scale antiviral response and most cells ultimately initiate ce

118 tion but also is a critical inhibitor of the antiviral response and one of the determinants of CHIKV

119 s during virus infection inhibits the host's antiviral response and promotes virus reactivation of la

120 learance, the host's ability to resolve this antiviral response and return to homeostasis is critical

121 hat this interaction may favor a more potent antiviral response and simultaneously facilitate cancer

122 s can palmitoylate IFITM3 to ensure a robust antiviral response and that ZDHHC20 may serve as a parti

123 nd lower expression of genes involved in the antiviral response and type I IFN signaling.

124 n, which consequently precludes the cellular antiviral response and/or induces cell death.

125 lammation by suppressing innate and adaptive antiviral responses and by instructing epithelial cells

126 nked to neurodegenerative diseases, aberrant antiviral responses and cancer(1-5).

127 priming leads to early activation of innate antiviral responses and cell intrinsic inhibition of vir

128 vivo RNA and DNA viral infections, limiting antiviral responses and enhancing viral growth early aft

129 ses translation of cellular mRNAs to support antiviral responses and explain how influenza virus uses

130 pleiotropic regulator of RIG-I/MDA5-mediated antiviral responses and further highlight the importance

131 CD8 depletion appeared to dysregulate early antiviral responses and possibly increase viral persiste

132 nventional anti-tumor therapeutics, enhanced antiviral responses and protected zebrafish and mice fro

133 red to uninfected cells, where they activate antiviral responses and restrict virus infection.

134 Type I interferon (IFN) antiviral responses and SARS-CoV-2-specific T cell respo

135 mitochondrial dysfunction, regulation of the antiviral response, and integrin-linked kinase (ILK) sig

136 ith both ISG15, an essential effecter of the antiviral response, and p62, a selective autophagy recep

137 to be an integral part of the macrophage IFN antiviral response, and we show that miR-342-5p exerts b

138 in an array of complex processes, including antiviral responses, and may also modulate the efficienc

139 egulation pathways involved in inflammation, antiviral responses, and stress-related neuroendocrine s

140 enes (ISGs) encoding molecules important for antiviral responses, antigen presentation, autoimmunity

141 Interferon (IFN)-mediated antiviral responses are central to host defence against

142 in to elucidate the mechanisms by which host antiviral responses are upregulated in myeloid cells des

143 t FOXO3a plays a critical role in regulating antiviral responses as well as limiting pro-inflammatory

144 nsition by repressing host genes involved in antiviral responses as well as viral proteins that suppo

145 ever, it is unclear how heterogeneity in the antiviral response at the single-cell level impacts vira

146 ying an armory of proteins that counter host antiviral responses at multiple levels.

147 Furthermore, the kinetics of initial antiviral responses at sites of infection remain unclear

148 ral infection and are thought to promote the antiviral response because many viruses encode inhibitor

149 athways involved in the establishment of the antiviral response, both dependent on STING expression.

150 LR activation; this can lead to an effective antiviral response but also immunopathology if RLR activ

151 ector CTL also contributed to the endogenous antiviral response but not to CTL memory generation.

152 Autophagy also plays a role in this neuronal antiviral response, but the mechanism remains obscure.

153 terferons (IFNs) play a crucial role in host antiviral response by activating the JAK/STAT (Janus kin

154 Thus, an arbovirus can evade the host antiviral response by inducing an acute immunosuppressio

155 r confirming the negative role of MYC in the antiviral response by pDC.

156 hHB enhances RIG-I-mediated antiviral responses by promoting RIG-I ubiquitination de

157 pport replication and protect the virus from antiviral responses by the host.

158 As part of their antiviral response, cells also trigger the translational

159 These inhibitors reveal new features of the antiviral response, clarify existing models of signaling

160 opts the host protein CypA to aid evasion of antiviral responses dependent on the effector protein ki

161 e immune cells to regulate antibacterial and antiviral responses downstream of phagocytosis, interfer

162 ing did not play a major role in the NK cell antiviral response during acute infection, but it strong

163 t a unique mechanism for how HCMV avoids the antiviral response during infection by hijacking the fun

164 sion of viral genes and activation of innate antiviral responses during infection result in an increa

165 geted protein degradation contributes to the antiviral response either by down-regulating various met

166 ntified the mechanism of RAB1B action in the antiviral response, finding that it forms a protein comp

167 mmune system cooperate to achieve an optimal antiviral response following influenza virus infection o

168 n active small interfering RNA (siRNA)-based antiviral response for both the wild-type and sfRNA1-def

169 e interaction of alphaviruses with host cell antiviral responses has been conducted using fibroblast

170 ntly induce antibody-dependent cell-mediated antiviral responses: (i) the interaction between the Fc

171 cognition serves as the major stimulus to an antiviral response, implying a requirement to limit the

172 enhance IFN production to mount an effective antiviral response.IMPORTANCE Double-stranded RNAs produ

173 unrecognized strategy for EV71 to evade the antiviral response.IMPORTANCE Recently, it has been repo

174 sm by which WNV NS1 interferes with the host antiviral response.IMPORTANCE WNV Nile virus (WNV) has r

175 and IFN-gamma pathways in achieving optimal antiviral responses.IMPORTANCE IFN-alpha/beta induction

176 We demonstrate an increased antiviral response in B cells and monocytes in HG patien

177 These data point to an untuned antiviral response in COVID-19, contributing to persiste

178 ve evidence of chloride-ion dependent innate antiviral response in epithelial cells, we conducted a p

179 ng out a single miRNA, miR-673, restores the antiviral response in ESCs through MAVS regulation.

180 for the local induction of an ERK-dependent antiviral response in flies.

181 DNA recombination by Cre instigates a robust antiviral response in mammalian cells, independent of le

182 fferent cellular processes, and as a natural antiviral response in plants, nematodes, and insects.

183 Finally, we measured the dynamics of the antiviral response in primary human epithelial cells, wh

184 ascertain the consequences of restoring the antiviral response in the context of pluripotency, we en

185 the innate immune system activates a potent antiviral response in the infected cell, a key component

186 The host antiviral response in tissues maintaining persistent FMD

187 is well tolerated and can induce a sustained antiviral response in WHV-infected woodchucks; the ident

188 erpes simplex virus type 1 (HSV-1)-triggered antiviral responses in a cGAS-dependent manner.

189 ze nucleotide second messengers and initiate antiviral responses in bacterial and animal cells.

190 roposed mechanism involves the activation of antiviral responses in cells receiving CD63-positive EVs

191 his suggests that ISG15 deficiency increases antiviral responses in humans, in stark contrast to expe

192 to whether other host factors participate in antiviral responses in intestinal mucosa.

193 genomes and may also play a crucial role in antiviral responses in mammals, including humans.

194 receptor 3, which triggers type I interferon antiviral responses in mothers infected by Zika virus du

195 in ex vivo vaginal tissue cultures triggered antiviral responses in myeloid and CD4(+) T cells.

196 evade host type I interferon (IFN)-mediated antiviral responses in order to enhance its own propagat

197 Viruses must negotiate cellular antiviral responses in order to replicate.

198 Initially, there was higher antiviral responses in the free HIV compared to compleme

199 t virus infection and correlates with faster antiviral responses in the host.

200 Neuro-COVID patients and suggest compromised antiviral responses in this setting.

201 t functions of STING mediate STING-dependent antiviral responses in vivo.

202 y occurring picornavirus that elicits strong antiviral responses in zebrafish and provides new strate

203 Honey bee antiviral responses include RNA interference and immune

204 Essential components of the innate immune antiviral response, including type I interferon (IFN) an

205 ent viral replication, as it undermines host antiviral responses, including stimulator of interferon

206 e virus has evolved strategies to counteract antiviral responses, including the gene-silencing and in

207 DCs, resulting in the greater activation of antiviral responses, including the type I IFN response.

208 The type I IFN antiviral response increased the pathology of L. guyanen

209 Additionally, loss of RAB1B dampened the antiviral response, indicated by enhanced Zika virus inf

210 pp71 PTM diminishes its ability to undermine antiviral responses induced by the STING pathway.

211 viruses centre on virus-triggered inducible antiviral responses initiated by RIG-I-like receptors or

212 istinct evasion mechanisms from the cellular antiviral response involving vMIA, a virally-encoded pro

213 Moreover, the noncytotoxic CD8(+) T cell antiviral response is a primary mediator of natural HIV

214 ediators in regulating anti-inflammation and antiviral response is also discussed.

215 The acute antiviral response is mediated by a family of interferon

216 Here, we show that the intestinal epithelial antiviral response is programmed to enable protection wh

217 Importantly, this MDA5-dependent antiviral response is specific to the pancreas of rotavi

218 Central to the execution of this particular antiviral response is the small ubiquitin-like modifier

219 hanism by which a type I interferon-mediated antiviral response is triggered.

220 l replication intermediate known to activate antiviral responses, is determined by the cellular locat

221 A better understanding of how recipient antiviral responses lead to breakthrough alloimmunizatio

222 We hypothesized that antiviral responses may impact the efficacy of immunopro

223 However, induction of such antiviral responses may not be exclusive to viruses, as

224 gers of type 1 diabetes (T1D) and macrophage antiviral responses may provide a link to virus-induced

225 virus 1, or cytomegalovirus induced a strong antiviral response measured by upregulation of interfero

226 Further, in contrast to wild-type virus, the antiviral response mediated by the viral DNA-sensing cyc

227 leukocyte antigen (HLA) proteins that limit antiviral responses mediated by natural killer (NK) cell

228 By obstructing the type I IFN-induced antiviral response, miR-BART16 provides a means to facil

229 eractions with proteins involved in cellular antiviral responses, nuclear activities, and biogenesis

230 cate that US11 facilitates the countering of antiviral response of infected cells and promotes the ef

231 Here, we addressed whether antiviral response of peripheral blood lymphocytes diffe

232 sented a potential solution to enhancing the antiviral response of these cells.

233 ic RLR receptor shifts the common interferon antiviral responses of infected cells to necroptosis and

234 independent of the known CD8(+) T cell-based antiviral responses or changes in lipid synthesis and li

235 ks that regulate viral replication or innate antiviral response pathways.

236 mplex cellular networks activated during the antiviral response, placing IFN-stimulated genes in a fu

237 as potential therapeutic targets to enhance antiviral responses postvaccination and postinfection.

238 g early illness are indicators of an altered antiviral response potentially contributing to disease s

239 f immunity is that interferon (IFN)-mediated antiviral responses precede pro-inflammatory ones, optim

240 a suggest that the temporal induction of the antiviral response primes iPSCs away from pluripotency a

241 This effective and durable antiviral response probably participates in a virtuous c

242 The interferon (IFN)-mediated antiviral response represents an important component of

243 Ifit5, Irf7, Isg15, orMx1), illustrating an antiviral response signature.

244 The master regulator of interferon-mediated antiviral responses - stimulator of interferon genes (ST

245 g the attenuating mutation induced decreased antiviral responses, suggesting why this subject could b

246 r ZIKV entry and lack components of a robust antiviral response system.

247 f autophagy, that promotes a cell-autonomous antiviral response that arose before evolution of the in

248 -1) is an effector of the host innate immune antiviral response that prevents propagation of virus in

249 ral infection causes the host to activate an antiviral response that, in part, is dependent on mitoch

250 cells recognize viruses is unclear, and the antiviral responses that are initiated following virus r

251 f preventing or counteracting the cascade of antiviral responses that double-stranded RNA (dsRNA) tri

252 doing so, is highly efficient in undermining antiviral responses that limit successful infections.

253 ed by a bacterial origin ultimately involves antiviral responses that result in host translation shut

254 ple viral proteins that antagonize each host antiviral response, thereby allowing for efficient viral

255 t viral glycoproteins induce a strong innate antiviral response through activating the ER stress path

256 antly surveying the cell to rapidly mount an antiviral response through the synthesis and downstream

257 rosis is associated with a defective mucosal antiviral response through ZEB1-initiated epigenetic sil

258 gene expression, mitochondrial activity, and antiviral responses through IFN activity.

259 r, immunoglobulin G (IgG) can also stimulate antiviral responses through its constant region.

260 ter understanding of the interferon-mediated antiviral response to dengue virus may aid in the develo

261 gh RIG-I is also known to have a role in the antiviral response to DNA viruses, physiological RNA spe

262 Additionally, inhibition rescued the antiviral response to exogenous type I IFN, as measured

263 The antiviral response to GS-9688 did not correlate with sys

264 r immune cell subsets may play a role in the antiviral response to GS-9688.

265 g and the HCMV U(L)26 protein in shaping the antiviral response to HCMV.IMPORTANCE Modulation of cell

266 S4A and defines a new role for Riplet in the antiviral response to HCV.

267 Silencing of RNA5SP141 strongly dampened the antiviral response to HSV-1 and the related virus Epstei

268 to IFN pathway genes that play a role in the antiviral response to HuNoVs, we developed knockout (KO)

269 nally, BMP6 enhanced the transcriptional and antiviral response to IFN, but BMP6 and related activin

270 must overcome the interferon (IFN)-mediated antiviral response to replicate and propagate to new hos

271 However, our understanding of the antiviral response to WNV infection is mostly derived fr

272 fect in NK cell metabolism, transcription or antiviral responses to MCMV infection.

273 s (80%) and particularly in blood (85%), and antiviral responses to oseltamivir appeared less pronoun

274 ggest potential differences in virulence and antiviral responses to oseltamivir that may explain the

275 ession.IMPORTANCE Viruses must suppress host antiviral responses to replicate and spread between host

276 We found evidence of strong innate antiviral responses together with induction of neutraliz

277 An integral component of the antiviral response, type I IFNs require regulation to mo

278 irus (CMV) antigens, which stimulates a host antiviral response: UL83 (pp65), UL123 (IE1-exon4), and

279 ole T cells play in the orchestration of the antiviral response underlying the pathogenesis of the di

280 etroviruses and activate ubiquitin-dependent antiviral responses upon capsid recognition.

281 In microglia, cytoplasmic DNA primes an antiviral response via the DNA sensor, STING (stimulator

282 rt the hypothesis that EVEs contribute to an antiviral response via the piRNA pathway, limited nucleo

283 suppresses NF-kappaB activation, a powerful antiviral response, via interactions with the NF-kappaB

284 ere pp71 is not protein S-nitrosylated, host antiviral response was inhibited.

285 In these animals, the antiviral response was maintained until the end of the s

286 An antiviral response was not evident in rat trophoblast st

287 d DNA levels by >95% in animals in which the antiviral response was sustained after treatment cessati

288 In contrast, no detectable antiviral response was triggered by the dsRNA from a beg

289 he initiation of both apoptosis and the host antiviral response, we analyzed the role of NF-kappaB du

290 ribonucleoproteins and measuring the cell's antiviral response, we were able to provide direct evide

291 o elucidate the role of FOXO3a in regulating antiviral responses, we generated airway epithelial cell

292 ficient in a variety of innate intracellular antiviral responses, we show that DVGs induce an unchara

293 ction is associated with an enhanced mucosal antiviral response, whereas FMDV persistence is associat

294 ction of primary human TEC did not induce an antiviral response, whereas infection with influenza A v

295 ither p62 or OPTN were able to mount greater antiviral responses, whereas cells expressing exogenous

296 ellular fate and a contributor to the innate antiviral response, which together control influenza vir

297 SARS-CoV-2 induced a strong antiviral response with up-regulation of antiviral facto

298 ins (GBPs), is involved in antimicrobial and antiviral responses within the cell.

299 In contrast to the induction of antiviral responses, WNV infection did not promote trans

300 on and appears adept at evading normal human antiviral responses, yet it remains poorly characterized