ライフサイエンスコーパス: antiviral response

1 ignaling and promote fly survival during the antiviral response.

2 of type I interferon, a key component of the antiviral response.

3 interfering RNA (siRNA) pathway is the major antiviral response.

4 ay be crucial for the onset of an early host antiviral response.

5 ecognizes viral RNA and signals to induce an antiviral response.

6 influenza A virus pathogenicity and the host antiviral response.

7 life cycle is an important mechanism of the antiviral response.

8 ve evolved strategies to subvert this potent antiviral response.

9 es (STING), leading to IFN production and an antiviral response.

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

11 specific molecules that aid in a productive antiviral response.

12 ase involved in autoimmune disorders and the antiviral response.

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

14 ompatibility complex class I (MHC-I) and the antiviral response.

15 f VEGF-mediated suppression of the intrinsic antiviral response.

16 dentified a role for SETX in controlling the antiviral response.

17 les required to activate IRF3 and trigger an antiviral response.

18 enes, resulting in significantly compromised antiviral response.

19 ble for viral activation of interferon (IFN) antiviral response.

20 detect pathogenic RNA and induce a systemic antiviral response.

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

22 diator also has several complex roles in the antiviral response.

23 nting inappropriate activation of the innate antiviral response.

24 uitin axis as critical for IFN signaling and antiviral response.

25 viral transcription and can trigger the host antiviral response.

26 ontributor to the overall development of the antiviral response.

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

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

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

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

31 echanism employed by viruses to counter this antiviral response.

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

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

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

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

36 the main viral factor counteracting the host antiviral response.

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

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

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

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

41 with RV1B to determine lung inflammation and antiviral response.

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

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

44 te immune receptors to promote an integrated antiviral response.

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

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

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

48 differential effects on HCMV replication and antiviral responses.

49 ulation that inhibition of AXL would promote antiviral responses.

50 ry DNA (ISD) pathway, which is essential for antiviral responses.

51 tinating enzyme USP7 to inhibit p53-mediated antiviral responses.

52 lead to induction of RNA-triggered cellular antiviral responses.

53 e-stranded RNA (dsRNA) and promotion of host antiviral responses.

54 AM receptor activation and downregulation of antiviral responses.

55 uclei of infected cells and counteracts host antiviral responses.

56 ponsible for increased infection and reduced antiviral responses.

57 antiviral signaling protein (MAVS)-mediated antiviral responses.

58 cycle and counteract intrinsic and extrinsic antiviral responses.

59 lls, potentially accelerating and broadening antiviral responses.

60 ntrol of viral infection in conjunction with antiviral responses.

61 s that can activate IRF3 to promote cellular antiviral responses.

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

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

64 ing, disrupts interferon gene expression and antiviral responses.

65 bsets of monocytic cells and interferes with antiviral responses.

66 protect viral RNAs from destruction by host antiviral responses.

67 Type I IFN plays a key role in antiviral responses.

68 ral demonstrating roles in regulating innate antiviral responses.

69 ocyte subsets function together to fine-tune antiviral responses.

70 ples collected to assess virus infection and antiviral responses.

71 at DENV has developed to manipulate cellular antiviral responses.

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

73 eurovirulence and regulates several cellular antiviral responses.

74 on and affect processes including immune and antiviral responses.

75 biological context for MDA5-RNA filaments in antiviral responses.

76 greater insight into viral pathogenicity and antiviral responses.

77 toimmune diabetes and, conversely, restrains antiviral responses.

78 favorable cell conditions and overcome cell antiviral responses.

79 wheezing but not increased atopy or reduced antiviral responses.

80 ge in macrophages to promote interferons and antiviral responses.

81 ruses accomplish this by repressing specific antiviral responses.

82 ncoded immune evasion molecules that inhibit antiviral responses.

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

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

85 tly related to aeroallergen sensitization or antiviral responses.

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

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

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

89 sitive regulatory role for NLRX1 in inducing antiviral responses.

90 rmeasures of HCV for suppression of the host antiviral response, a miRNA array was performed by using

91 NV or CHIKV infection generated a protective antiviral response against both pathogens in immune and

92 bda (but not IFN-alpha) produced a sustained antiviral response against HCV.

93 tigate the role of p38 MAPK signaling in the antiviral response against HPAIV in mice as well as in h

94 achieve a maximal RIG-I-mediated protective antiviral response against human-pathogenic RNA viruses.

95 butes to the elucidation of the lepidopteran antiviral response against infection of segmented double

96 stered, RIG-I stimulation generated a robust antiviral response against these two viruses.

97 Thus, knockdown of RIOK3 inhibits cellular antiviral responses against both DNA and RNA viruses (he

98 mechanism is likely to shield the priming of antiviral responses against inhibition or abrogation by

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

100 ng viruses outcompete or subvert the initial antiviral response, allowing the establishment of chroni

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

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

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

104 , the roles of pulmonary eosinophilia in the antiviral response and in disease pathogenesis are inade

105 nknown mechanism by which HCV attenuates the antiviral response and indicate new potential therapeuti

106 FN-lambda1), a type III IFN, showed a strong antiviral response and induced viral clearance.

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

108 ypes of factors that both undermine the host antiviral response and regulate viral replication, inclu

109 the physiological role of miRNAs during the antiviral response and suggests their contribution is li

110 itute a platform for evasion of the cellular antiviral response and that the human cytomegalovirus ha

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

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

113 hat prevents the virus from suppressing host antiviral responses and a gene encoding bacterial flagel

114 in an evolutionary arms race with the host's antiviral responses and adaptation of viruses to new hos

115 numerous ways to subvert these intracellular antiviral responses and directly inhibit cellular signal

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

117 in an evolutionary arms race with the host's antiviral responses and facilitates adaptation of viruse

118 FN-alpha/beta), which promotes intracellular antiviral responses and helps initiates the adaptive res

119 a deficiency of TAM receptors would enhance antiviral responses and protect against viral infection.

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

121 tomegalovirus (HCMV) is known to up-regulate antiviral responses and suppress virus replication.

122 luded genes associated with inflammatory and antiviral responses and was particularly apparent among

123 de an apoptotic cytopathic effect, an innate antiviral response, and a metabolic shift toward aerobic

124 lifications for genes that drive cell cycle, antiviral response, and inhibit cell differentiation.

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

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

127 HCV encodes several strategies to evade this antiviral response, and this evasion of innate immunity

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

129 included expression of NLRX1, which inhibits antiviral responses, and activation of the TGF-beta path

130 al reservoir, elicit efficient cell-mediated antiviral responses, and induce intermittent posttherapy

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

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

133 on pattern of regulators of Ag presentation, antiviral responses, and transcription factors.

134 ion, viral proteins that modulate immune and antiviral responses, and virulence factors that increase

135 Here we demonstrate that, to escape this antiviral response, antibody-opsonized DENV coligates le

136 ype I and type II interferon responses, RNAi antiviral responses, antigen presentation, T-cell-depend

137 However, the roles of RXRalpha in host antiviral response are unknown.

138 Neuronal antiviral responses are driven by type I interferon (IFN

139 ral immunity and suggest, rather, that their antiviral responses are predominated by IFN-lambda respo

140 e uncommon in untreated CLL, suggesting that antiviral responses are uncompromised.

141 mune regulatory responses that dampen Th1/M1 antiviral responses as well as promote reactivation of l

142 -dependent mTORC1 activation functions as an antiviral response, as mTORC1 inhibition increases the e

143 e ability to circumvent the interferon (IFN) antiviral response, as suggested for PEDV, promotes vira

144 ing of the contribution of IFN-lambda to the antiviral response at anatomic barriers and the immune r

145 pathology while still allowing for effective antiviral responses at a site of infection.

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

147 infection MAVS does not only elicit a type I antiviral response but also recruits caspase-8 to mitoch

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

149 and NLRX1 as important players in the innate antiviral response, but their roles in the generation of

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

151 transcription factor IRF-3 mediates cellular antiviral response by inducing the expression of interfe

152 ing of activating FcgammaRs signals an early antiviral response by inducing the type-I IFN-stimulated

153 rus nucleocapsid protein counteracts the PKR antiviral response by inhibiting PKR dimerization, which

154 in virus replication and inhibition of host antiviral response by means of its host protein synthesi

155 We envision that evasion of the PKR antiviral response by NP has likely helped hantaviruses

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

157 P) proteins are key regulators of the innate antiviral response by virtue of their capacity to respon

158 t the D10 decapping enzyme may help restrict antiviral responses by accelerating host mRNA degradatio

159 ) on bronchial epithelial cell innate immune antiviral responses by assessing interferon (IFN-beta an

160 More importantly, the induction of antiviral responses by BTV resulted in significant suppr

161 f the 5' cap of viral RNA subverts mammalian antiviral responses by evading restriction of Ifit1, an

162 uble-stranded RNA (dsRNA), which can trigger antiviral responses by inducing phosphorylation-mediated

163 which remove caps from mRNAs, inhibit these antiviral responses by preventing dsRNA accumulation.

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

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

166 ence of positive selection in genes encoding antiviral responses, components of the Toll and JAK/STAT

167 Colonization events and antiviral responses consisting of total specific immunog

168 ting that the same virus can induce distinct antiviral responses depending on the MOI.

169 rovide opportunities to activate cytoplasmic antiviral responses directed against capsid or viral DNA

170 Thus, an effective antiviral response does require MyD88, but TLR2 is not r

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

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

173 ivities have been suggested to suppress host antiviral responses during infection.

174 on of host cell cycle regulators, as well as antiviral response factors.

175 irus (Ad) infection triggers a cell-specific antiviral response following exposure of viral DNA to th

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

177 s to enhance virus replication by regulating antiviral responses following viral infection.

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

179 unique mechanism for DENV to evade an early antiviral response for enhanced infection.

180 ry pressure on hantaviruses to evade the PKR antiviral response for survival.

181 t methods for detecting viral infections and antiviral responses have limited throughput and coverage

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

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

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

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

186 with virus resulted in a marked reduction of antiviral response in conditionally deleted adults.

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

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

189 Viruses efficiently block the host antiviral response in order to replicate and spread befo

190 lammatory gene expression and down-regulated antiviral response in people experiencing perceived soci

191 a key role for IRF-5 in modulating the host antiviral response in peripheral organs that controls bu

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

193 es have been little studied, and the initial antiviral response in the midgut has not been examined.

194 The host antiviral response in tissues maintaining persistent FMD

195 mily of cytokines that are essential for the antiviral response in vertebrates.

196 ne-rich RIG-I agonist generated a protective antiviral response in vitro and in vivo and was effectiv

197 in the regulation of innate immunity and the antiviral response in zebrafish, and point to the need f

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

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

200 ted effective RSV antagonism of IFN-mediated antiviral responses in infected cells.

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

202 sphorylation, IFN-alpha/beta production, and antiviral responses in MEFs in response to RNA virus inf

203 USP21 also restricted antiviral responses in peritoneal macrophages (PMs) and

204 To study antiviral responses in PRRSV-infected monocytic cells, w

205 espite this view, several pathogens activate antiviral responses in the absence of type I interferons

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

207 ted evasion mechanism controlling endogenous antiviral responses in the liver.

208 nsible for the inability to mount protective antiviral responses in this setting.

209 Honey bee antiviral responses include RNA interference and immune

210 ) infection in hepatocytes stimulates innate antiviral responses including the production of type III

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

212 Only a few of these cytokines mount an antiviral response, including type I, II, and III interf

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

214 ontraction-to-memory phase transition of the antiviral response increased autophagic activity and enh

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

216 ory factors prior to infection, a more rapid antiviral response, increased resistance to virus infect

217 FN receptor knockout mice suggested that the antiviral response induced by Ad5-poIRF7/3(5D) was depen

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

219 The interferon (IFN)-driven antiviral response is critical for the control of HSV-1

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

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

222 ws that the expression of many gene involved antiviral responses is dependent on RIOK3.

223 biological processes, but their role in host antiviral responses is largely unknown.

224 ategies to evade this powerful, IFN-mediated antiviral response, it is not well-defined if IAV manipu

225 fend against hantavirus infection, but those antiviral responses may also contribute to hantavirus di

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

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

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

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

230 a lncRNA that we call negative regulator of antiviral response (NRAV) was dramatically downregulated

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

232 he level of viral replication, and the early antiviral response observed in the plasma is predominant

233 We conclude that deficits in the interferon antiviral response of cancer cells do not contribute to

234 ese results further our understanding of the antiviral response of neurons and highlight the importan

235 aviruses and primarily serves to inhibit the antiviral response of the host.

236 The main limiting factor in the antiviral response of twp mice was impaired T cell proli

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

238 that adult TG neurons can mount an effective antiviral response only if provided with an exogenous so

239 also implicated miRNAs as regulators of the antiviral response, others have found that the RISC comp

240 many cellular processes, particularly innate antiviral response pathways.

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

242 vive but also that they acquire a heightened antiviral response phenotype after surviving.

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

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

245 the liver while inducing an inflammatory and antiviral response remains unclear.

246 fection to allow the generation of effective antiviral responses remains largely unclear.

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

248 Given the potency of this antiviral response, RLRs are tightly regulated at variou

249 ses to interfere with the development of the antiviral response strongly complicate identification of

250 r recruiting signaling molecules involved in antiviral responses such as apoptosis and innate immunit

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

252 s, or exogenous IFN-beta restored protective antiviral responses, suppressed infection, and improved

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

254 te that alpha cells trigger a more efficient antiviral response than beta cells, including higher bas

255 bies virus itself would induce a more robust antiviral response than would occur naturally in mice.

256 by human trophoblast cells elicits a strong antiviral response that alters the recruitment and activ

257 interferon system exerts an extremely potent antiviral response that efficiently restricts virus repl

258 receptors RIG-I, LGP2, and MDA5 initiate an antiviral response that includes production of type I in

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

260 ystem, a component of the interferon-induced antiviral response that senses double-stranded RNA and a

261 3 replicates rapidly, but is unable to evade antiviral responses that constrain its spread hence also

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

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

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

265 USP21 acts as a novel negative regulator in antiviral responses through its ability to bind to and d

266 The antiviral response to a 12- to 16-week course of SOF/RBV

267 findings are important in understanding the antiviral response to CCHFV and support continued invest

268 ghlights a critical signaling pathway in the antiviral response to CCHFV.

269 IG-I as a receptor involved in initiating an antiviral response to CCHFV.

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

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

272 gh the adapter protein STING to initiate the antiviral response to DNA viruses.

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

274 id-induced type I IFN production and for the antiviral response to gammaherpesvirus through two indep

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

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

277 f murine cGAS reveals its requirement in the antiviral response to two DNA viruses, and an unapprecia

278 molecules that activate IRF3 to promote host antiviral responses to broadly suppress infections cause

279 e cultured to determine pro-inflammatory and antiviral responses to IL-13 and RV16.

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

281 nules is central in orchestrating stress and antiviral responses to restrict viral replication.

282 Here we show that RIG-I also mediates antiviral responses to RNAs bearing 5'-diphosphates (5'p

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

284 sm that enhances specificity and prevents an antiviral response upon encounter with host RNA molecule

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

286 cancer cells due in part to defects in their antiviral responses upon exposure to type I interferons

287 l and critical role for ATR as a mediator of antiviral responses utilizing LT.

288 RIG-I binds to viral RNA, eliciting an antiviral response via the cellular adaptor MAVS.

289 However, viral regulation of the antiviral responses via mDRM remains incompletely unders

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

291 The magnitude of the IRF3/IFN/ISG antiviral response was strongly influenced by serotype,

292 nstable capsid that induces a strong IFNbeta antiviral response, we identify three sensors, IFI203, D

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 on or RXR antagonist treatment benefits host antiviral response, whereas RXR agonist treatment may in

296 ght to allow viruses to escape from the host antiviral response, which restricts virus replication an

297 PD to influenza likely results from impaired antiviral responses, which are mediated by increased PI3

298 ss to viral infection is modulated by innate antiviral responses, which vary among different cell typ

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

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