ライフサイエンスコーパス: antiviral

1 ed for future development of new Lassa virus antivirals.

2 delay relapse while patients were receiving antivirals.

3 tablished vaccination programme and approved antivirals.

4 g LT, with lower costs and lower exposure to antivirals.

5 The antiviral actions of IRF-1 appeared to be independent of

6 The antiviral actions of IRF-1 resulted in decreased local i

7 HCV subverts the antiviral actions of these miRNAs by dampening their exp

8 The antiviral activities of synthesized Kalpha2-helix peptid

9 thieno[3,2-b]pyrrole 1b that displayed good antiviral activity against CHIKV infection in vitro.

10 in an interferon-dependent manner, displays antiviral activity against DENV, and localizes to the DE

11 on-sulfur (Fe/S) cluster is critical for its antiviral activity against many different viruses.

12 RNA production and displayed broad-spectrum antiviral activity against other alphaviruses and CHIKV

13 egrase strand transfer inhibitor with potent antiviral activity and a long half-life when administere

14 ulator in innate immune responses due to its antiviral activity and association with autoimmune disea

15 Thus, caution must be taken when predicting antiviral activity based on percent channel blockage in

16 60 new analogues and determination of their antiviral activity in a single-cycle and a multicycle in

17 Drugs with demonstrated antiviral activity in the nonhuman primate models alread

18 These insights into the mechanism of antiviral activity of CD4mc should assist efforts to opt

19 These results confirm the robust antiviral activity of N6-LS in vivo, supporting the furt

20 JUNV's ability to antagonize the antiviral activity of PKR appears to be complete, as sil

21 The antiviral activity of these compounds in an Ebola pseudo

22 We further sought to correlate the antiviral activity of these peptides and their effects o

23 t monotherapy studies to evaluate safety and antiviral activity should be conducted prior to proceedi

24 r enzymes, ZDHHC20 uniquely increased IFITM3 antiviral activity when both proteins were overexpressed

25 f HLA-C expression demonstrated by increased antiviral activity when exposed to viral strains with di

26 maller than 10(-6) while they do not exhibit antiviral activity when kd is 10(-5) or higher although

27 /M2 channels, and (ii) the compounds display antiviral activity when they have kd equal or smaller th

28 omatic hypermutations are required for broad antiviral activity, and germline-approximating variants

29 a membrane localization is required for Ser5 antiviral activity, and Ser5-001 is the predominant isof

30 as potent viral DNA mutators and have broad antiviral activity.

31 ht into the mechanism of IFN-lambda-mediated antiviral activity.IMPORTANCE Human noroviruses (HNoVs)

32 ucture are a step towards the development of antivirals against ZIKV and other flaviviruses.

33 Resumption of direct-acting antiviral agent therapy after a temporary interruption a

34 n and the potential use of 25HC as a natural antiviral agent to combat ZIKV infection and prevent ZIK

35 been treated previously with a direct-acting antiviral agent were assigned randomly to groups given s

36 and safety of a once-daily, 2-direct-acting-antiviral-agent (2-DAA) combination of simeprevir + TMC6

37 enal transplant population but direct acting antiviral agents (DAA) provide an effective cure of HCV

38 tment with regimens containing direct-acting antiviral agents (DAAs) have limited retreatment options

39 nt attractive targets for the development of antiviral agents against chronic HBV infection.

40 urrent therapies with all-oral direct-acting antiviral agents are associated with high rates of susta

41 Survival data with direct-acting antiviral agents are not available.

42 In the event of a pandemic, antiviral agents are the mainstay for treatment, but bro

43 inclusion (with interferon then with direct antiviral agents) and underwent an ultrasound examinatio

44 In this study we tested the antiviral and anti-inflammatory activity of the H2S slow

45 inhibit HBV replication alone, enhanced the antiviral and antifibrotic activities of single and dual

46 eas defects in TH1 and TH17 cells compromise antiviral and antifungal immunity, respectively, explain

47 occur in parallel with development of novel antiviral and immune modulatory therapies such that appr

48 ctivated, this MX1 construct phenocopies the antiviral and NP binding activity of wild type MX1.

49 These differences may inform antiviral and vaccine strategies.

50 state, thus facilitating the development of antivirals and latency reactivating agents.

51 igen stimulation is necessary for successful antiviral, and antitumor immune responses.

52 Further trials of immunosuppression, antiviral, and immunomodulating therapies are needed.

53 fits for human health, such as anti-oxidant, antiviral, and liver-protective properties.

54 paves the way for lead optimization for VEEV antivirals, and is an exciting prospect to identify inhi

55 history of clinical and scientific use as an antiviral, antibacterial, and antitumor agent.

56 e HIV-1 envelope, with the goal of eliciting antiviral antibodies.

57 with significant antibacterial, antifungal, antiviral, antiparasitic, antitumour, anti-inflammatory,

58 ctivation of T, B, and NK cells and exhibits antiviral, antiproliferative, and antibacterial activiti

59 epatitis B virus and development of curative antivirals are hampered by a scarcity of models that mim

60 Broad-spectrum antivirals are highly sought after and studied because t

61 Continuation of prolonged antivirals beyond initial clearance was not associated w

62 actic vaccine exists and currently available antivirals can suppress but rarely cure chronic infectio

63 unctionality and contribute to the increased antiviral capacity of HIV-specific CD8(+) T cells in eli

64 together, these data suggest that the potent antiviral capacity of some HIV-specific CD8(+) T cells i

65 istinct viral proteins, thereby limiting its antiviral capacity.

66 V controllers develop particularly efficient antiviral CD4(+) T cell responses mediated by shared hig

67 therapy or in rare cases spontaneously, most antiviral CD8 T cells do not enter B-cell follicles, and

68 R5+ CD8 T cells represent a unique subset of antiviral CD8 T cells that expand in LNs during chronic

69 s are considered to be immune privileged for antiviral CD8 T cells.

70 hed cross-priming and expansion of cytolytic antiviral CD8(+) T cells.

71 ll receptor (TCR) clonotypes in differential antiviral CD8(+) T-cell function, we performed detailed

72 Hyperthermia increases expression of the antiviral cellular factors APOBEC3A and APOBEC3G and ind

73 es and suggest that this property influences antiviral cellular immune responses.IMPORTANCE Primate l

74 hat, in this context, Drosha functions as an antiviral clamp, conferring steric hindrance on the RNA-

75 Through this pathway, the antiviral compound ribavirin 5'-monophosphate is signifi

76 LJ001 is a broad-spectrum antiviral compound that inhibits enveloped virus infecti

77 our studies, we used LJ001, a broad-spectrum antiviral compound that specifically inhibits enveloped

78 be used to better model disease and develop antiviral countermeasures.

79 ltispecificity of the VSTs ensures extensive antiviral coverage, which facilitates the treatment of p

80 genic types, by treatment with IFN-gamma, an antiviral cytokine that is released from stimulated immu

81 individuals who can produce IFN-lambda4, an antiviral cytokine, are also less likely to clear hepati

82 mice had a transiently reduced production of antiviral cytokines and an impaired CD4(+) T cell respon

83 capacity of the VA to deliver direct-acting antiviral (DAA) HCV therapy, supported by an infrastruct

84 GROUND & AIMS: Interferon-free direct-acting antiviral (DAA) therapies are effective in patients with

85 Although direct-acting antiviral (DAA) therapies for chronic hepatitis C virus

86 infected individuals receiving direct-acting antiviral (DAA) therapy.

87 fectiveness of two alternative direct-acting antiviral (DAA) treatment policies in a real-life cohort

88 virus (HCV) patients involves direct-acting antivirals (DAA).

89 a on the effectiveness of oral direct-acting antivirals (DAAs) in predominantly minority HIV/HCV coin

90 stained virologic responses to direct-acting antivirals (DAAs), which lack immunomodulatory propertie

91 ulation represents a pivotal balance between antiviral defences and autoimmunity.

92 hway activation, but their relative roles in antiviral defense are not well understood.

93 -beta in response to VSV plays a key role in antiviral defense during infection.

94 antiviral protein and provide insights into antiviral defense mechanisms.

95 ng elicits interferon production for primary antiviral defense through cascades controlled by protein

96 r characterize the mechanism(s) of honey bee antiviral defense, bees were infected with a model virus

97 sizing a critical role for NK cells in human antiviral defense.

98 connect epithelial cells, evading immune and antiviral defenses and provide an explanation for the in

99 ing human cytomegalovirus (HCMV), blunt host antiviral defenses by limiting ISG expression, the overa

100 tion, and egress as well as the avoidance of antiviral defenses through the sequestration of key cell

101 to facilitate viral replication and inhibit antiviral defenses.

102 Targeting the TP domain for antiviral development is difficult due to the lack of ho

103 on was not completely blocked at established antiviral doses.

104 ent data and the addition of host factor and antiviral drug components.

105 Moreover, binding of the antiviral drug, amantadine, at the N-terminal pore at lo

106 ave the potential for further development as antiviral drugs against CHIKV infection.

107 as a potential target in the development of antiviral drugs against EBOV.

108 esis and to assess the efficacy of candidate antiviral drugs and new vaccines.IMPORTANCE Early pathog

109 ry illness for which no vaccines or suitable antiviral drugs are available.

110 However, no specific vaccines or antiviral drugs are currently available to prevent or tr

111 Licensed vaccines or suitable antiviral drugs are not available.

112 New direct-acting antiviral drugs for the treatment of chronic hepatitis C

113 DNA and L-dCTP or the triphosphate forms of antiviral drugs lamivudine ((-)3TC-TP) and emtricitabine

114 0 years, there are no commercially available antiviral drugs or vaccines.

115 g of the mode of action of the highly potent antiviral drugs that are targeted to NS5A.

116 rse combination therapies with direct-acting antiviral drugs that might be explored in future clinica

117 used to study polio pathogenesis, candidate antiviral drugs, and the efficacy of new vaccines.

118 ial avenues for the development of alternate antiviral drugs.

119 ural 5A protein (NS5A) is the target for new antiviral drugs.

120 as a valuable tool for evaluating promising antiviral drugs.

121 attenuation and new targets for screening of antiviral drugs.

122 y complex internalization could result in an antiviral effect, since it may interfere with virus part

123 Current antivirals effectively target diverse viruses at various

124 eted, specific signaling pathways leading to antiviral effectors are affected.

125 Lambda interferon (IFN-lambda) has potent antiviral effects against multiple enteric viral pathoge

126 l(s) upon which IFN-lambda acts to exert its antiviral effects is unclear.

127 The antiviral effects of bat IFNs appeared not to correlate

128 The antiviral effects of hepatitis C virus (HCV)-specific CD

129 rategies used by flavivirus NS5 to evade the antiviral effects of IFN-I and how this information can

130 ed with TNF before infection, the subsequent antiviral effects of IFNs were increased.

131 ated the role of type I IFN induction in the antiviral effects of the miR-34 family and confirmed tha

132 fic CD8 T-cell activation with cytolytic and antiviral effects was blunted by PD-L1 expression on HCV

133 HCV-specific CD8 T cells and the downstream antiviral effects.

134 argues for the need to maximize breadth and antiviral efficacy by combining bnAbs for therapeutic in

135 eased functional CD4 T cell avidity improved antiviral efficacy of CD8 T cells.

136 ost-LT HCV treatment with oral direct-acting antivirals for patients with MELD scores between 10 and

137 tive immune responses and having potentially antiviral functions against HIV using a novel focused om

138 Surprisingly, and despite the antiviral functions of ISG15 described in mice, humans b

139 tigated whether the potent antibacterial and antiviral functions of LL-37 were inhibited by exposure

140 circulating inflammatory chemokines, blunted antiviral gene signature within the pancreas, and reduce

141 ults provide insight into a newly identified antiviral gene, as well as broadening our understanding

142 faster than other type III IFNs in inducing antiviral genes, as well as negative regulators of the I

143 t as Prevention (TasP) using directly-acting antivirals has been advocated for Hepatitis C Virus (HCV

144 regulating epithelial cell proliferation and antiviral host defense during the normal wound healing r

145 Apoptosis is an important antiviral host defense mechanism.

146 ergic respiratory disease is able to promote antiviral host defenses against the influenza virus.

147 navirus nucleoproteins and uncovers a potent antiviral host protein that is neutralized during Junin

148 cular immunization of mice results in strong antiviral humoral and cellular immune responses.

149 activating endosomal toll-like receptors and antiviral humoral immunity.

150 interplay of immune cell subsets involved in antiviral humoral immunity.

151 attached to any protein, to induce efficient antiviral IFN-I-mediated responses.

152 important role for the regulation of the bee antiviral immune response by ATP-sensitive inwardly rect

153 T cells in AGMs may lead to tissue-specific antiviral immune responses in lymphoid follicles that li

154 f class I PI3K played a role in induction of antiviral immune responses.

155 acerbation; however, only anti-IL-33 boosted antiviral immunity and decreased viral replication.

156 studies reveal a novel function for CFTR in antiviral immunity and demonstrate that the DeltaF508 mu

157 toid dendritic cells (pDCs) are important in antiviral immunity and in maintaining tolerance to inert

158 dapted poxvirus MCV can so effectively evade antiviral immunity and suppress inflammation to persist

159 nstrated role in shaping innate and adaptive antiviral immunity by inducing the expression of IFN-sti

160 Because HLA-E plays an important role in antiviral immunity by regulating natural killer and CD8(

161 irus replication are the primary triggers of antiviral immunity in many RNA virus infections.

162 athway and has emerged as a key mechanism of antiviral immunity in metazoans, including the selective

163 utophagy plays a paramount role in mammalian antiviral immunity including direct targeting of viruses

164 However, whether YAP has a role in innate antiviral immunity is largely unknown.

165 necroptosis has been shown to contribute to antiviral immunity, death-independent roles for RIPK3 in

166 using several immunomodulators for boosting antiviral immunity, immunotherapy that is able to induce

167 t orthogonal therapies designed to stimulate antiviral immunity, such as therapeutic vaccines or broa

168 so promotes transgenerational inheritance of antiviral immunity.

169 es exacerbates Tfr cell responses to subvert antiviral immunity.

170 rotein translation, autophagy, apoptosis and antiviral immunity.

171 Antiviral inflammatory responses are a crucial component

172 ion and also determine which of the approved antiviral inhibitor drugs is likely to be the most effec

173 HIV infection.IMPORTANCE The greater ex vivo antiviral inhibitory activity of CD8(+) T cells from eli

174 alization and ability to negatively regulate antiviral innate immunity dependent on the adaptors MAVS

175 lines, transcription factor DMRTA1 (27%) and antiviral interferon epsilon (IFNE, 19%).

176 n ligase that activates RIG-I to promote the antiviral interferon response.

177 infection not only through the induction of antiviral interferons and pro-inflammatory cytokines, bu

178 blocking PKR kinase activity.IMPORTANCE The antiviral kinase PKR plays a critical role in controllin

179 ytomegalovirus (HCMV) infection activate the antiviral kinase protein kinase R (PKR), which potently

180 derived macrophages rescued the inflammatory antiviral M1 macrophage response, revealing reduction-ox

181 Thus, a novel antiviral mechanism for IFN-gamma has been revealed.

182 esistance to the innate immune response, and antiviral mechanisms affecting the viral RNA sequence an

183 nd activated a panel of IFN-regulated genes, antiviral mediators and transcriptional regulators.

184 Preclinical data suggest that combining antivirals might be more effective than administering os

185 nalyses, we identify three proviral and nine antiviral miRNAs that interact with HCV.

186 The administration of IAP or the antiviral neuraminidase inhibitor zanamivir was therapeu

187 Viral loss was specific to antiviral nucleoside treatment and not induced by growth

188 n children (72%); only 56% of cases received antivirals on the day of admission.

189 ry engaged by arenavirus NPs and identify an antiviral pathway that is subverted by JUNV.IMPORTANCE A

190 The regulation by rotaviruses (RVs) of antiviral pathways mediated by multiple IFN types is not

191 Direct-acting antivirals produce high SVR rates in white, black, Hispa

192 This study reveals the effect of antiviral programmed cell death pathways on inflammation

193 , and show that these cells recapitulate the antiviral properties of primary trophoblasts through the

194 Long-term antiviral prophylaxis is required to prevent hepatitis B

195 udies involving 1,672 patients not receiving antiviral prophylaxis, the reactivation risk was 14% (95

196 ible, third-party donors could provide broad antiviral protection to recipients of HSCT as an immedia

197 ll inhibitory RNAs revealed that zinc-finger antiviral protein (ZAP) inhibited virion production by c

198 tify ZMPSTE24 as an intrinsic broad-spectrum antiviral protein and provide insights into antiviral de

199 The host antiviral protein APOBEC3G (A3G) antagonizes the early s

200 sion, yet many have evolved to counteract an antiviral protein called tetherin, which may selectively

201 Viperin (RSAD2) is an interferon-stimulated antiviral protein that belongs to the radical S-adenosyl

202 d protein kinase (PKR), a well-characterized antiviral protein that inhibits cap-dependent protein tr

203 ribavirin-free, pangenotypic, direct-acting antiviral regimen, glecaprevir coformulated with pibrent

204 our search for novel and effective drugs in antiviral research.

205 genome targeting has shown its potential in antiviral research.

206 hanisms underpinning antigenic evolution and antiviral resistance.

207 This event showed that antiviral-resistant (AVR) strains can be intrinsically m

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

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

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

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

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

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

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

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

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

217 detect pathogenic RNA and induce a systemic antiviral response.

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

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

220 Honey bee antiviral responses include RNA interference and immune

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

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

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

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

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

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

227 greater insight into viral pathogenicity and antiviral responses.

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

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

230 sitive regulatory role for NLRX1 in inducing antiviral responses.

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

232 The antiviral restriction factor IFN-induced transmembrane p

233 viral replication is marked by expression of antiviral restriction factors, it was intuitive to find

234 A 5'-diphosphate form of antiviral ribavirin weakly inhibited the GpppA formation

235 cells, even in nematodes defective in their antiviral RNA interference (RNAi) response, and is neith

236 Our results suggest that the antiviral RNAi response not only inhibits vertical VSV t

237 ll, Tassetto et al. describe a mechanism for antiviral RNAi spreading that parallels mammalian adapti

238 Our results clearly define an antiviral role of PI3K by modulating immune responses an

239 ore transmissible than their contemporaneous antiviral-sensitive (AVS) counterpart.

240 All viruses must antagonize antiviral signaling events for survival.

241 of human cancer cells that harbor defects in antiviral signaling, but a minority are nonpermissive be

242 er shuttles NS3 to the mitochondria to block antiviral signaling.

243 ere, we determined the role of mitochondrial antiviral-signaling protein (MAVS), the adaptor protein

244 Systemic immunity mediates the spread of antiviral signals from infection sites to distant uninfe

245 ata from recent trials of oral direct-acting antivirals (SOLAR 1 and 2), the United Network for Organ

246 Although type I IFN induces an antiviral state in many cell types, HIV-1 can replicate

247 sting that ExoN(-) virus generated during an antiviral state is less viable to establish a subsequent

248 pe I interferon (IFN) signaling engenders an antiviral state that likely plays an important role in c

249 ector cells in establishing a broad-spectrum antiviral state, as well as providing a better understan

250 ity, and antigenicity for the development of antiviral strategies to control human bocavirus infectio

251 tribute to the development of more effective antiviral strategies.

252 sis and validate PLK1 inhibition a potential antiviral strategy.

253 rish, creating the need for an RNA-targeting antiviral system.

254 dentify a novel role of IL-22 in controlling antiviral T cell responses in the non-lymphoid and lymph

255 ults open a pathway for directing engineered antiviral T cells into these viral sanctuaries to help e

256 in tissue sites; however, knowledge of human antiviral T cells is largely derived from blood.

257 hibited HBV infection, validating PLK1 as an antiviral target in vivo.

258 enzymatic function yet to be exploited as an antiviral target.

259 cells and offers opportunities for designing antiviral therapeutic cellular targets.

260 on VP24 that may serve as a novel target for antiviral therapeutic intervention.

261 approved vaccines do not exist and effective antiviral therapeutics are needed.

262 ons for the combined use of CoRAs and FIs in antiviral therapies and point to a multifaceted role for

263 n in affected areas, no licensed vaccines or antiviral therapies are available.

264 Additionally, no specific antiviral therapies or vaccines currently exist for huma

265 nts of rational strategies for the design of antiviral therapies, including monoclonal antibodies (mA

266 patocytes, even in the presence of available antiviral therapies, lies in the accumulation of covalen

267 ding survival, and reduce the need for toxic antiviral therapies.

268 KO hamster model for evaluation of promising antiviral therapies.

269 ough it was lower than those recommended for antiviral therapy (78.2%).

270 ter informed consent, all patients underwent antiviral therapy (AVT) with sofosbuvir/ledipasvir and c

271 Oral antiviral therapy alone without hepatitis B immune globu

272 Studies on antiviral therapy are undergoing to elucidate the optima

273 spective cohort, we report on the success of antiviral therapy combined with a short course (in hospi

274 systematically assessed before starting the antiviral therapy for early detection and the improvemen

275 In recent years, short-term antiviral therapy for pregnant women in the third trimes

276 e supporting the use of intravenous and oral antiviral therapy for the treatment of ARN.

277 d/or HBsAg are critical endpoints for future antiviral therapy in chronic HBV.

278 s B e antigen (HBeAg) status and response to antiviral therapy in patients with chronic hepatitis B (

279 ave potential implications for the timing of antiviral therapy to achieve better virus control.

280 odes (18 = brincidofovir; 23 = cidofovir) of antiviral therapy were observed in 27 patients.

281 ve observational cohort study, direct-acting antiviral therapy with SOF/ledipasvir, ombitasvir/parita

282 onic HCV infection before, during, and after antiviral therapy with sofosbuvir and velpatasvir, we fo

283 Even after years of fully effective antiviral therapy, a persistent reservoir of virus-infec

284 h detectable viremia who received preemptive antiviral therapy, suggesting that the adaptive NK cell

285 versal hepatitis B vaccination and effective antiviral therapy, the estimated overall seroprevalence

286 imicking chronic infections with and without antiviral therapy, which prevents de novo viral replicat

287 at the SLII domain is a potential target for antiviral therapy.

288 ovides a novel target for the development of antiviral therapy.

289 e pathway can provide a potential target for antiviral therapy.

290 rn sericulture but also shed light on future antiviral therapy.IMPORTANCE Pathogen genome targeting h

291 The efficacy of antiviral treatment for chronic hepatitis C virus (HCV)

292 Once the diagnosis is made, antiviral treatment is recommended to decrease the colit

293 Appropriate antiviral treatment of influenza-positive patients was m

294 Design of antiviral treatment options and elucidation of the mecha

295 Antiviral treatment options for chronic Hepatitis E Viru

296 We assess the potential effect of an antiviral treatment that blocks viral replication, showi

297 itional applicable studies regarding new HBV antiviral treatment.

298 While induction of antiviral type I interferons (IFNs) is the major outcome

299 of stay and improved influenza detection and antiviral use, and appeared to be safe.

300 timization effort yielded a number of potent antivirals with submicromolar efficacy against several h