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1 this nucleotide analogue as a direct-acting antiviral.
2 failure in clinical trials of direct-acting antivirals.
3 immune protection, and down-select candidate antivirals.
4 erve as novel targets for the development of antivirals.
5 llular functions potential targets for novel antivirals.
11 vel analogue, NBD-14189 (Ref1), which showed antiviral activity against HIV-1(HXB2), with a half maxi
15 n structure of HBV RNA was important for its antiviral activity and cleaved by MCPIP1 in the cell-fre
16 nto an antibody combination that potentiates antiviral activity and is able to prevent EVD in nonhuma
17 IRF3 activation, interferon production, and antiviral activity are compromised in cell cultures and
18 rferon-stimulated gene with well-established antiviral activity but limited mechanistic understanding
19 Molecular docking of analogues that retained antiviral activity demonstrated a relationship between p
22 HPV16) infection in vitro and maintain their antiviral activity in vivo, while the glycooligomers exe
23 In this study, we assessed the influenza antiviral activity of 10 compounds previously shown to i
24 dels have been extensively used to study the antiviral activity of IFIT (interferon-induced protein w
30 -1 accessory protein Nef can antagonize this antiviral activity of TIM-1 while host restriction facto
31 via a structure-based approach and performed antiviral activity screening to identify compounds 29 an
35 ecurring RBD-specific antibodies with potent antiviral activity were found in all individuals tested,
37 to determine the molecular mechanisms of its antiviral activity, we show that PG specifically inhibit
38 disrupt membrane integrity but with no known antiviral activity, were tested for the ability to inhib
45 f the CpG in the viral genome determines its antiviral activity.IMPORTANCE Some RNA virus genomes are
46 ques in human brains, and treatment with the antiviral acyclovir (ACV) was reported to block the accu
51 dies in both populations is the need for new antiviral agents and the necessity for combination thera
55 n multiple therapeutic domains, for example, antiviral agents, corticosteroids, or immunoglobulin.
59 signaling pathways, essential for respective antiviral and antibacterial responses, is common in prev
60 iptase inhibitors (NRTIs) are widely used as antiviral and anticancer agents, although they require i
61 institution of aggressive intensive care and antiviral and immune treatment to reduce the complicatio
64 g for HCC in persons at risk, treatment with antivirals, and an emerging role for immunotherapy in HC
65 ural products and pharmaceuticals, including antiviral, antibacterial, anticancer and cardiac drugs(6
68 5 who were tested (91.1%) were seropositive; antiviral antibody titers assayed by two pan-Ig assays i
70 , accompanied by suppression of IFN-mediated antiviral, apoptotic, and inflammatory functions, during
71 recognition specificity by a broad-spectrum antiviral aptamer, and they open new possibilities for a
75 nant CD4(+) T cell epitopes induced a robust antiviral CD4(+) T cell response in the cornea that was
76 HSCT) during chronic infection generated new antiviral CD8 T cells, despite sustained virus replicati
79 A-protein interactions to repurpose powerful antiviral chromatin silencing machinery for sex chromoso
82 ogether, our results identified a new set of antiviral compounds for the potential treatment of influ
85 -Cas13-based strategy, PAC-MAN (prophylactic antiviral CRISPR in human cells), for viral inhibition t
89 s a lack of data on the use of direct-acting antivirals (DAA) on the risk of death and tumoral recurr
90 limination by sofosbuvir-based direct-acting antivirals (DAAs) and addition of RBV improves NK cell f
93 robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammato
95 llers, NK cells are also key helper cells in antiviral defense, influencing adaptive immune responses
99 viruses is important in understanding innate antiviral defenses in birds.IMPORTANCE Birds are importa
101 ell as effects on the host cell that enhance antiviral defenses.IMPORTANCE Kaposi's sarcoma-associate
102 s for replication and to avoid the litany of antiviral detection mechanisms in the cytoplasm remains
105 cap methylation is an attractive target for antiviral discovery and development of new live attenuat
107 ve care as background therapy, including the antiviral drug remdesivir and, when indicated, supplemen
109 ctions and facilitate future applications in antiviral drug research to manage flavivirus infections.
110 treatment failure upon standard care due to antiviral drug resistance and treatment-limiting side ef
111 he mammalian SKI complex as a broad-spectrum antiviral drug target and identifies lead compounds for
112 time, only one FDA-approved anti-SARS-CoV-2 antiviral drug, remdesivir, is available, and unfortunat
114 infection, to repurpose currently available antiviral drugs and to develop new therapies and vaccine
117 ; yet currently, no vaccines or FDA-approved antiviral drugs are available to counter these pathogens
118 national economies as effective vaccines or antiviral drugs are not currently available (according t
120 ions that should facilitate the discovery of antiviral drugs for this important zoonotic pathogen.
126 ies are required to assess whether a similar antiviral effect is achievable in humans without toxic e
128 se subpopulations and their association with antiviral effector CD8+ T cell subsets were also charact
130 ic individuals develop a higher frequency of antiviral effector memory CD4(+) T(EM) cells specific to
131 leus, and contributes to the upregulation of antiviral effectors in response to type I interferons.IM
132 s exhibit permanent, low-level expression of antiviral effectors that safely protect them from variou
133 y blocks NF-kappaB, likely to counteract its antiviral effects and promote efficient viral replicatio
139 t stem cells, and apilimod also demonstrated antiviral efficacy in a primary human lung explant model
142 K2, CDK, AXL, and PIKFYVE kinases to possess antiviral efficacy, representing potential COVID-19 ther
143 highlight an ever-evolving arms race between antiviral factors and viral pathogens and provide a new
145 ong antiviral response with up-regulation of antiviral factors such as OAS1-3 and IFIT1-3 and T helpe
147 ates such a nano-inhibitor might be a potent antiviral for the treatment of influenza infection.
149 is article provide further insights into the antiviral function of NK cells and the pathways involved
151 bited characteristics associated with potent antiviral function: memory T cells secreted cytokines an
152 O(2) increased IAV replication and inhibited antiviral gene and protein expression in macrophages in
154 nalysis shows that ERBs upregulate canonical antiviral genes typical of mammalian systems, such as IS
159 tory demyelination due to loss of protective antiviral host immunity.IMPORTANCE The current trend in
161 deployable surrogate viral assays to screen antiviral humoral responses, define correlates of immune
163 in thus demonstrates that LY6E is a critical antiviral immune effector that controls CoV infection an
165 disease 2019 (COVID-19) severity, beneficial antiviral immune responses may be identified in detail.
166 st widespread 2'3'-cGAMP signaling in insect antiviral immunity and explain how a family of cGAS-STIN
167 Interferon (IFN)-Is are crucial mediators of antiviral immunity and homeostatic immune system regulat
168 Thus, symbiotic intestinal bacteria modulate antiviral immunity and levels of circulating alphaviruse
169 Type I interferon (IFN-I) provides effective antiviral immunity but can exacerbate harmful inflammato
171 was associated with IFN-gamma signaling and antiviral immunity controlled by T cells (T(H)1 and CD8(
173 ating the mechanisms by which CHIKV subverts antiviral immunity to establish and maintain a persisten
180 ibavirin (PegIFN-RBV) plus one direct-acting antiviral in 53.4%, PegIFN-RBV in 34.5%, and sofosbuvir/
187 of ZIKV NS5 as critical in the regulation of antiviral ISG and cell cycle responses that permit ZIKV
189 ur results shed light on a potentially broad antiviral mechanism by 25HC through depleting accessible
192 ity that targeting this cytokine may restore antiviral mechanisms.FUNDINGThis study was supported by
194 with paralogs MItochondrial STress Response AntiViral (MISTRAV) and/or MItochondrial STress Response
195 veloping highly selective and broad-spectrum antiviral molecules active against emerging and dangerou
196 and safely deployed, the rapidity with which antiviral monoclonal antibodies can be isolated and engi
198 capacity of herpesvirus mutants that trigger antiviral necroptotic cell death upon early viral gene e
199 aling a cell-extrinsic downregulation of the antiviral NK cell response by adrenergic neuroendocrine
200 , which functions as novel chain-terminating antiviral nucleotide when misincorporated by viral RNA-d
204 is imperative to address this challenge, and antiviral peptides (AVPs) represent a valuable resource
205 5 binding to STAT2, disrupt the formation of antiviral PML-STAT2 NBs, and direct PML degradation.
207 OI and DMF induce a distinct IFN-independent antiviral program that is broadly effective in limiting
210 the use of preemptive therapy, compared with antiviral prophylaxis, resulted in a lower incidence of
211 ISG expression during infection that confers antiviral protection but minimizes disruption of intesti
212 ith the role of these receptors in mediating antiviral protection in various viral infections, necess
215 ual twist, human cytomegalovirus co-opts the antiviral radical SAM enzyme viperin (virus-inhibitory p
216 activation from latency.IMPORTANCE While HSV antivirals reduce the severity and duration of clinical
217 CTs of DAA therapy vs placebo or an outdated antiviral regimen, 48 other treatment studies, and 33 co
218 t in VEEV, the trajectory and penetration of antiviral resistance reflected the microenvironment in w
220 lymphocyte populations that are key for the antiviral response and immune reconstitution.FUNDINGNIH
221 is well tolerated and can induce a sustained antiviral response in WHV-infected woodchucks; the ident
223 g early illness are indicators of an altered antiviral response potentially contributing to disease s
224 ole T cells play in the orchestration of the antiviral response underlying the pathogenesis of the di
227 ossmann fold domain(6), sculpting a powerful antiviral response(7-10) that can drive viruses to extin
228 mplex cellular networks activated during the antiviral response, placing IFN-stimulated genes in a fu
233 sion of viral genes and activation of innate antiviral responses during infection result in an increa
239 and IFN-gamma pathways in achieving optimal antiviral responses.IMPORTANCE IFN-alpha/beta induction
240 de compelling evidence for the regulation of antiviral RNAi by the jasmonate hormone signaling in pla
243 ls enhances DCV replication independently of antiviral RNAi, and VINR-knockout adult flies exhibit en
246 le gene I (RIG-I) and initiate mitochondrial antiviral signaling (MAVS) protein-dependent antiviral i
247 acid-inducible gene I (RIG-I)/mitochondrial antiviral signaling (MAVS)-dependent remodeling of the c
249 er proteins, that this interaction modulates antiviral signaling via disruption of USP7 interactions
251 n limits CNS viral spread by establishing an antiviral state, but also promotes blood brain barrier i
252 overy sets HR3 as a new candidate target for antiviral strategies for NiV and likely for related viru
255 B12 inhibition as a promising broad-spectrum antiviral strategy for the treatment of Flaviviridae inf
257 ntiviral function of EDAL resides in a 56-nt antiviral substructure through which its 18-nt helix-loo
259 trix layer have not been available, impeding antiviral targeting and understanding of the pH-dependen
260 the viral life cycle that may be amenable to antiviral targeting as well as key features of its biolo
262 04 is a promising candidate for an effective antiviral that can be used to prevent SARS-CoV-2 infecti
264 stop the pandemic are prophylactic vaccines, antiviral therapeutics are important to limit morbidity
266 s, which could facilitate the development of antiviral therapeutics targeting the CHIKV attachment st
268 d RNA [(+)RNA] viruses, the major target for antiviral therapies is genomic RNA replication, which oc
275 virus (HCV) screening found interferon-based antiviral therapy associated with increased likelihood o
277 reduces the risk of HCC development, even if antiviral therapy fails to completely eliminate HCC risk
279 adhere to frequent, consistent follow-up so antiviral therapy may begin at the earliest sign of reac
280 = 24 686) found inconsistent associations of antiviral therapy vs no therapy with risk of hepatocellu
282 R 1.07, 95% C.I. 1.02-1.13, p<0.01) and dual antiviral therapy(OR 12.46, 95% C.I. 2.09-74.20, p<0.1)
284 basal QTc values, basal heart rate and dual antiviral therapy, age(OR 1.06, 95% C.I. 1.00-1.13, p<0.
285 ge, baseline viral load, vaccination status, antiviral therapy, and emergence of drug resistance on v
288 espite combination systemic and intravitreal antiviral therapy; however, none of the 19 patients demo
289 cterized according to age; sex; comorbidity; antiviral therapy; viral load, expressed as cycle thresh
292 remains a barrier to accessing direct-acting antiviral treatment (DAA) for hepatitis C virus (HCV) in
295 NA level >=1250 IU/mL, CMV viremia requiring antiviral treatment, or end-organ disease), nonrelapse m
296 wn, the formulation of strategies concerning antiviral treatment, vaccination, and epidemiological co
298 eta complexed with nucleic acids triggers an antiviral type I interferon response in neuroglia, resul
299 assay to engineer stabilized GP variants for antiviral vaccines and to discover and improve drugs tha
300 ultures infected with HSV-1, with or without antivirals, were assessed for Abeta and p-tau expression