戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
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.
6 ), antibiotics (74%), tocilizumab (13%), and antivirals (14%).
7 ly effective vaccines to generate protective antiviral Ab responses.
8                                              Antiviral Abs were measured by ELISA.
9  responsible for their demonstrated in vitro antiviral activities against COVID-19.
10 ulate lung inflammation but it has no direct antiviral activity against ECTV.
11 vel analogue, NBD-14189 (Ref1), which showed antiviral activity against HIV-1(HXB2), with a half maxi
12 upted IFITM3 oligomerization and reduced its antiviral activity against Influenza A virus.
13                     RDV shows broad-spectrum antiviral activity against RNA viruses, and previous stu
14                            Investigations of antiviral activity against the human respiratory syncyti
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
20                                  Strikingly, antiviral activity in infected chicken cells, accompanie
21 e-dependent pharmacokinetics, and had potent antiviral activity in patients with CHB.
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
25                    Despite this promise, the antiviral activity of ivermectin has not been consistent
26               In this study, we examined the antiviral activity of natural compounds against the foll
27                                          The antiviral activity of nucleoside reverse transcriptase i
28                                          The antiviral activity of the eight identified compounds aga
29 irming that resistance was due to the direct antiviral activity of the IFN response.
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
32 that remdesivir (RDV) and IFNb have superior antiviral activity to LPV and RTV in vitro.
33                      Translation of in vitro antiviral activity to the in vivo setting is crucial to
34            Target exposures were reached and antiviral activity was observed.
35 ecurring RBD-specific antibodies with potent antiviral activity were found in all individuals tested,
36                                  Besides its antiviral activity, chloroquine might also mitigate the
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
39                      Some ISGs have specific antiviral activity, whereas others regulate the cellular
40 erpinning this unusual enzyme's wide-ranging antiviral activity.
41 ing affinity with a concomitant reduction in antiviral activity.
42 nhibition of JAK activity contributes to its antiviral activity.
43 f literature suggesting ivermectin has broad antiviral activity.
44 ith the treatment appear to be important for antiviral activity.
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
47 t regulator of the sheddase, ADAM17, and the antiviral adaptor protein, stimulator of IFN genes.
48                    Influenza vaccination and antiviral administration could be increased in both IC a
49 ing this kinase in developing small-molecule antivirals against SARS-CoV-2.
50          Remdesivir (RDV) is a direct-acting antiviral agent that is used to treat patients with seve
51 dies in both populations is the need for new antiviral agents and the necessity for combination thera
52                          Anticoagulation and antiviral agents are standard treatments for DIC but are
53                                        While antiviral agents provide effective prophylaxis, there ar
54 ng the possibility to develop broad-spectrum antiviral agents targeting host factors.
55 n multiple therapeutic domains, for example, antiviral agents, corticosteroids, or immunoglobulin.
56             With the advent of direct-acting antiviral agents, there has been a rapid rise in hepatit
57 ly no approved treatments with direct-acting antiviral agents.
58 ected neurons, as well as in the presence of antivirals alone.
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
62      Initial high dose and extended taper of antiviral and steroid prophylaxis for MK in high-risk, v
63 es, DVGs may also be used therapeutically as antivirals and vaccine adjuvants.
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
66                    Our results indicate that antiviral antibodies against SARS-CoV-2 did not decline
67 tralizing or cross-reactive non-neutralizing antiviral antibodies.
68 5 who were tested (91.1%) were seropositive; antiviral antibody titers assayed by two pan-Ig assays i
69           They combat pathogens due to their antiviral, antifungal and antibacterial properties, and
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
72 demic virus for which Remdesivir is the only antiviral available.
73 he basis of lung disease and test immune and antiviral-based countermeasures.
74 ue chemical scaffolds and enhanced influenza antiviral capabilities.
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
77                       These findings confirm antiviral CD8(+) T cell exhaustion during SYMP herpes in
78 family member 5 (PGAM5) is important for the antiviral cellular response.
79 A-protein interactions to repurpose powerful antiviral chromatin silencing machinery for sex chromoso
80 resents a screenable process for identifying antiviral compounds effective against SARS-CoV-2.
81                                              Antiviral compounds exert one such pressure on virus pop
82 ogether, our results identified a new set of antiviral compounds for the potential treatment of influ
83 ntial and to generate effective vaccines and antiviral compounds.
84 e I interferon (IFN) system is important for antiviral control in the brain.
85 -Cas13-based strategy, PAC-MAN (prophylactic antiviral CRISPR in human cells), for viral inhibition t
86                                Direct-acting antiviral (DAA) therapy has transformed the management o
87  metabolic parameters early in direct-acting antiviral (DAA) therapy.
88 irological response (SVR) with direct-acting antiviral (DAA).
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
91                  The advent of direct-acting antivirals (DAAs) has transformed the landscape of hepat
92 d after viral eradication with direct acting antivirals (DAAs).
93  robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammato
94 PRRs) which are known to be involved in host antiviral defences.
95 llers, NK cells are also key helper cells in antiviral defense, influencing adaptive immune responses
96 ly controlled to ensure timely activation of antiviral defense.
97  important indication of their relevance for antiviral defense.
98 ighest viral loads and initial engagement of antiviral defenses are expected.
99 viruses is important in understanding innate antiviral defenses in birds.IMPORTANCE Birds are importa
100  exert effects on the host cell that promote antiviral defenses.
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
103  in addition to RNA cap and SAM pockets, for antiviral development.
104 provide potential anti-influenza targets for antiviral development.
105  cap methylation is an attractive target for antiviral discovery and development of new live attenuat
106                        The APOBEC3 family of antiviral DNA cytosine deaminases is implicated as the s
107 ve care as background therapy, including the antiviral drug remdesivir and, when indicated, supplemen
108                                          The antiviral drug remdesivir, dexamethasone, transfusion of
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
113                                         Some antiviral drugs and broadly reactive influenza vaccines
114  infection, to repurpose currently available antiviral drugs and to develop new therapies and vaccine
115                                 With limited antiviral drugs and vaccines available, vector control i
116 ins, is direly needed for the development of antiviral drugs and vaccines.
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
119                                      Because antiviral drugs can have side effects and show reduced c
120 ions that should facilitate the discovery of antiviral drugs for this important zoonotic pathogen.
121 al; however, small-molecule orally available antiviral drugs have yet to be developed.
122                             Additionally, no antiviral drugs or vaccines were developed against the c
123 effect of glycans on the binding kinetics of antiviral drugs to the influenza neuraminidase.
124                                 There are no antiviral drugs with proven clinical efficacy for the tr
125 ional design of live attenuated vaccines and antiviral drugs.
126 ies are required to assess whether a similar antiviral effect is achievable in humans without toxic e
127 into the immune mechanisms that mediate this antiviral effect.
128 se subpopulations and their association with antiviral effector CD8+ T cell subsets were also charact
129 ultures that correlated with upregulation of antiviral effector genes.
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
134  infected cell surface, and LIF enhanced the antiviral effects of antibody.
135             To determine the extent to which antiviral effects of IRF-1 are B cell intrinsic, we gene
136         Here, we show that Vpr mitigates the antiviral effects of REAF, a protein highly expressed in
137                                    To assess antiviral effects, RSV RNA viral load from nasal swabs w
138 ed to induce both therapeutic and preventive antiviral effects.
139 t stem cells, and apilimod also demonstrated antiviral efficacy in a primary human lung explant model
140                                          The antiviral efficacy of many nucleoside analogues is stron
141        We therefore provide evidence for the antiviral efficacy of remdesivir in vivo, and its potent
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
144             Intriguingly, mRNAs encoding for antiviral factors bypass this translational shutoff, sug
145 ong antiviral response with up-regulation of antiviral factors such as OAS1-3 and IFIT1-3 and T helpe
146                Pimodivir is a first-in-class antiviral for influenza A under development for these pa
147 ates such a nano-inhibitor might be a potent antiviral for the treatment of influenza infection.
148                                          The antiviral function of EDAL resides in a 56-nt antiviral
149 is article provide further insights into the antiviral function of NK cells and the pathways involved
150 munotherapeutic strategies to increase their antiviral function.
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
153 splenic viral burden and reduction in global antiviral gene pathways.
154 nalysis shows that ERBs upregulate canonical antiviral genes typical of mammalian systems, such as IS
155 ression of an array of interferon-stimulated antiviral genes, is a vital part of host defense.
156 in turn induce the expression of hundreds of antiviral genes.
157                                  And yet, no antivirals have been identified to treat astrovirus infe
158  compensates for the absence of apoptosis in antiviral host defense.
159 tory demyelination due to loss of protective antiviral host immunity.IMPORTANCE The current trend in
160                                              Antiviral human monoclonal antibodies (mAbs) are promisi
161  deployable surrogate viral assays to screen antiviral humoral responses, define correlates of immune
162 and IFN-gamma signaling pathways to optimize antiviral IFN-gamma activity.
163 in thus demonstrates that LY6E is a critical antiviral immune effector that controls CoV infection an
164 uitination of MAVS and thus shuts off innate antiviral immune response.
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
170  Antibodies are typically thought to mediate antiviral immunity by blocking host-cell infection.
171  was associated with IFN-gamma signaling and antiviral immunity controlled by T cells (T(H)1 and CD8(
172                                              Antiviral immunity in insects is mediated by the RNA int
173 ating the mechanisms by which CHIKV subverts antiviral immunity to establish and maintain a persisten
174 3 and thus allows timely induction of innate antiviral immunity.
175 ferentiation that can be targeted to improve antiviral immunity.
176 FN-alpha, suggesting a potential weakness in antiviral immunity.
177 e principally recognized as key mediators of antiviral immunity.
178 NV impacting some, but not all, mediators of antiviral immunity.
179         Our work contributes to the field of antiviral immunology by discovering and characterizing a
180 ibavirin (PegIFN-RBV) plus one direct-acting antiviral in 53.4%, PegIFN-RBV in 34.5%, and sofosbuvir/
181       Including the effects of direct acting antivirals in our models, we found that in spite of decr
182                                     Licensed antivirals inhibit virus replication, but do not affect
183 ce could be exploited for the development of antiviral inhibitors.
184 antiviral signaling (MAVS) protein-dependent antiviral interferon (IFN) responses.
185 Vs are complex and regulated in part through antiviral interferons.
186 als, and humans, can lead to new targets for antiviral interventions.
187 of ZIKV NS5 as critical in the regulation of antiviral ISG and cell cycle responses that permit ZIKV
188                                          The antiviral lectin, Griffithsin (GRFT), has been shown to
189 ur results shed light on a potentially broad antiviral mechanism by 25HC through depleting accessible
190                The results have uncovered an antiviral mechanism through inhibitor-induced tetrameriz
191 striction by ZAP and whether CpGs have other antiviral mechanisms.
192 ity that targeting this cytokine may restore antiviral mechanisms.FUNDINGThis study was supported by
193 duction of type I interferons, which are key antiviral mediators, is reportedly blunted.
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
197 ar among patients treated with DAA, IFN, and antiviral naive, respectively (P < 0.001).
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
201 (mAbs) represent a highly promising class of antiviral or anti-inflammatory agents.
202                           There is no proven antiviral or immunomodulatory therapy for coronavirus di
203                        However, no effective antivirals or vaccines are available.
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.
206 esults are significant for the design of new antiviral prodrugs.
207 OI and DMF induce a distinct IFN-independent antiviral program that is broadly effective in limiting
208                    Our findings reveal novel antiviral properties of PG, suggesting its high potentia
209 alganciclovir, 900 mg, daily for 100 days as antiviral prophylaxis (n = 105).
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
213                         Tetherin/BST-2 is an antiviral protein that blocks the release of enveloped v
214                                          The antiviral protein ZAP binds viral RNA containing CpGs an
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
219           NK cells play an important role in antiviral resistance.
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
222                   Here, we addressed whether antiviral response of peripheral blood lymphocytes diffe
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
225                        In these animals, the antiviral response was maintained until the end of the s
226                  SARS-CoV-2 induced a strong antiviral response with up-regulation of antiviral facto
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
229 ction and are important in the host's innate antiviral response.
230  and viral RNA during the type VI CRISPR-Cas antiviral response.
231 t may have roles during the RNase L-mediated antiviral response.
232                      Type I interferon (IFN) antiviral responses and SARS-CoV-2-specific T cell respo
233 sion of viral genes and activation of innate antiviral responses during infection result in an increa
234 ze nucleotide second messengers and initiate antiviral responses in bacterial and animal cells.
235 in ex vivo vaginal tissue cultures triggered antiviral responses in myeloid and CD4(+) T cells.
236 r, immunoglobulin G (IgG) can also stimulate antiviral responses through its constant region.
237 Rylating) PARPs are associated with cellular antiviral responses.
238 ies at the intersection of antibacterial and antiviral responses.
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
241 onse to the viral suppression of the primary antiviral RNAi immunity.
242  and eri-6/7-defective mutants because of an antiviral RNAi response to dsRNA.
243 ls enhances DCV replication independently of antiviral RNAi, and VINR-knockout adult flies exhibit en
244                       While RSK2 displays an antiviral role, we demonstrate a virus-supportive functi
245 ease 2019 (COVID-19) serological testing and antiviral screening.
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
248 g lytic replication and inhibit a variety of antiviral signaling pathways.
249 er proteins, that this interaction modulates antiviral signaling via disruption of USP7 interactions
250  (PDE) domain to counteract RNase L-mediated antiviral signaling.
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
253                           Efforts to develop antiviral strategies for treating MS are underway.
254                                              Antiviral strategies targeting early steps of infection
255 B12 inhibition as a promising broad-spectrum antiviral strategy for the treatment of Flaviviridae inf
256  factors upon which viruses rely as a viable antiviral strategy.
257 ntiviral function of EDAL resides in a 56-nt antiviral substructure through which its 18-nt helix-loo
258 ing host translational machinery and evading antiviral surveillance.
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
261 h purified proteins are crucial advances for antiviral targeting of influenza viruses.
262 04 is a promising candidate for an effective antiviral that can be used to prevent SARS-CoV-2 infecti
263 l polymerases have been attractive and major antiviral therapeutic targets.
264 stop the pandemic are prophylactic vaccines, antiviral therapeutics are important to limit morbidity
265                             Without approved antiviral therapeutics or vaccines to this ongoing globa
266 s, which could facilitate the development of antiviral therapeutics targeting the CHIKV attachment st
267 urgent need for the accelerated discovery of antiviral therapeutics.
268 d RNA [(+)RNA] viruses, the major target for antiviral therapies is genomic RNA replication, which oc
269                         The discovery of new antiviral therapies is imperative to address this challe
270                   Ongoing trials are testing antiviral therapies, immune modulators, and anticoagulan
271 edge that may guide development of effective antiviral therapies.
272 % and few short-term harms relative to older antiviral therapies.
273 d the effective monitoring of the associated antiviral therapies.
274 to persist in individuals during combination antiviral therapy (ART).
275 virus (HCV) screening found interferon-based antiviral therapy associated with increased likelihood o
276               Based on 18 trials (n = 2972), antiviral therapy compared with placebo or no treatment
277 reduces the risk of HCC development, even if antiviral therapy fails to completely eliminate HCC risk
278 nce is a critical problem limiting effective antiviral therapy for HIV/AIDS.
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
281                                 An SVR after antiviral therapy was associated with decreased adjusted
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)
283                   Cohort A: After 3 years of antiviral therapy, 33% and 30% had detectable HBcrAg and
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
286 e been sought as novel molecular targets for antiviral therapy.
287 se functionalities, represent a milestone in antiviral therapy.
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
290           This assay may help identify novel antivirals to control the COVID-19 pandemic.
291 om direct effector function to regulation of antiviral transcription.
292 remains a barrier to accessing direct-acting antiviral treatment (DAA) for hepatitis C virus (HCV) in
293 lowed by 400 mg once daily for 6 days) or no antiviral treatment (not-placebo controlled).
294  diagnosis can help initiate early effective antiviral treatment and isolation.
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
297 28 patients (21.4%) had previously undergone antiviral treatment.
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

 
Page Top