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1 ivo under selective pressure by a host-based antiviral drug.
2 he potential to function as a broad-spectrum antiviral drug.
3 ny of them, there is no effective vaccine or antiviral drug.
4 d and developed into a potent broad-spectrum antiviral drug.
5  controlled clinical trial of an efficacious antiviral drug.
6 velopment of verdinexor (KPT-335) as a novel antiviral drug.
7  but it lacks a licensed vaccine or suitable antiviral drug.
8 function as an anticoagulant, anticancer, or antiviral drug.
9 ial avenues for the development of alternate antiviral drugs.
10 g virus are essential for the development of antiviral drugs.
11 n sensory neurons and cannot be cleared with antiviral drugs.
12 ing is a novel target for the development of antiviral drugs.
13 ality largely because of a lack of effective antiviral drugs.
14 g pathways potential therapeutic targets for antiviral drugs.
15 e interactions may represent new targets for antiviral drugs.
16 ed for a next generation of highly effective antiviral drugs.
17 ns could facilitate the development of novel antiviral drugs.
18 and the development of resistance to current antiviral drugs.
19 eral strains with variable susceptibility to antiviral drugs.
20 table levels of viremia despite not being on antiviral drugs.
21 t round of rational design of broad-spectrum antiviral drugs.
22 road-spectrum targets for the development of antiviral drugs.
23  selective pressure, such as the presence of antiviral drugs.
24 determine the efficacy of novel or available antiviral drugs.
25 e used to test preclinically the efficacy of antiviral drugs.
26 tion as potent broad-spectrum, host-oriented antiviral drugs.
27 creening, and structure-based development of antiviral drugs.
28 by the viruses and facilitate development of antiviral drugs.
29 trimerization and are a potential target for antiviral drugs.
30 tion forks are widely used as anticancer and antiviral drugs.
31  that is targeted by the amantadine class of antiviral drugs.
32 ely replicating and thus is not inhibited by antiviral drugs.
33 dying pathogenicity, immunity, vaccines, and antiviral drugs.
34 f which may lead to the development of novel antiviral drugs.
35  substitutions associated with resistance to antiviral drugs.
36 esistance to HIV that supplants the need for antiviral drugs.
37 suppression of viruses that are resistant to antiviral drugs.
38 ent serum from a recovered HCV patient or by antiviral drugs.
39 o allows one to evaluate the efficacy of new antiviral drugs.
40  replication and assembly complex as well as antiviral drugs.
41 p the possibility for the rapid screening of antiviral drugs.
42 ural 5A protein (NS5A) is the target for new antiviral drugs.
43 immunity, develop novel vaccines, or develop antiviral drugs.
44 ses, HBx represents an attractive target for antiviral drugs.
45 developing LIMK inhibitors as broad-spectrum antiviral drugs.
46  as a valuable tool for evaluating promising antiviral drugs.
47 atitis C virus (HCV) vaccines and affordable antiviral drugs.
48 attenuation and new targets for screening of antiviral drugs.
49 ce necessitate the development of new potent antiviral drugs.
50 esent great potential for the development of antiviral drugs.
51 thus a primary target for the development of antiviral drugs.
52 , there is an urgent need for more effective antiviral drugs.
53 r compound testing, including potential ZIKV antiviral drugs.
54 ckaging might lead to the development of new antiviral drugs.
55 he rational design of vaccines and potential antiviral drugs.
56 inactivated virus was not stimulatory and an antiviral drug, 2'-C-methyladenosine, reduced induction
57  genetic associations found has been for the antiviral drug abacavir, which causes severe adverse rea
58           In this study, the removal of five antiviral drugs (abacavir, acyclovir, emtricitabine, lam
59 nous nucleoside analogues for anticancer and antiviral drug actions.
60                         The oxidation of the antiviral drug acyclovir (ACV) and its main biotransform
61  The U.S. Food and Drug Administration (FDA) Antiviral Drugs Advisory Committee reviewed these studie
62  for the clinical development of UV-4B as an antiviral drug against DENV, and it provides a framework
63 eviously reported, ribavirin is an effective antiviral drug against many RNA viruses.
64 t can serve as a novel target for developing antiviral drugs against arenavirus pathogens.
65 ave the potential for further development as antiviral drugs against CHIKV infection.
66  as a potential target in the development of antiviral drugs against EBOV.
67          This indicates that the efficacy of antiviral drugs against H7N9-R292K will be reduced.
68                    In order to develop novel antiviral drugs against HBV, we established a cell-based
69 tial target for discovery and development of antiviral drugs against HCV.
70 n 3 position of pyrimidine ring as potential antiviral drugs against HCV.
71  The availability of curative, direct-acting antiviral drugs against hepatitis C virus (HCV) sparks a
72 opment of novel prophylactic and therapeutic antiviral drugs against hRSV is imperative to control th
73 al development of a promising class of novel antiviral drugs against virulent neurotropic alphaviruse
74          Certain IN mutations (class II) and antiviral drugs (allosteric IN inhibitors [ALLINIs]) adv
75                               Binding of the antiviral drug amantadine suppressed both proton exchang
76 2 proton channel (A/M2) is the target of the antiviral drugs amantadine and rimantadine, whose use ha
77                     Moreover, binding of the antiviral drug, amantadine, at the N-terminal pore at lo
78 s the seasonal H1N1, tend to be sensitive to antiviral drugs, amantadine and rimantadine, while the S
79 unique target for developing a novel type of antiviral drug and improved options of broad-spectrum an
80 linical applications in cancer treatment, as antiviral drugs and as immunosuppressants, and have also
81 will likely require the broad application of antiviral drugs and development of an effective vaccine.
82 esis and to assess the efficacy of candidate antiviral drugs and new vaccines.IMPORTANCE Early pathog
83 pre-emptive therapy with lamivudine or other antiviral drugs and no one showed episodes of viral reac
84                                 There are no antiviral drugs and no preventive vaccine.
85 ction, as well as help in the development of antiviral drugs and protective vaccines.
86 mall-primate animal model for studying novel antiviral drugs and T-cell-based vaccines against HCV in
87 will likely require the broad application of antiviral drugs and the development of an effective vacc
88          Phototransformation rates of parent antiviral drugs and their biotransformation products wer
89 though far less advanced than for influenza, antiviral drugs and vaccines are in different stages of
90  impediment to the eventual licensing of new antiviral drugs and vaccines for NIRVs.
91  and boost research and development into new antiviral drugs and vaccines for these viruses.
92 rational design of novel and highly specific antiviral drugs and will aid in the detailed understandi
93 SV isolates being multiresistant to standard antiviral drugs, and infection was fully resolved in 7/8
94  used to study polio pathogenesis, candidate antiviral drugs, and the efficacy of new vaccines.
95 re critical for basic research, diagnostics, antiviral drugs, and vaccines to combat IBV.
96 be effectively treated with a broad-spectrum antiviral drug approved for use in Japan.
97 Currently, there are no licensed vaccines or antiviral drugs approved for human use.
98                                          The antiviral drug arbidol (ARB), already in clinical use in
99                           The broad-spectrum antiviral drug Arbidol shows efficacy against influenza
100                                              Antiviral drugs are a proposed medical intervention to r
101 ry illness for which no vaccines or suitable antiviral drugs are available.
102             However, no specific vaccines or antiviral drugs are currently available to prevent or tr
103                                              Antiviral drugs are effective against severe VZV infecti
104                                              Antiviral drugs are important components for the control
105                                              Antiviral drugs are needed for clinical practice and pub
106                Licensed vaccines or suitable antiviral drugs are not available.
107                                      Because antiviral drugs are of limited efficacy in patients hosp
108 e a new pandemic strain has been identified, antiviral drugs are often considered the first line of d
109         In addition to vaccination, however, antiviral drugs are required for individuals with uncert
110                                      Current antiviral drugs are susceptible to drug resistance, and
111                                         Four antiviral drugs are used for preventing or treating CMV:
112                                              Antiviral drugs are used to treat herpes simplex virus (
113                                    Available antiviral drugs are virus-specific and active against a
114 diagnostics, and identification of candidate antiviral drugs argue that the major obstacles to drug d
115 ed with oral corticosteroids alone, are oral antiviral drugs associated with improved outcomes when c
116 ignificance for which there is no vaccine or antiviral drug available.
117 (NA) inhibitors (NAIs) are the only class of antiviral drugs available for therapeutic intervention f
118          Currently, there are no vaccines or antiviral drugs available to counter these highly contag
119 y of these viruses, there are no vaccines or antiviral drugs available.
120 f these synergistic interactions is with the antiviral drug azidothymidine (AZT).
121 tantial differences in kinetics of different antiviral drugs, biotransformation reactions mainly invo
122  not only to suppress viral replication with antiviral drugs but also potentially to eliminate or "cu
123     Addition of a third potent direct-acting antiviral drug can reduce the duration of treatment requ
124                Neuraminidase inhibitor (NAI) antiviral drugs can shorten the duration of uncomplicate
125 affirm that M2-S31N inhibitors are promising antiviral drug candidates that warrant further developme
126               Treatment of the mice with the antiviral drug cidofovir reduced the numbers of effector
127 ated knockdown of pp71 or treatment with the antiviral drug cidofovir resulted in decreased expressio
128 g clinical drug concentrations and selecting antiviral drug combinations most likely to suppress resi
129 ent data and the addition of host factor and antiviral drug components.
130 t RNA polymerase, which is a major target of antiviral drugs currently in the clinic.
131              Phase 3 trials of direct acting antiviral drugs (DAAs) for hepatitis C virus (HCV) exclu
132                       All-oral direct-acting antiviral drugs (DAAs) for hepatitis C virus, which have
133                Development of broad-spectrum antiviral drugs depends on a better mechanistic understa
134 ent RNA polymerase complex should facilitate antiviral drug design and provide a precedent for other
135  provides insights into specific targets for antiviral drug design for improved efficacy.
136 tures and mechanisms that can be targeted in antiviral drug design.
137 ad in the long run to a structural basis for antiviral drug design.
138 y CpAMs, indicating a more complex basis for antiviral drug design.
139                                              Antiviral drugs designed to accelerate viral mutation ra
140 ich is a potential target for broad-spectrum antiviral drug development.
141  replication and could be a target for broad antiviral drug development.
142 a new, potentially broad-spectrum target for antiviral drug development.
143  model is a critical step in the path toward antiviral drug development.
144 o identify targetable host factors and guide antiviral drug development.
145 lluminates potential targets for vaccine and antiviral drug development.
146 esponses and may be important to vaccine and antiviral drug development.
147  hence represents a promising target for new antiviral drug development.
148 P1 and PLP2) represent potential targets for antiviral drug development.
149 dings may provide a new structural basis for antiviral drug development.
150 r VZV skin infection and may be targeted for antiviral drug development.
151                        Moreover, because new antiviral drugs directly inhibit hepatitis C virus, vira
152             One of the promising targets for antiviral drug discovery against dengue and related flav
153 put based assays are beginning to accelerate antiviral drug discovery and improve on current strategi
154     We present an unconventional approach to antiviral drug discovery, which is used to identify pote
155  HBV replication and an important target for antiviral drug discovery.
156 se of dengue virus is a promising target for antiviral drug discovery.
157 cription that PKD may represent a target for antiviral drug discovery.
158 ny that are resistant to treatment; and (ii) antiviral drugs do not directly inhibit immune-mediated
159 evirus infection, and can be used to predict antiviral drug efficacy.
160                              For preclinical antiviral drug evaluation, the GMP version of the myrist
161 cant limitations to their effective use: (i) antiviral drugs exert selective pressure on the virus, r
162 tcomes, but was rather associated with lower antiviral drug exposure (6.4 +/- 13 days vs 38.6 +/- 14
163 a murine CMV that is highly sensitive to the antiviral drug famciclovir to modulate virus replication
164            Currently, there is no vaccine or antiviral drug for hMPV.
165  patients with fatal outcomes and the use of antiviral drug for SFTS.
166  Food and Drug Administration (FDA)-approved antiviral drug for which genotypic resistance analyses w
167                                  The role of antiviral drugs for HHV-8 prevention and treatment is ye
168  novel, live attenuated vaccines, as well as antiviral drugs for pneumoviruses.
169  develop live attenuated vaccines as well as antiviral drugs for pneumoviruses.
170 hreat, which underscores the need to develop antiviral drugs for rapid response in the event of an at
171  target for the development of direct-acting antiviral drugs for the treatment of chronic HCV infecti
172                            New direct-acting antiviral drugs for the treatment of chronic hepatitis C
173  search for human adenovirus (HAdV)-specific antiviral drugs for the treatment of HAdV infections in
174                        Resurgent interest in antiviral drugs for the treatment of herpesvirus has led
175 dates for the development of a new family of antiviral drugs for the treatment of infections by DNA v
176 xycytidine analogs, have been widely used as antiviral drugs for years, a structural basis for D-ster
177 idine (telbivudine) have been widely used as antiviral drugs for years.
178  potential in various applied areas, e.g. as antiviral drugs, for the vaccine development and as nove
179           Here we show that the FDA-approved antiviral drug ganciclovir (GCV) induces a type I interf
180          We discovered unexpectedly that the antiviral drug ganciclovir (GCV) inhibits the proliferat
181                                          The antiviral drug ganciclovir prevents CMV disease in heart
182 CMV prophylaxis consisted in all patients of antiviral drugs (ganciclovir/valganciclovir) combined wi
183 ted with supportive therapy and experimental antiviral drug GS-5734 (Gilead Sciences, San Francisco,
184                                Direct-acting antiviral drugs have a high cure rate and favourable tol
185 ublic health threat, to date, no vaccines or antiviral drugs have been developed for human use.
186                               Unlike AM2, no antiviral drugs have been developed to block the BM2 cha
187 nfection, but efforts to develop TAR-binding antiviral drugs have not yet yielded a successful candid
188 y and mortality worldwide, with vaccines and antiviral drugs having limited efficacy thus far.
189 e developed as a new class of broad-spectrum antiviral drugs.IMPORTANCE The actin cytoskeleton is a s
190 ccination as a viable alternative to chronic antiviral drugs in the treatment and control of genital
191  critically evaluate the rationale for using antiviral drugs in the treatment of patients with glioma
192  reported the effectiveness of direct-acting antiviral drugs in these patients.
193             The viral resistance of marketed antiviral drugs including the emergence of new viral res
194  can successfully modify an HSV-TK-dependent antiviral drug into an anti-tumor drug.
195                         To date, no specific antiviral drug is available to treat or prevent this dis
196                                Currently, an antiviral drug is not available and information on thera
197             A vaccine or generally effective antiviral drug is not yet available.
198                              A wide range of antiviral drugs is currently available; however, drug-re
199            Resistance to one of the two main antiviral drugs is differentially acquired by the two di
200 t therapies, as resistance to currently used antiviral drugs is emerging rapidly.
201 of the virus genome, resistance to available antiviral drugs is frequently observed, and new targets
202  DNA and L-dCTP or the triphosphate forms of antiviral drugs lamivudine ((-)3TC-TP) and emtricitabine
203 using the triphosphates of chain-terminating antiviral drugs lamivudine ((-)3TC-TP) and emtricitabine
204           Moreover, current highly effective antiviral drugs make efforts to treat hepatitis C with h
205              Furthermore, treatment with one antiviral drug might promote the development of antivira
206 xanthine alkaloids, nucleosides, and related antiviral drug molecules.
207 s approaching 30% despite treatment with the antiviral drug of choice, acyclovir.
208                                   Poliovirus antiviral drugs offer the only mitigation of these risks
209 therapies that combine immunosuppressive and antiviral drugs, offering a window into the effects of i
210 efficacy and safety of the two direct-acting antiviral drugs ombitasvir, an NS5A inhibitor, and parit
211 showed that treatment of pregnant women with antiviral drugs or hyperimmunoglobulins significantly re
212 uld be a target for development of new small antiviral drugs or peptidomimetics.
213                        To date, there are no antiviral drugs or specific therapies to treat MERS-CoV.
214 0 years, there are no commercially available antiviral drugs or vaccines.
215 influenza infection, infections resistant to antiviral drugs, or as an interim therapy during a pande
216                             Furthermore, the antiviral drug oseltamivir is less effective for treatin
217 ses that were resistant and sensitive to the antiviral drug oseltamivir, resistance was propagated th
218 " Preexisting variants resistant to specific antiviral drugs, overlooked in traditional hit-to-lead d
219 ination therapies with other directly acting antiviral drugs, particularly in difficult-to-treat pati
220 nfluence of HBV genotypes on the response to antiviral drugs, particularly TDF, is poorly understood.
221 ncluding modulation of immunosuppression and antiviral drug regimens.
222                                              Antiviral drugs represent important means of influenza v
223        Our results uncovered a novel form of antiviral drug resistance and suggest that host-based RB
224 kthrough (VBT) is the first manifestation of antiviral drug resistance during nucleos(t)ide analogue
225 important implications for the assessment of antiviral drug resistance in research and clinical pract
226                                              Antiviral drug resistance is a crucial factor that frequ
227 sitic nature of viruses and the emergence of antiviral drug resistance necessitate the development of
228                                              Antiviral drug resistance should be suspected when CMV v
229 ients are highly susceptible to emergence of antiviral drug resistance, most probably due to prolonge
230 idate a previously unidentified mechanism of antiviral drug resistance.
231           Among treated individuals, 27% had antiviral drug resistance.
232 ng of various mechanisms by which RT confers antiviral drug resistance.
233 t nearly 40% of the VBTs were not related to antiviral drug resistance.
234 nts may predict CMV infection resolution and antiviral drug resistance.
235 covery was observed in mice treated with the antiviral drug ribavirin during the persistent stage of
236 tide polymerase inhibitor sofosbuvir and the antiviral drug ribavirin was associated with high respon
237 on renders the virus more susceptible to the antiviral drug ribavirin, suggesting that recombination
238 mechanism of resistance of a poxvirus to the antiviral drug rifampin.
239 (VGX-1027) named GIT-27NO or the NO-modified antiviral drug saquinavir (Saq) named Saq-NO on two colo
240 Virus (HIV) mutants developing resistance to antiviral drugs show that the dose response curve may no
241                                              Antiviral drugs such as neuraminidase (NA) inhibitors wi
242 er drugs (such as Ara-C and gemcitabine) and antiviral drugs (such as zidovudine and ribavirin), have
243 vailable for CMV infection and the available antiviral drugs suffer from toxicity, poor efficacy and
244 investigate the impact of this tryptophan on antiviral drug susceptibility and viral replicative capa
245 hese results have important implications for antiviral drug susceptibility, vaccine efficacy, transmi
246 esent here will allow future studies on EV71 antiviral drug susceptibility, vaccine efficacy, transmi
247 investigate the impact of this tryptophan on antiviral drug susceptibility.
248  RT-IN interaction can be exploited as a new antiviral drug target.
249 us (HCV) NS3 helicase, which is an important antiviral drug target.
250 elp to guide the development of vaccines and antiviral drugs targeting astrovirus.
251 act should accelerate the development of new antiviral drugs targeting cis-acting RNA regulatory sign
252 de a small-animal model for evaluating novel antiviral drugs targeting HCV NS3-NS4A protease and T-ce
253 this finding, we reviewed the development of antiviral drugs targeting viral DNA-packaging motors.
254  not only will facilitate the development of antiviral drugs targeting viral entry steps but also wil
255 ntivirals (DAAs) are being developed and new antiviral drug targets are being explored.
256 al and human DEDDh exonucleases can serve as antiviral drug targets due to their critical roles in vi
257  life cycle of many viruses and can serve as antiviral drug targets, further investigations into a po
258 hange factor 1 (GBF1) and JAK1, as potential antiviral drug targets.
259  development of a new efficient synthesis of antiviral drug telaprevir.
260   Nelfinavir (NFV) is a clinically important antiviral drug that inhibits production of infectious HI
261 HV-8, and we propose ARB as a broad-spectrum antiviral drug that may be useful against hemorrhagic vi
262 his shift was blocked by ribavirin (RBV), an antiviral drug that reduces relapse in HCV patients.
263 both targets for highly potent and promising antiviral drugs that are in the late stages of clinical
264 g of the mode of action of the highly potent antiviral drugs that are targeted to NS5A.
265                                              Antiviral drugs that inhibit influenza virus replication
266  acid (PFA, foscarnet) belongs to a class of antiviral drugs that inhibit the human cytomegalovirus D
267 rse combination therapies with direct-acting antiviral drugs that might be explored in future clinica
268 led to development of many new direct-acting antiviral drugs that target key components of virus repl
269 indings can lead to the development of novel antiviral drugs that target viral genomes and block vira
270  screening may facilitate the development of antiviral drugs that target viruses other than the influ
271 ng site is potentially a good target for new antiviral drugs that will directly inhibit viral replica
272 es it a major unmet target for a vaccine and antiviral drug therapy.
273 f attempts to develop vaccine candidates and antiviral drugs, there is a lack of approved therapeutic
274 al reactivation in order to be vulnerable to antiviral drugs, these findings identify a new way to in
275 hether the addition of a third direct-acting antiviral drug to sofosbuvir and ledipasvir would allow
276 ts a potential target for the development of antiviral drugs to combat human-pathogenic arenaviruses.
277 erged in 2011 with the approval of the first antiviral drugs to directly inhibit HCV NS3/4A protease,
278 ents of the ability of novel CMV vaccines or antiviral drugs to reduce or even interrupt such transmi
279 t groundwork for the eventual development of antiviral drugs to treat AIDS.
280            Currently, there are no effective antiviral drugs to treat RSV infection.
281 ssess the efficacy of control strategies via antiviral drug treatment during an outbreak of pandemic
282  which can be inhibited with directly acting antiviral drug treatment, thereby providing evidence for
283 ic adaptive immune responses, and respond to antiviral drug treatment.
284 ses of Food and Drug Administration-approved antiviral drugs used for the prevention and treatment of
285 Sofosbuvir and daclatasvir are direct-acting antiviral drugs used to treat chronic hepatitis C virus
286                            The host-targeted antiviral drug UV-4B reduces viral replication and promo
287                                   The use of antiviral drugs was more common in clubfoot cases than i
288 ial for disease and subsequent need for such antiviral drugs, we aimed to assess safety and efficacy
289  AM2 is inhibited by the amantadine class of antiviral drugs, whereas BM2 has no known inhibitors.
290          We show that commercially available antiviral drugs which target HIV-1 protease can be divid
291       Here we show that DAS181 (Fludase), an antiviral drug with sialidase activity, potently inhibit
292 ovir and valganciclovir are highly effective antiviral drugs with a well-established role in primary
293 rted a structural platform for the design of antiviral drugs with activities against these viruses or
294 sidered a potential target for the design of antiviral drugs with broad-spectrum activities against t
295 d to novel vaccine approaches or targets for antiviral drugs with broad-spectrum activity.
296 on relationships of 3CLpro for the design of antiviral drugs with broader antiviral activities.
297 of the discovery and characterization of new antiviral drugs with different mechanisms of action and
298 otion will promote the development of potent antiviral drugs with high specificity and efficiency.
299 sistant to current therapy make the need for antiviral drugs with novel mechanisms of action compelli
300 dase (NA) that confer drug resistance to two antiviral drugs, zanamivir and oseltamivir.

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