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1  mutagenesis is a key antiviral mechanism of T-705.
2  oseltamivir (a neuraminidase inhibitor) and T-705 (a nonspecific inhibitor of viral polymerases) cou
3             We investigated the mechanism of T-705 activity against influenza A (H1N1) viruses by app
4 so explain the broad spectrum of activity of T-705 against viruses of multiple families.
5         The anti-influenza virus activity of T-705 and T-1105 (3-hydroxy-2-pyrazinecarboxamide; the a
6                 Enzymatic assays showed that T-705 and T-1105 are poor substrates for human HGPRT hav
7 ase did not change the antiviral activity of T-705 and T-1105.
8                          Since conversion of T-705 by HGPRT appears to be inefficient, T-705-RMP prod
9                                One of these, T-705 (favipiravir), has a mechanism of action that is n
10 ed the therapeutic potential of favipiravir (T-705) for Lassa fever, both alone and in combination wi
11                 Our results demonstrate that T-705 induces a high rate of mutation that generates a n
12 e phosphoribosyltransferase (HGPRT) converts T-705 into its ribose-5'-monophosphate (RMP) prior to fo
13      Which enzymes perform the activation of T-705 is unknown.
14    6-Fluoro-3-hydroxy-2-pyrazinecarboxamide (T-705) is a novel antiviral compound with broad activity
15 ys based on cell viability confirmed that no T-705-resistant variants were selected.
16                       Its active metabolite, T-705-ribose-5'-triphosphate (T-705-RTP), is recognized
17                     The crystal structure of T-705-RMP in complex with human HGPRT showed how this co
18 of T-705 by HGPRT appears to be inefficient, T-705-RMP prodrugs may be designed to increase the antiv
19 ve metabolite, T-705-ribose-5'-triphosphate (T-705-RTP), is recognized by influenza virus RNA polymer
20 5'-monophosphate (RMP) prior to formation of T-705-RTP.
21                           In the presence of T-705, titers of infectious virus decreased significantl
22  sequencing showed that virus populations in T-705-treated mice had greater genetic variability, with
23                                We found that T-705 treatment did not select specific mutations in pot
24               Susceptibility to favipiravir (T-705) was assessed using plaque reduction assays.
25 associated with resistance to oseltamivir or T-705 were detected.

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