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Concerning the spread of mutant viruses, however, the fitness of the viruses needs further investigation.
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However, mutant viruses probably would have been discovered in the immunocompromised population.
However, mutant viruses that carry a phenylalanine instead of the tyrosine at position 89 of the NS1 only showed marginal differences to wt viruses with regard to their replication fitness.
However, the mutant viruses often revert to a common or "optimal" form of the virus throughout the course of infection.
Following recombination with gp64-null bacmid DNA, all mutants except the Thogoto loop swap rescued viable viruses; however, reflecting the poor level of syncytium formation, mutant RR RR grew slowly.
However, total IgG against all mutant viruses tested peaked at day 71 and remained stable to the end of the study at day 142.
However, many issues remain, including drug toxicity and the emergence of drug-resistant mutant viruses, even in treated patients.
However, the reliance on EBV's immortalizing ability prevents study of 3CKO and E3KO mutant viruses, as LCLs could not be established with these viruses (data not shown).
However, the therapeutic effect of ART is weakened by the emergence of drug-resistant mutant viruses.
However, treatment with NAIs against H7N9 infections has resulted in the emergence of drug-resistant mutant viruses, as soon as 1~9 days after administration (Gao et al., 2013; Hu et al., 2013).
However, the higher replication efficiency might also result from virus adaptation to MARC-145 cells because the mutant viruses were rescued after 13 or 22 sequential passages.
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