Key result
Influenza A viruses lacking M mRNA3 show no replication defect versus wild-type.
Why the study?
The function of influenza A virus M mRNA3 is unknown and its necessity for viral replication was undetermined.
Does the lack of M mRNA3 affect influenza A virus replication in tissue culture?
Does the lack of M mRNA3 affect influenza A virus replication in tissue culture?
The influenza A virus spliced messenger RNA M mRNA3 is not essential for viral replication in tissue culture.
M mRNA3 dispensability in culture does not alter antiviral targets; leaves open its role in vivo or pathogenesis.
Influenza A virus genome RNA segment 7 encodes three known mRNAs, two of which, M2 mRNA and M mRNA3, are derived by alternative splicing of the primary collinear mRNA transcript using alternative 5' splice sites. The function of M mRNA3 is currently unknown, therefore we attempted to determine whether it is essential for virus replication. Recombinant viruses unable to produce M mRNA3 and/or M2 mRNA were created by mutating the shared 3' splice site. Growth of the mutant viruses in M2-expressing MDCK cells was not significantly affected by the lack of M mRNA3. During the course of a wild-type virus infection, levels of M mRNA3 began to decrease while those of M2 mRNA increased, which may indicate a potential mechanism of alternative splicing control. These data suggest that neither M mRNA3 nor any potential protein product are essential for influenza virus replication in tissue culture.
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Jackson et al. (2008) studied Influenza A virus infection. Mutation of shared 3' splice site to prevent M mRNA3 production vs. Wild-type virus was evaluated on Virus replication/growth in M2-expressing MDCK cells. Recombinant influenza A viruses unable to produce M mRNA3 showed no significant growth defect in tissue culture, indicating that M mRNA3 is not essential for viral replication.
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