1. N-terminal region of the PB1-F2 protein is responsible for increased expression of influenza A viral protein PB1.
- Author
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Košík I, Krejnusová I, Bystrická M, Poláková K, and Russ G
- Subjects
- Amino Acid Sequence, Animals, Cells, Cultured, DNA-Directed RNA Polymerases metabolism, Dogs, Female, Humans, Influenza A Virus, H1N1 Subtype genetics, Mice, Mice, Inbred BALB C, Puerto Rico, RNA, Viral genetics, Reading Frames, Vaccines, DNA genetics, Viral Proteins genetics, Influenza A Virus, H1N1 Subtype metabolism, Viral Proteins biosynthesis, Viral Proteins metabolism
- Abstract
Influenza A virus (IAV) PB1-F2 protein is encoded by an alternative reading frame (+1) within the PB1 gene. PB1-F2 has been shown to contribute to the pathogenesis of influenza virus infection as well as to the secondary bacterial infection. More recently has been shown that PB1-F2 protein may regulate a viral RNA (vRNA) polymerase activity by the interaction with PB1 protein. We proved that PB1-F2 protein increased the level of expression of PB1 protein and vRNA in the infected cells. Moreover, we demonstrated that a higher level of vRNA expression resulted in the increase of expression of multiple viral proteins, including NP, M1, and NS1. Finally, we used plasmids expressing N-terminal (1-50 aa) or C-terminal (51-87 aa) region of the PB1-F2 molecule for transfection of MDCK cells co-infected with influenza A/Puerto Rico/8/34 (H1N1) virus deficient in the PB1-F2 protein expression (PR8ΔPB1-F2). These experiments clearly showed that N-terminal region of PB1-F2 protein was responsible for the increase in PB1 protein expression. C-terminal region of PB1-F2 protein had no effect. Thus, we have identified the important function for N-terminal region of PB1-F2 protein.
- Published
- 2011
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