2018 Fiscal Year Final Research Report
Effect of cytoplasmic tail of CM2 protein on influenza C virus replications
| Project/Area Number |
16K19136
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Virology
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Research Collaborator |
HONGO Seiji
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | C型インフルエンザウイルス / CM2 |
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| Outline of Final Research Achievements |
To investigate whether the residues 73-75 of CM2, which are involved in protein expression level, N-glycosylation processing and tetrameric formation of CM2, affect influenza C virus replication, we generated a recombinant virus (rCM2 Ala 73-75) in which the residues were substituted with alanine. The rCM2 Ala 73-75 replicated significantly lower than the wild-type virus (rWT). The amount of CM2 in the rCM2 Ala 73-75 virions and virus-infected cells was lower than that in rWT virions and rWT-infected cells. The amount of CM2 expressed on the cell membranes of rCM2 Ala 73-75-infected cells was less than that observed with rWT-infected cells. However, these mutations did not affect the N-glycosylation and oligomerization of CM2 in the virions. These results suggested that the mutation at residues 73-75 of CM2 decreased the amount of CM2 on the cell membrane of infected cells and in the virions, thereby affecting the genome packaging and uncoating.
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| Free Research Field |
ウイルス学
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| Academic Significance and Societal Importance of the Research Achievements |
CM2はA型インフルエンザウイルスのM2と同様に、水素イオンをエンベロープ内に流入させ、M1の殻を崩壊させ脱殻に寄与すると考えられている。本研究により、この機能に関与する新たなアミノ酸配列(73-75位)を発見できたことは学術的意義がある。また、この配列は感染性に必須なウイルスゲノムの取り込みにも関与することが明らかになり、ウイルス増殖機構の解明に一歩近づいたこともウイルス学的に意義が大きい。上記の機能はウイルス増殖に必須であるため、これを標的とした抗ウイルス薬の開発に繋がる可能性がある。
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