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Isolation of a novel type of interfering influenza B virus defective in the function of M gene
Abstract:
A novel type of interfering influenza B virus which is defective in the function of M gene has been reported. Clone 301, a B type virus clone obtained by successive back-crosses of A/Aichi/2/68 (H 3 N 2) with B/Yamagata/1/73, grew normally in MDCK cells when inoculated at a low multiplicity, but was easily converted to a hemagglutinating but non-infectious form by one cycle of high multiplicity infection. Within MDCK cells infected with infectious clone 301 at a high multiplicity, synthesis of M protein was greatly reduced. The virus particle produced by a high multiplicity infection was devoid of RNA segment 7 (M gene), contained less amount of M protein compared with the standard virus, and interfered with the replication of wild type B/Yamagata, again accompanied by a selective suppression of M protein synthesis within the co-infected cells.
Insights
A novel influenza B virus variant defective in M gene function was identified. This variant interferes with wild-type influenza B virus replication by suppressing M protein synthesis.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Influenza B viruses possess segmented RNA genomes, with M gene encoding matrix proteins crucial for viral assembly and replication.
- Interfering virus particles can modulate the replication of standard viruses, a phenomenon with potential therapeutic implications.
Purpose of the Study:
- To characterize a novel influenza B virus clone (Clone 301) exhibiting defective M gene function and interfering properties.
- To investigate the mechanism by which this defective virus interferes with wild-type influenza B virus replication.
Main Methods:
- Generation of Clone 301 through successive back-crossing of influenza A and B strains.
- Infection of Madin-Darby Canine Kidney (MDCK) cells at varying multiplicities.
- Analysis of viral protein synthesis, RNA content, and hemagglutination properties.
- Co-infection experiments to assess interference with wild-type B/Yamagata virus.
Main Results:
- Clone 301 replicated normally at low multiplicity but produced non-infectious, hemagglutinating virions at high multiplicity.
- High multiplicity infection of Clone 301 led to significantly reduced M protein synthesis within MDCK cells.
- Virus particles produced under high multiplicity conditions lacked RNA segment 7 (M gene) and contained reduced M protein.
- These defective particles interfered with wild-type B/Yamagata virus replication, correlating with suppressed M protein synthesis in co-infected cells.
Conclusions:
- A novel interfering influenza B virus, defective in M gene function, has been characterized.
- The M gene defect and subsequent reduction in M protein synthesis are critical for the observed interference with wild-type influenza B virus replication.
- This finding provides insights into virus-host interactions and potential mechanisms for viral interference.