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[Proteolytic mechanism of deproteinization of influenza virus by plasmatic membranes]
Abstract:
A mechanism responsible for proteolytic deproteinization of influenza virus A2 Hong-Kong (I)68 by plasmatic membranes of sensitive cells was studied. Presence of trypsinlike protease in plasmatic membranes of white mice lungs was demonstrated. A considerable inhibition of the membrane proteolitic activity was obtained in the presence of epsilon-aminocaproic acid. Disintegration of the virus labeled by [3H]uridine by plasmatic membranes was investigated and it was found that this process required ATP. Inhibition of the protease activity by epsilon-aminocaproic acid led to the suppression of deproteinization of influenza virus. The experimental data obtained indicate that the proteolytic enzymes of plasmatic membranes participate in the complex process of virus "uncoating".
Insights
Influenza virus deproteinization by cell membranes involves a trypsin-like protease. Epsilon-aminocaproic acid inhibits this protease, suggesting its role in virus uncoating.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Context:
- Influenza virus entry into host cells involves a complex uncoating process.
- Plasmatic membranes of host cells possess enzymatic machinery that can interact with viruses.
- Understanding virus-host interactions is crucial for developing antiviral strategies.
Purpose:
- To investigate the mechanism of proteolytic deproteinization of influenza virus A2 Hong-Kong (I)68 by plasmatic membranes.
- To identify the enzymes involved in virus deproteinization and their role in the uncoating process.
- To explore the potential of inhibiting this process using specific agents.
Summary:
- A trypsin-like protease was identified in the plasmatic membranes of white mice lungs, capable of deproteinizing influenza virus.
- The proteolytic activity of these membranes was significantly inhibited by epsilon-aminocaproic acid.
- Virus disintegration by plasmatic membranes was found to be ATP-dependent, and protease inhibition suppressed deproteinization, indicating enzyme involvement in virus uncoating.
Impact:
- This study elucidates a key step in the influenza virus replication cycle, specifically the initial deproteinization.
- The findings highlight the role of host cell proteolytic enzymes in viral uncoating.
- Identifying the involvement of specific proteases and inhibitors like epsilon-aminocaproic acid may offer new avenues for antiviral therapies targeting influenza virus entry.