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Effect of cellular function inhibitors on the infection of Frp/3 cells by hepatitis A virus
1Istituto di Microbiologia, Facoltà di Medicina, Università La Sapienza, Roma, Italy.
Abstract:
The effect of some cellular function inhibitors on hepatitis A virus (HAV) adsorption and on the successive events of infection in a monkey cell line (Frp/3 cells) was investigated. Treatments of Frp/3 cells with colcemide, vinblastine and cytochalasin D, which affect cytoskeleton organization, indicated that neither microtubules nor microfilaments play an important role in the early events of HAV infection. Monensin, which acts as an ionophore on intracellular vesicle compartments inhibited HAV infection probably at the uncoating step. Inhibition of viral replication to a different degree was observed with both inhibitors of oxidative phosphorylation, such as dinitrophenol and sodium azide, and with an inhibitor of glycolysis, 2-deoxy-D-glucose. However, none of these compounds significantly affected the early steps of infection, thus demonstrating that HAV replication is largely dependent upon cell energy.
Insights
Cellular function inhibitors reveal that hepatitis A virus (HAV) entry is independent of cytoskeleton. However, viral replication heavily relies on cellular energy metabolism.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Background:
- Hepatitis A virus (HAV) is a significant human pathogen.
- Understanding the cellular mechanisms of HAV infection is crucial for developing antiviral strategies.
Purpose of the Study:
- To investigate the role of cellular functions and energy metabolism in HAV infection.
- To identify potential targets for antiviral interventions.
Main Methods:
- Treatment of Frp/3 monkey cells with various cellular function inhibitors.
- Assessment of HAV adsorption, uncoating, and replication.
- Utilizing cytoskeleton inhibitors (colcemide, vinblastine, cytochalasin D), an ionophore (monensin), and metabolic inhibitors (dinitrophenol, sodium azide, 2-deoxy-D-glucose).
Main Results:
- Cytoskeleton inhibitors did not affect early HAV infection events.
- Monensin inhibited HAV infection, likely at the uncoating stage.
- Metabolic inhibitors significantly impacted viral replication but not early infection steps.
Conclusions:
- HAV entry and adsorption are independent of microtubule and microfilament organization.
- HAV uncoating may involve intracellular vesicle transport.
- Viral replication is highly dependent on cellular energy production through oxidative phosphorylation and glycolysis.