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Influenza

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Influenza is an acute, highly communicable viral disease that affects the respiratory tract and is responsible for seasonal epidemics worldwide. Influenza A is the most prevalent type associated with widespread outbreaks and is subtyped based on two surface glycoproteins: hemagglutinin (H) and neuraminidase (N), as in H1N1. These glycoproteins are essential for viral infectivity, transmission, and immune recognition. Transmission occurs primarily through respiratory droplets and contaminated...

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Related Experiment Video

Updated: Jun 4, 2026

Identifying Caspases and their Motifs that Cleave Proteins During Influenza A Virus Infection

Identifying Caspases and their Motifs that Cleave Proteins During Influenza A Virus Infection

Published on: July 21, 2022

Pepstatin A alters host cell autophagic machinery and leads to a decrease in influenza A virus production.

Paola Matarrese¹, Lucia Nencioni, Paola Checconi

¹Department of Drug Research and Medicine Evaluation, Istituto Superiore di Sanita', Rome, Italy.

Journal of Cellular Physiology

|February 24, 2011

Summary

Pepstatin A, an inhibitor of cathepsin D, significantly hindered influenza A virus replication by modulating host cell autophagy and apoptosis. This finding offers insights into viral replication pathways and potential antiviral targets.

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Identifying Caspases and their Motifs that Cleave Proteins During Influenza A Virus Infection

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Affinity Purification of Influenza Virus Ribonucleoprotein Complexes from the Chromatin of Infected Cells

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siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

Area of Science:

Cellular Biology
Virology
Molecular Medicine

Background:

Autophagy is a cellular survival mechanism crucial for recycling waste under metabolic stress.
Dysfunctional autophagy is linked to various human pathologies, including viral infections.
Viruses may exploit or subvert host cell autophagy for replication.

Purpose of the Study:

To investigate the role of autophagy in influenza A virus replication.
To evaluate the impact of lysosomal protease inhibitors on viral production.
To identify potential antiviral strategies targeting host cell pathways.

Main Methods:

Biochemical and morphological analyses were employed.
Influenza A/Puerto Rico/8/34 H1N1 virus production was modulated.
The effects of cathepsin B inhibitor (CA074) and cathepsin D inhibitor (Pepstatin A) were assessed.

Main Results:

Pepstatin A significantly inhibited influenza virus replication.
CA074 did not significantly affect viral replication.
Pepstatin A's effect was likely due to modulation of host cell autophagic/apoptotic responses.

Conclusions:

Cathepsin D activity, modulated by Pepstatin A, plays a role in influenza A virus replication.
Host cell autophagy and apoptosis are likely pathways exploited by influenza A virus.
These findings suggest novel antiviral strategies targeting host-pathogen interactions.