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Measurement of γHV68 Infection in Mice

Measurement of γHV68 Infection in Mice

Published on: November 22, 2011

Starvation after infection restricts enterovirus D68 replication.

Alagie Jassey¹, Michael A Wagner¹, Ganna Galitska¹

¹Department of Microbiology and Immunology and Center for Pathogen Research, University of Maryland School of Medicine, Baltimore, MD, USA.

|April 21, 2022

Summary

Starvation after infection (SAI) effectively reduces enterovirus D68 (EV-D68) replication by enhancing autophagy and blocking viral membrane production. This broad-spectrum strategy shows promise against picornaviruses lacking vaccines or treatments.

Keywords:

Autophagic flux EV-D68 SAI SBI picornavirus

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Area of Science:

Virology
Cell Biology
Autophagy Research

Background:

Enterovirus D68 (EV-D68) is a significant respiratory pathogen linked to acute flaccid myelitis in children.
Current therapeutic options, including vaccines and antivirals, are unavailable for EV-D68 infections.
EV-D68 hijacks the host cell's autophagy pathway, promoting autophagosome formation for replication but inhibiting lysosome fusion.

Purpose of the Study:

To investigate the impact of modulating autophagy through starvation on EV-D68 replication.
To determine if starvation, applied before or after infection, affects viral propagation.
To explore the potential of autophagy modulation as a broad-spectrum antiviral strategy against picornaviruses.

Main Methods:

EV-D68 infected cell cultures were subjected to starvation either before infection (SBI) or after infection (SAI).
Viral replication, host protein cleavage, autophagic flux, and viral membrane formation were analyzed.
Pharmacological inhibitors of autophagic flux were used to assess the role of downstream autophagy steps.

Main Results:

Starvation after infection (SAI) significantly attenuated EV-D68 replication across multiple cell lines, unlike SBI.
SAI prevented viral-induced cleavage of key autophagy-related proteins and restored autophagic flux during infection.
SAI inhibited the formation of virus-induced membranes essential for picornavirus replication and restricted other picornaviruses.

Conclusions:

Autophagosome maturation and fusion are critical for picornavirus replication.
SAI represents a promising, broad-spectrum antiviral strategy against EV-D68 and related picornaviruses.
Targeting host autophagy flux offers a novel therapeutic avenue for enterovirus infections.