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Related Experiment Video

Updated: Feb 15, 2026

Experimental Infection with Listeria monocytogenes as a Model for Studying Host Interferon-γ Responses

Experimental Infection with Listeria monocytogenes as a Model for Studying Host Interferon-γ Responses

Published on: November 16, 2016

Interferons: Reprogramming the Metabolic Network against Viral Infection.

Kavita Raniga^1,2, Chen Liang^3,4,5

¹Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC H3T 1E2, Canada. kavita.raniga@mail.mcgill.ca.

|January 19, 2018

Summary

Viruses alter host metabolism for replication, but the host counters with interferon signaling. Interferon-stimulated genes (ISGs) reprogram cellular metabolism to fight viral infections.

Keywords:

25HC IDO1 ISGs SAMHD1 SAT1 interferons metabolism viruses

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Published on: June 17, 2019

Area of Science:

Virology
Immunology
Metabolic studies

Background:

Viruses manipulate host cell metabolism to favor replication.
Host cells employ innate immune responses, including interferon signaling, to counteract viral infections.
Interferon signaling induces interferon-stimulated genes (ISGs) that impact cellular metabolism and antiviral defense.

Purpose of the Study:

To review the intricate relationship between viral infection and host cellular metabolism.
To highlight the role of interferon-stimulated genes (ISGs) in modulating host metabolism against viruses.
To discuss specific ISGs (CH25H, SAT1, IDO1, SAMHD1) and their metabolic functions in antiviral defense.

Main Methods:

Literature review of recent studies on virus-host metabolic interactions.
Analysis of the role of interferon signaling in cellular metabolic reprogramming.
Focus on specific ISGs and their impact on metabolic pathways.

Main Results:

Interferons and ISGs significantly alter host cellular metabolism.
Specific ISGs like CH25H, SAT1, IDO1, and SAMHD1 directly modulate metabolic events.
These metabolic modulations by ISGs contribute to limiting viral replication and infection.

Conclusions:

The interplay between viral manipulation and host metabolic response is complex.
ISGs are critical mediators in rewiring host metabolism to establish an antiviral state.
Targeting ISG-mediated metabolic pathways presents a potential strategy for antiviral therapies.