Related Experiment Video
Updated: Jul 4, 2025

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies
Published on: September 13, 2024
Virus-induced host cell metabolic alteration.
Syed Shahariar Bappy1, Md Muzammal Haque Asim1, Mohammad Mainul Ahasan1
1R&D, Vaccine Division, Incepta Pharmaceutical Ltd, Dhaka, Bangladesh.
This review summarizes how viruses change the metabolism of the cells they infect to support their replication. By altering pathways like glycolysis and fatty acid synthesis, viruses ensure they have enough energy and materials to make new virus particles. The study highlights that each virus has a unique way of changing host cell metabolism, and these changes may help viruses survive and spread. Understanding these metabolic shifts could lead to new treatments that block viral replication by targeting key metabolic enzymes. The findings also suggest that these changes may increase the risk of cancer in infected cells. Future research should focus on comparing these changes across different viruses to develop more effective antiviral therapies.
Area of Science:
- Virology
- Cellular metabolism
- Antiviral drug development
Background:
Understanding how viruses alter host cell metabolism remains a key challenge in virology. Prior research has shown that viruses manipulate energy and biosynthesis pathways to support replication. However, the extent of these changes and their variability across viral types is still unclear. No prior work had resolved how specific metabolic shifts correlate with viral life stages. This gap motivated a systematic review of recent findings on virus-induced metabolic reprogramming. Researchers have long known that glycolysis and lipid metabolism are affected, but the mechanisms remain poorly characterized. The field lacks a unified framework to compare metabolic responses across different viruses. This review aims to clarify how diverse viruses influence host cell metabolism.
Purpose Of The Study:
The goal of this review is to synthesize current knowledge on how viruses alter host cell metabolism. The authors aim to highlight the diversity of metabolic changes induced by different viruses. They focus on identifying common and unique metabolic signatures across viral infections. The study addresses the need for a comprehensive overview of virus-host metabolic interactions. By compiling recent findings, the authors seek to improve understanding of viral metabolic dependencies. This work may help identify new therapeutic targets for antiviral treatments. The review also aims to guide future research on virus-induced metabolic reprogramming. It provides a foundation for comparing metabolic responses across viral species.
Main Methods:
The authors conducted a literature review of recent metabolomics studies on virus-host interactions. They analyzed data from various eukaryotic viruses and their effects on host cell metabolism. The review includes findings from studies on glycolysis, fatty acid synthesis, and glutaminolysis. The authors compared metabolic changes across different viral families and life cycles. They evaluated how these changes support viral replication and energy needs. The study also examined the role of specific enzymes and pathways in viral metabolism. The authors synthesized data from in vitro and in vivo experiments. They focused on identifying patterns and exceptions in virus-induced metabolic reprogramming.
Main Results:
The review found that viruses broadly alter host cell metabolism to support replication. Glycolysis is commonly upregulated to provide energy for viral processes. Fatty acid synthesis is modified to supply membrane components for new virions. Glutaminolysis is often increased to support biosynthesis and redox balance. Each virus has a distinct metabolic signature based on its replication strategy. Some viruses prioritize lipid metabolism, while others focus on amino acid pathways. The study identified multiple antiviral drug targets linked to metabolic enzymes. These findings suggest that metabolic reprogramming is a conserved viral strategy. The review also highlighted gaps in understanding the full scope of these changes.
Conclusions:
The authors conclude that viruses manipulate host cell metabolism in diverse ways. These changes are essential for viral replication and survival. The review emphasizes the need for further study of virus-specific metabolic signatures. Improved monitoring of metabolic shifts could lead to better antiviral therapies. The authors suggest that targeting metabolic enzymes may be a promising treatment approach. They also note that virus-induced metabolic reprogramming may contribute to oncogenesis. The findings support the idea that metabolic pathways are key to viral life cycles. This work provides a foundation for future research on virus-host metabolic interactions.
Frequently Asked Questions
Viruses modify glycolysis, fatty acid synthesis, and glutaminolysis to provide energy and building blocks for replication.
Each virus alters specific pathways based on its replication strategy, such as prioritizing lipid or amino acid metabolism.
Glycolysis provides ATP and intermediates needed for viral RNA and protein synthesis during replication.
Glutaminolysis supports biosynthesis and redox balance, which are critical for viral replication.
Altered metabolism may promote uncontrolled cell growth and survival, increasing cancer risk in infected cells.
Targeting metabolic enzymes could disrupt viral replication and reduce pathogenesis.
Related Concept Videos
Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Viral Mutations
Mechanisms of Retrovirus-induced Cancers
Immune Response Against Viral Pathogens
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...

