# Molecular Maneuvers and Host Sabotage: A Comprehensive Review of CSFV’s Multifaceted Strategies to Subvert Immune Defenses and Cellular Metabolism

## TL;DR

This paper reviews how classical swine fever virus evades the immune system and manipulates host cells to spread, offering insights for new antiviral approaches.

## Contribution

The paper provides a comprehensive synthesis of CSFV's immune evasion and host manipulation strategies, highlighting recent discoveries and potential therapeutic targets.

## Key findings

- CSFV manipulates host cell death pathways like apoptosis and necroptosis to aid its replication.
- The virus exploits intracellular transport systems and exosomes to enhance its spread.
- Recent advances in understanding CSFV entry receptors are summarized for potential antiviral development.

## Abstract

Classical swine fever virus (CSFV) remains a significant threat to the global swine industry, causing a highly contagious and often fatal disease in pigs. This review comprehensively examines the molecular biology of CSFV and the intricate mechanisms it employs to establish infection. We detail the structure and functions of viral proteins, highlighting their roles in virus entry, replication, and immune evasion. A major focus is placed on the virus–host interaction, specifically how CSFV subverts host innate immune responses and hijacks critical cellular processes, including metabolism and cell death pathways. The virus strategically manipulates host cell death programs (apoptosis, mitophagy, necroptosis) and exploits intracellular transport systems to promote its propagation. Furthermore, we summarize recent advances in understanding the cellular receptors involved in CSFV entry and the role of exosomes in viral spread. This synthesis of current knowledge aims to provide a deeper insight into the pathogenesis of CSFV and identify potential vulnerabilities that could be targeted for the development of novel antiviral strategies.