Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection

TL;DR

This paper reviews how influenza viruses upregulate and use host proteins to support their infection and spread, offering insights for developing new antiviral drugs.

Contribution

The paper provides a comprehensive review of pro-viral host factors upregulated by influenza and their roles in viral propagation and pathogenicity.

Findings

Influenza viruses upregulate various host proteins essential for viral replication and immune evasion.

Pro-viral factors are often indispensable for efficient viral propagation and pathogenicity.

Understanding these interactions could lead to host-targeted antiviral therapies.

Abstract

Influenza viruses cause annual epidemics and occasional pandemics through respiratory tract infections, giving rise to substantial morbidity and mortality worldwide. Influenza viruses extensively interact with host cellular proteins and exploit a variety of cellular pathways to accomplish their infection cycle. Some of the cellular proteins that display negative effects on the virus are degraded by the virus. However, there are also various proteins upregulated by influenza at the expression and/or activation levels. It has been well-established that a large number of host antiviral proteins such as type I interferon-stimulated genes are elevated by viral infection. On the other hand, there are also many cellular proteins that are induced directly by the virus, which are considered as pro-viral factors and often indispensable for rigorous viral propagation or pathogenicity. Here, we review the recent advances in our understanding of the cellular factors deemed to be upregulated and utilized by the influenza virus. The focus is placed on the functions of these pro-viral proteins and the mechanisms associated with promoting viral amplification, evading host immunity, or enhancing viral pathogenicity. Investigating the process of how influenza viruses hijack cellular proteins could provide a framework for inventing the host-factor-targeted drugs to conquer influenza.

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