Opinion - (2025) Volume 9, Issue 6
Received: 01-Nov-2025, Manuscript No. vcrh-26-180186;
Editor assigned: 03-Nov-2025, Pre QC No. P-180186;
Reviewed: 17-Nov-2025, QC No. Q-180186;
Revised: 24-Nov-2025, Manuscript No. R-180186;
Published:
29-Nov-2025
, DOI: 10.37421/2736-657X.2025.9.335
Citation: Dubois, Antoine. ”Autophagy: A Viral Infection’s Double-Edged Sword.” Virol Curr Res 09 (2025):335.
Copyright: © 2025 Dubois A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Autophagy, a fundamental cellular process responsible for the degradation and recycling of damaged organelles and misfolded proteins, plays a remarkably complex and often contradictory role in the context of viral infections. Initially recognized as a crucial component of host defense, autophagy can directly combat viral invaders by sequestering viral particles and infected cellular components within autophagosomes for lysosomal degradation, thereby limiting viral spread and reducing viral load [1].
This cytoprotective function is vital in mounting an effective innate immune response against intracellular pathogens, offering a mechanism for eliminating viruses that have successfully entered host cells [3].
However, the evolutionary adaptability of viruses has led many to develop sophisticated strategies to subvert this cellular machinery. Instead of being eliminated, viruses can hijack the autophagy pathway to facilitate their own replication, assembly, or egress from infected cells [2].
This intricate dance between host defense and viral manipulation underscores the dynamic nature of the host-pathogen interaction, making autophagy a fascinating and critical area of study for understanding viral pathogenesis and developing novel therapeutic interventions [7].
The dual role of autophagy, acting as both a defense mechanism and a target for viral exploitation, necessitates a nuanced understanding of its involvement in various viral infections to devise effective treatment strategies [1, 2]. For instance, in the case of influenza A virus, autophagy is induced, but specific viral proteins are employed to disrupt autophagic degradation, creating an environment conducive to viral assembly and release [4].
Similarly, herpes simplex virus 1 has been shown to selectively induce autophagy to promote the encapsidation of its genome and subsequent virion assembly, highlighting a novel pathway for viral pathogenesis [5].
This intricate interplay extends to other viruses like Dengue virus, where autophagy has been demonstrated to enhance viral replication, suggesting that targeting autophagy could be a viable antiviral strategy [6].
Coronaviruses, including SARS-CoV-2, also engage with the autophagy machinery, with specific viral proteins modulating the process to influence viral replication and release, emphasizing the role of autophagy dysregulation in disease pathogenesis [7].
Hepatitis C virus (HCV) presents another example where autophagy modulation is implicated; while HCV can induce autophagy, it also develops mechanisms to evade degradation, contributing to persistent infections and pointing towards autophagy modulation as a therapeutic target [8].
Even Human Immunodeficiency Virus (HIV) is susceptible to autophagy-mediated clearance, with enhanced autophagy leading to the degradation of viral particles and infected cellular components, presenting a potential avenue for host defense [9].
Finally, cytomegalovirus (CMV) is known to hijack the autophagy pathway to promote viral replication and evade host immunity, further solidifying autophagy as a critical target for therapeutic intervention in viral infections [10].
The intricate relationship between autophagy and viral infections is characterized by a dual role, acting as both a host defense mechanism and a target for viral exploitation. Autophagy, a cellular process of self-degradation and recycling, can eliminate viral components and infected cells, thereby limiting viral spread [1].
This intrinsic host defense is crucial for controlling intracellular pathogens [3].
However, numerous viruses have evolved mechanisms to manipulate the autophagy pathway for their own benefit, utilizing it to enhance replication, assembly, or egress [2].
Understanding this complex interplay is paramount for developing effective antiviral therapies that can either boost autophagy for viral clearance or inhibit viral interference with the process [1].
For example, influenza A virus induces autophagy but simultaneously employs viral proteins to obstruct autophagic degradation, thus facilitating viral assembly and release [4].
Herpes simplex virus 1 utilizes autophagy to promote the encapsidation of its genome and the assembly of new virions, demonstrating a novel role in viral pathogenesis [5].
Dengue virus replication is significantly enhanced by autophagy, indicating that targeting this pathway could be a promising antiviral strategy [6].
Coronaviruses, including SARS-CoV-2, interact with autophagy machinery through specific viral proteins that modulate the process, influencing viral replication and release and highlighting the impact of autophagy dysregulation on disease [7].
Hepatitis C virus (HCV) demonstrates a complex interaction where it induces autophagy but also evades its degradative functions, contributing to persistent infections and suggesting autophagy modulation as a therapeutic target [8].
Autophagy also plays a role in the clearance of Human Immunodeficiency Virus (HIV), as enhanced autophagy can lead to the degradation of viral particles and infected cells, presenting a host defense strategy [9].
Cytomegalovirus (CMV) infection is another instance where the virus hijacks the autophagy pathway to foster its replication and evade host immunity, making autophagy a potential therapeutic target for CMV infections [10].
This review delves into the specific mechanisms by which viruses manipulate the autophagy pathway, providing examples of viruses that use autophagosomes for replication or transport, or that disrupt autophagic flux to avoid degradation. The context-dependent nature of autophagy's role, varying with the virus, host cell, and cellular environment, is a recurring theme [2].
The authors emphasize the potential of autophagy inducers to enhance viral clearance and reduce viral loads, suggesting therapeutic avenues [3].
The findings on influenza A virus highlight how viral proteins can interfere with autophagic degradation to support viral replication [4].
Similarly, the research on HSV-1 underscores its selective induction of autophagy for genome encapsidation and virion assembly [5].
The enhanced replication of Dengue virus in the presence of autophagy points to the exploitation of autophagosomal pathways [6].
The modulation of autophagy by specific viral proteins in coronaviruses is critical for viral replication and release [7].
The evasion of autophagic degradation by HCV contributes to persistent infection and indicates a therapeutic target [8].
The clearance of HIV through autophagy-mediated degradation of viral components signifies a host defense mechanism [9].
Finally, the hijacking of autophagy by CMV for replication and immune evasion highlights its role as a therapeutic target [10].
Autophagy, a cellular recycling process, plays a dual role in viral infections. It can act as a host defense by degrading viral components and infected cells, thus limiting viral spread. Conversely, many viruses have evolved strategies to exploit autophagy for their own replication, assembly, and egress. Understanding this complex interaction is crucial for developing antiviral therapies. Different viruses, including influenza A virus, herpes simplex virus 1, Dengue virus, coronaviruses, Hepatitis C virus, HIV, and cytomegalovirus, have been shown to either utilize or be targeted by autophagy in unique ways. Some viruses induce autophagy to aid their lifecycle, while others manipulate it to evade degradation. This context-dependent role of autophagy, varying by virus and host cell, highlights its significance as a therapeutic target. Activating autophagy can enhance viral clearance, while inhibiting viral manipulation of the process offers another therapeutic avenue.
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