Abstract: Zhang et al.
Cellular & Molecular Biology Letters
(2025) 30:55
https://doi.org/10.1186/s11658-025-00722-w
Cellular & Molecular
Biology Letters
Open Access
REVIEW
Rho‑GTPases subfamily: cellular defectors
orchestrating viral infection
Beibei Zhang1† , Shuli Li1†, Juntao Ding1, Jingxia Guo2, Zhenghai Ma1, Hong Duan3*
†
Beibei Zhang and Shuli Li have
contributed equally to this work
and share first authorship.
*Correspondence:
duanhong0924@126.com
1
Xinjiang Key Laboratory
of Biological Resources
and Genetic Engineering, College
of Life Science and Technology,
Xinjiang University, Urumqi,
Xinjiang, China
2
Disease Prevention and Control
Center of Xinjiang Production
and Construction Corps, Urumqi,
Xinjiang, China
3
College of Veterinary Medicine,
Henan Agricultural University,
Zhengzhou, Henan, China
Abstract
Ras homolog gene family-guanosine triphosphatases (Rho-GTPases), key
molecular switches regulating cytoskeletal dynamics and cellular signaling, play
a pivotal role in viral infections by modulating critical processes such as viral
entry, replication, and release. This review elucidates the intricate mechanisms
through which Rho-GTPases, via interactions with guanine nucleotide exchange
factors (GEFs), GTPase-activating proteins (GAPs), and other signaling pathways,
including the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), rat sarcoma
(Ras), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)
pathways, facilitate viral pathogenesis. Specific viruses, such as influenza A virus (IAV),
herpesviruses, human immunodeficiency virus (HIV), and respiratory syncytial virus
(RSV), exploit Rho-GTPase-mediated cytoskeletal reorganization to enhance infectivity.
For example, Rho-GTPases promote actin remodeling and membrane fusion, which
are essential for viral entry and intracellular transport. Furthermore, Rho-GTPases
modulate immune responses, often suppressing antiviral defenses to favor viral
replication. Despite these insights, the molecular mechanisms underlying Rho-GTPase
regulation during viral infections remain incompletely understood. Future research
should focus on delineating the precise roles of Rho-GTPases in distinct viral life cycles,
uncovering novel regulatory mechanisms, and developing targeted antiviral therapies
that selectively inhibit Rho-GTPase signaling without compromising host cell functions.
Such advancements could pave the way for broad-spectrum antiviral strategies,
particularly against viruses that heavily rely on cytoskeletal manipulation for infection.
Keywords: Rho-GTPases, Molecule switch, Viral infection, Regulatory mechanism,
Therapeutic target
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"abstract": "<jats:title>Abstract</jats:title>\n <jats:p>Ras homolog gene family-guanosine triphosphatases (Rho-GTPases), key molecular switches regulating cytoskeletal dynamics and cellular signaling, play a pivotal role in viral infections by modulating critical processes such as viral entry, replication, and release. This review elucidates the intricate mechanisms through which Rho-GTPases, via interactions with guanine nucleotide exchange factors (GEFs), GTPase-activating proteins (GAPs), and other signaling pathways, including the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), rat sarcoma (Ras), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways, facilitate viral pathogenesis. Specific viruses, such as influenza A virus (IAV), herpesviruses, human immunodeficiency virus (HIV), and respiratory syncytial virus (RSV), exploit Rho-GTPase-mediated cytoskeletal reorganization to enhance infectivity. For example, Rho-GTPases promote actin remodeling and membrane fusion, which are essential for viral entry and intracellular transport. Furthermore, Rho-GTPases modulate immune responses, often suppressing antiviral defenses to favor viral replication. Despite these insights, the molecular mechanisms underlying Rho-GTPase regulation during viral infections remain incompletely understood. Future research should focus on delineating the precise roles of Rho-GTPases in distinct viral life cycles, uncovering novel regulatory mechanisms, and developing targeted antiviral therapies that selectively inhibit Rho-GTPase signaling without compromising host cell functions. Such advancements could pave the way for broad-spectrum antiviral strategies, particularly against viruses that heavily rely on cytoskeletal manipulation for infection.</jats:p>",
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