CRISPR/Cas-Mediated Genome Editing in Viral Research

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "General Virology".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 1208

Special Issue Editor


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Guest Editor
School of Nursing, Tung Wah College, Kowloon, Hong Kong
Interests: Epstein–Barr virus (EBV); molecular virology; CRISPR–Cas-mediated viral genome editing; host innate immune responses

Special Issue Information

Dear Colleagues,

CRISPR/Cas technologies have revolutionized virology by providing precise, programmable tools that accelerate fundamental discovery and translational applications. In viral genome editing, CRISPR systems enable the targeted modification of DNA viruses and proviral sequences, facilitating the functional dissection of viral genes, the generation of attenuated strains, and the engineering of viral vectors for vaccines and gene delivery. Genome-wide CRISPR knockout, activation, and interference screens have likewise transformed host–pathogen research: unbiased screens identify proviral and antiviral host factors, map entry and replication pathways, and reveal novel therapeutic targets with unprecedented throughput and resolution. Beyond editing, CRISPR-based diagnostics—particularly collateral cleavage systems like Cas12 and Cas13—offer rapid, sensitive, and field-deployable detection of viral RNA or DNA, reshaping outbreak response and point-of-care testing. Finally, CRISPR is emerging as a direct antiviral modality: sequence-specific nucleases can selectively disrupt viral genomes or transcripts, suppress latent infections, and potentially clear reservoirs when coupled with delivery strategies. Together, these capabilities make CRISPR/Cas a versatile platform that spans basic virology, diagnostics, and therapeutic development. This Special Issue highlights advances and challenges in leveraging CRISPR tools responsibly and effectively to deepen our understanding of viruses and to innovate next-generation antiviral strategies.

Dr. Kit San Yuen
Guest Editor

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Keywords

  • CRISPR–Cas systems
  • viral genome engineering
  • antiviral gene therapy
  • host factor discovery (proviral and antiviral)
  • CRISPR-based diagnostics

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Published Papers (1 paper)

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Research

25 pages, 9678 KB  
Article
Tree Shrew Genome-Wide CRISPR Screen Identifies RNF6 as a Proviral Host Factor for Zika Virus Replication in Brain Microvascular Endothelial Cells
by Mengdi Qi, Xin Liu, Wenguang Wang, Meili Lu, Qingwei Zeng, Na Li, Yuanyuan Han, Shengtao Fan, Caixia Lu and Jiejie Dai
Viruses 2026, 18(3), 323; https://doi.org/10.3390/v18030323 - 5 Mar 2026
Viewed by 935
Abstract
Zika virus (ZIKV), a unique flavivirus with neurotropic and teratogenic potential, can cross the blood–brain barrier and persist in human brain microvascular endothelial cells (BMECs); however, no approved vaccines or specific antivirals exist, and its barrier-crossing and neuroinvasive mechanisms remain elusive. Innovative strategies [...] Read more.
Zika virus (ZIKV), a unique flavivirus with neurotropic and teratogenic potential, can cross the blood–brain barrier and persist in human brain microvascular endothelial cells (BMECs); however, no approved vaccines or specific antivirals exist, and its barrier-crossing and neuroinvasive mechanisms remain elusive. Innovative strategies to identify additional host factors mediating ZIKV infection could yield key insights and help address these challenges. To uncover novel host factors, we established the first tree shrew (Tupaia belangeri) genome-wide CRISPR/Cas9 knockout (GeCKO) library and performed a screen in BMECs, identifying ring finger protein 6 (RNF6) as a novel proviral factor for ZIKV. ZIKV infection in BMECs was significantly reduced following RNF6 knockout or knockdown but enhanced upon RNF6 overexpression or rescue. Mechanistically, RNF6 interacts with the ZIKV NS5 protein and acts as a potential negative regulator of the type I interferon and MAPK signaling pathways. Evolutionary and structural analyses revealed that RNF6 is highly conserved between humans and tree shrews; molecular docking further identified shared NS5-binding residues (Gln-59, Arg-140), supporting the conserved proviral role of human RNF6 in ZIKV infection. Our findings highlight tree shrew GeCKO screening as an efficient approach for identifying novel host factors and establish RNF6 as a critical proviral factor for ZIKV replication in BMECs, providing new insights into ZIKV neurotropic pathogenesis and informing potential antiviral strategies. Full article
(This article belongs to the Special Issue CRISPR/Cas-Mediated Genome Editing in Viral Research)
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