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Related Experiment Video

Updated: Mar 15, 2026

Author Spotlight: Exploring Cloning Techniques for Full-Length DNA Fragments

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Published on: May 17, 2024

Pigs with CD163 Mutation Conferred PRRSV Resistance.

Changbao Wu¹, Heyao Wang¹, Wei Zhang¹

¹College of Life Science, Inner Mongolia University, Hohhot 010000, China.

Animals : an Open Access Journal From MDPI

|March 14, 2026

Summary

Researchers created pigs lacking the CD163 receptor using gene editing. These pigs were completely resistant to Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) infection, offering a new strategy for disease control.

Keywords:

CD163 CRISPR/Cas9 LWps PRRSV disease resistance

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Last Updated: Mar 15, 2026

Author Spotlight: Exploring Cloning Techniques for Full-Length DNA Fragments

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piggyBac Transposon System Modification of Primary Human T Cells

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Published on: November 5, 2012

Forward Genetic Approach to Uncover Stress Resistance Genes in Mice — A High-throughput Screen in ES Cells

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Published on: November 11, 2015

Area of Science:

Veterinary Virology
Animal Genetics

Background:

Porcine Reproductive and Respiratory Syndrome (PRRS) causes significant economic losses in swine production.
Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) utilizes the CD163 receptor on porcine alveolar macrophages for cellular entry.

Purpose of the Study:

To investigate the role of CD163 as the essential receptor for PRRSV infection in vivo.
To develop a genetically resistant pig model against PRRSV.

Main Methods:

CRISPR/Cas9 gene editing was employed to generate CD163-/- Landrace pigs.
Experimental challenge with two distinct Type II PRRSV strains was performed on edited and wild-type pigs.
Virological and pathological examinations were conducted to assess infection and disease progression.

Main Results:

CD163-/- pigs demonstrated complete resistance to PRRSV infection following experimental challenge.
Absence of viral replication and characteristic pulmonary lesions was observed in edited pigs.
Wild-type control pigs exhibited high viral loads and severe pathology, including pulmonary lesions and organ damage.

Conclusions:

CD163 is confirmed as an essential in vivo receptor for PRRSV entry.
The generated CD163-/- pig model provides a viable genetic strategy for breeding PRRSV-resistant swine.
This research offers a promising avenue for mitigating PRRSV economic impact on the global swine industry.