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Nasal Wipes for Influenza A Virus Detection and Isolation from Swine

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Published on: December 4, 2015

Swine Enteric Coronavirus: Diverse Pathogen-Host Interactions.

Quanhui Yan^1,2,3, Xiaodi Liu^1,2,3, Yawei Sun^1,2,3

¹College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.

International Journal of Molecular Sciences

|April 12, 2022

Summary

This summary is machine-generated.

Swine enteric coronaviruses (SeCoVs) cause severe piglet gastroenteritis. This review details how SeCoVs manipulate host cell processes like autophagy, apoptosis, and immunity, impacting viral spread and disease.

Keywords:

apoptosis autophagy coronavirus host–virus interaction innate immunity

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Area of Science:

Veterinary Virology
Molecular Biology
Immunology

Background:

Swine enteric coronaviruses (SeCoVs) cause significant economic losses in swine farming globally.
Historically, porcine transmissible gastroenteritis virus (TGEV) and porcine epidemic diarrhea virus (PEDV) have caused widespread outbreaks.
Emerging SeCoVs, including porcine delta coronavirus (PDCoV) and swine acute diarrhea syndrome coronavirus (SADS-CoV), complicate the epidemic landscape, with some exhibiting cross-species transmission.

Purpose of the Study:

To review and synthesize current knowledge on the intricate interactions between SeCoVs and their hosts.
To elucidate the roles of autophagy, apoptosis, and innate immunity in SeCoV pathogenesis.
To provide insights into how these host-pathogen interactions influence viral replication and cellular signaling pathways.

Main Methods:

Literature review of recent studies on SeCoV-host interactions.
Analysis of research focusing on cellular responses such as autophagy and apoptosis.
Examination of studies investigating innate immune responses to SeCoV infection.

Main Results:

SeCoV infections trigger complex host responses involving autophagy and apoptosis.
Innate immunity plays a critical role in the host's defense against SeCoV.
These host-pathogen interactions are integral to viral replication and the modulation of cellular signaling.

Conclusions:

Understanding SeCoV-host interactions is crucial for managing swine enteric coronavirus diseases.
Modulation of autophagy, apoptosis, and innate immunity by SeCoVs offers potential targets for therapeutic interventions.
Further research into these mechanisms will enhance strategies for controlling viral spread and reducing economic impact in the swine industry.