The Strategies Used by Animal Viruses to Antagonize Host Antiviral Innate Immunity: New Clues for Developing Live Attenuated Vaccines (LAVs)

As an essential type of vaccine, live attenuated vaccines (LAVs) play a crucial role in animal disease prevention and control. Nevertheless, developing LAVs faces the challenge of balancing safety and efficacy. Understanding the mechanisms animal viruses use to antagonize host antiviral innate immun...

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Main Authors: Na Chen, Baoge Zhang
Format: Article
Language:English
Published: MDPI AG 2025-01-01
Series:Vaccines
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Online Access:https://www.mdpi.com/2076-393X/13/1/46
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author Na Chen
Baoge Zhang
author_facet Na Chen
Baoge Zhang
author_sort Na Chen
collection DOAJ
description As an essential type of vaccine, live attenuated vaccines (LAVs) play a crucial role in animal disease prevention and control. Nevertheless, developing LAVs faces the challenge of balancing safety and efficacy. Understanding the mechanisms animal viruses use to antagonize host antiviral innate immunity may help to precisely regulate vaccine strains and maintain strong immunogenicity while reducing their pathogenicity. It may improve the safety and efficacy of LAVs, as well as provide a more reliable means for the prevention and control of infectious livestock diseases. Therefore, exploring viral antagonistic mechanisms is a significant clue for developing LAVs, which helps to explore more viral virulence factors (as new vaccine targets) and provides a vital theoretical basis and technical support for vaccine development. Among animal viruses, ASFV, PRRSV, PRV, CSFV, FMDV, PCV, PPV, and AIV are some typical representatives. It is crucial to conduct in-depth research and summarize the antagonistic strategies of these typical animal viruses. Studies have indicated that animal viruses may antagonize the antiviral innate immunity by directly or indirectly blocking the antiviral signaling pathways. In addition, viruses also do this by antagonizing host restriction factors targeting the viral replication cycle. Beyond that, viruses may antagonize via regulating apoptosis, metabolic pathways, and stress granule formation. A summary of viral antagonistic mechanisms might provide a new theoretical basis for understanding the pathogenic mechanism of animal viruses and developing LAVs based on antagonistic mechanisms and viral virulence factors.
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spelling doaj-art-558fc4278b7d44a2a42a37c297fc101f2025-01-24T13:51:46ZengMDPI AGVaccines2076-393X2025-01-011314610.3390/vaccines13010046The Strategies Used by Animal Viruses to Antagonize Host Antiviral Innate Immunity: New Clues for Developing Live Attenuated Vaccines (LAVs)Na Chen0Baoge Zhang1MOE Joint International Research Laboratory of Animal Health and Food Safety, Engineering Laboratory of Animal Immunity of Jiangsu Province, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, ChinaCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, ChinaAs an essential type of vaccine, live attenuated vaccines (LAVs) play a crucial role in animal disease prevention and control. Nevertheless, developing LAVs faces the challenge of balancing safety and efficacy. Understanding the mechanisms animal viruses use to antagonize host antiviral innate immunity may help to precisely regulate vaccine strains and maintain strong immunogenicity while reducing their pathogenicity. It may improve the safety and efficacy of LAVs, as well as provide a more reliable means for the prevention and control of infectious livestock diseases. Therefore, exploring viral antagonistic mechanisms is a significant clue for developing LAVs, which helps to explore more viral virulence factors (as new vaccine targets) and provides a vital theoretical basis and technical support for vaccine development. Among animal viruses, ASFV, PRRSV, PRV, CSFV, FMDV, PCV, PPV, and AIV are some typical representatives. It is crucial to conduct in-depth research and summarize the antagonistic strategies of these typical animal viruses. Studies have indicated that animal viruses may antagonize the antiviral innate immunity by directly or indirectly blocking the antiviral signaling pathways. In addition, viruses also do this by antagonizing host restriction factors targeting the viral replication cycle. Beyond that, viruses may antagonize via regulating apoptosis, metabolic pathways, and stress granule formation. A summary of viral antagonistic mechanisms might provide a new theoretical basis for understanding the pathogenic mechanism of animal viruses and developing LAVs based on antagonistic mechanisms and viral virulence factors.https://www.mdpi.com/2076-393X/13/1/46animal virusesantagonismhost antiviral innate immunityinterferon productioninterferon responsespathogenicity
spellingShingle Na Chen
Baoge Zhang
The Strategies Used by Animal Viruses to Antagonize Host Antiviral Innate Immunity: New Clues for Developing Live Attenuated Vaccines (LAVs)
Vaccines
animal viruses
antagonism
host antiviral innate immunity
interferon production
interferon responses
pathogenicity
title The Strategies Used by Animal Viruses to Antagonize Host Antiviral Innate Immunity: New Clues for Developing Live Attenuated Vaccines (LAVs)
title_full The Strategies Used by Animal Viruses to Antagonize Host Antiviral Innate Immunity: New Clues for Developing Live Attenuated Vaccines (LAVs)
title_fullStr The Strategies Used by Animal Viruses to Antagonize Host Antiviral Innate Immunity: New Clues for Developing Live Attenuated Vaccines (LAVs)
title_full_unstemmed The Strategies Used by Animal Viruses to Antagonize Host Antiviral Innate Immunity: New Clues for Developing Live Attenuated Vaccines (LAVs)
title_short The Strategies Used by Animal Viruses to Antagonize Host Antiviral Innate Immunity: New Clues for Developing Live Attenuated Vaccines (LAVs)
title_sort strategies used by animal viruses to antagonize host antiviral innate immunity new clues for developing live attenuated vaccines lavs
topic animal viruses
antagonism
host antiviral innate immunity
interferon production
interferon responses
pathogenicity
url https://www.mdpi.com/2076-393X/13/1/46
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