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Deletion of the H240R Gene in African Swine Fever Virus Partially Reduces Virus Virulence in Swine
African swine fever (ASF) is a highly contagious disease that affects wild and domestic swine. Currently, the disease is present as a pandemic affecting pork production in Eurasia and the Caribbean region. The etiological agent of ASF is a large, highly complex structural virus (ASFV) harboring a do...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10384018/ https://www.ncbi.nlm.nih.gov/pubmed/37515164 http://dx.doi.org/10.3390/v15071477 |
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author | Ramirez-Medina, Elizabeth Rai, Ayushi Espinoza, Nallely Valladares, Alyssa Silva, Ediane Velazquez-Salinas, Lauro Borca, Manuel V. Gladue, Douglas P. |
author_facet | Ramirez-Medina, Elizabeth Rai, Ayushi Espinoza, Nallely Valladares, Alyssa Silva, Ediane Velazquez-Salinas, Lauro Borca, Manuel V. Gladue, Douglas P. |
author_sort | Ramirez-Medina, Elizabeth |
collection | PubMed |
description | African swine fever (ASF) is a highly contagious disease that affects wild and domestic swine. Currently, the disease is present as a pandemic affecting pork production in Eurasia and the Caribbean region. The etiological agent of ASF is a large, highly complex structural virus (ASFV) harboring a double-stranded genome encoding for more than 160 proteins whose functions, in most cases, have not been experimentally characterized. We show here that deletion of the ASFV gene H240R from the genome of the highly virulent ASFV-Georgia2010 (ASFV-G) isolate partially decreases virus virulence when experimentally inoculated in domestic swine. ASFV-G-∆H240R, a recombinant virus harboring the deletion of the H240R gene, was produced to evaluate the function of the gene in the development of disease in pigs. While all animals intramuscularly inoculated with 10(2) HAD(50) of ASFV-G developed a fatal form of the disease, forty percent of pigs receiving a similar dose of ASFV-G-∆H240R survived the infection, remaining healthy during the 28-day observational period, and the remaining sixty percent developed a protracted but fatal form of the disease compared to that induced by ASFV-G. Additionally, all animals inoculated with ASFV-G-∆H240R presented protracted viremias with reduced virus titers when compared with those found in animals inoculated with ASFV-G. Animals surviving infection with ASFV-G-∆H240R developed a strong virus-specific antibody response and were protected against the challenge of the virulent parental ASFV-G. |
format | Online Article Text |
id | pubmed-10384018 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-103840182023-07-30 Deletion of the H240R Gene in African Swine Fever Virus Partially Reduces Virus Virulence in Swine Ramirez-Medina, Elizabeth Rai, Ayushi Espinoza, Nallely Valladares, Alyssa Silva, Ediane Velazquez-Salinas, Lauro Borca, Manuel V. Gladue, Douglas P. Viruses Article African swine fever (ASF) is a highly contagious disease that affects wild and domestic swine. Currently, the disease is present as a pandemic affecting pork production in Eurasia and the Caribbean region. The etiological agent of ASF is a large, highly complex structural virus (ASFV) harboring a double-stranded genome encoding for more than 160 proteins whose functions, in most cases, have not been experimentally characterized. We show here that deletion of the ASFV gene H240R from the genome of the highly virulent ASFV-Georgia2010 (ASFV-G) isolate partially decreases virus virulence when experimentally inoculated in domestic swine. ASFV-G-∆H240R, a recombinant virus harboring the deletion of the H240R gene, was produced to evaluate the function of the gene in the development of disease in pigs. While all animals intramuscularly inoculated with 10(2) HAD(50) of ASFV-G developed a fatal form of the disease, forty percent of pigs receiving a similar dose of ASFV-G-∆H240R survived the infection, remaining healthy during the 28-day observational period, and the remaining sixty percent developed a protracted but fatal form of the disease compared to that induced by ASFV-G. Additionally, all animals inoculated with ASFV-G-∆H240R presented protracted viremias with reduced virus titers when compared with those found in animals inoculated with ASFV-G. Animals surviving infection with ASFV-G-∆H240R developed a strong virus-specific antibody response and were protected against the challenge of the virulent parental ASFV-G. MDPI 2023-06-29 /pmc/articles/PMC10384018/ /pubmed/37515164 http://dx.doi.org/10.3390/v15071477 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Ramirez-Medina, Elizabeth Rai, Ayushi Espinoza, Nallely Valladares, Alyssa Silva, Ediane Velazquez-Salinas, Lauro Borca, Manuel V. Gladue, Douglas P. Deletion of the H240R Gene in African Swine Fever Virus Partially Reduces Virus Virulence in Swine |
title | Deletion of the H240R Gene in African Swine Fever Virus Partially Reduces Virus Virulence in Swine |
title_full | Deletion of the H240R Gene in African Swine Fever Virus Partially Reduces Virus Virulence in Swine |
title_fullStr | Deletion of the H240R Gene in African Swine Fever Virus Partially Reduces Virus Virulence in Swine |
title_full_unstemmed | Deletion of the H240R Gene in African Swine Fever Virus Partially Reduces Virus Virulence in Swine |
title_short | Deletion of the H240R Gene in African Swine Fever Virus Partially Reduces Virus Virulence in Swine |
title_sort | deletion of the h240r gene in african swine fever virus partially reduces virus virulence in swine |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10384018/ https://www.ncbi.nlm.nih.gov/pubmed/37515164 http://dx.doi.org/10.3390/v15071477 |
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