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Deletion of the L7L-L11L Genes Attenuates ASFV and Induces Protection against Homologous Challenge

African swine fever (ASF), caused by the African swine fever virus (ASFV), is a major epidemic disease endangering the swine industry. Although a number of vaccine candidates have been reported, none are commercially available yet. To explore the effect of unknown genes on the biological characteris...

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Autores principales: Zhang, Jingyuan, Zhang, Yanyan, Chen, Teng, Yang, Jinjin, Yue, Huixian, Wang, Lidong, Zhou, Xintao, Qi, Yu, Han, Xun, Ke, Junnan, Wang, Shuchao, Yang, Jinmei, Miao, Faming, Zhang, Shoufeng, Zhang, Fei, Wang, Ying, Li, Min, Hu, Rongliang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7915138/
https://www.ncbi.nlm.nih.gov/pubmed/33567491
http://dx.doi.org/10.3390/v13020255
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author Zhang, Jingyuan
Zhang, Yanyan
Chen, Teng
Yang, Jinjin
Yue, Huixian
Wang, Lidong
Zhou, Xintao
Qi, Yu
Han, Xun
Ke, Junnan
Wang, Shuchao
Yang, Jinmei
Miao, Faming
Zhang, Shoufeng
Zhang, Fei
Wang, Ying
Li, Min
Hu, Rongliang
author_facet Zhang, Jingyuan
Zhang, Yanyan
Chen, Teng
Yang, Jinjin
Yue, Huixian
Wang, Lidong
Zhou, Xintao
Qi, Yu
Han, Xun
Ke, Junnan
Wang, Shuchao
Yang, Jinmei
Miao, Faming
Zhang, Shoufeng
Zhang, Fei
Wang, Ying
Li, Min
Hu, Rongliang
author_sort Zhang, Jingyuan
collection PubMed
description African swine fever (ASF), caused by the African swine fever virus (ASFV), is a major epidemic disease endangering the swine industry. Although a number of vaccine candidates have been reported, none are commercially available yet. To explore the effect of unknown genes on the biological characteristics of ASFV and the possibility of a gene-deleted isolate as a vaccine candidate, the strain SY18ΔL7-11, with deletions of L7L–L11L genes from ASFV SY18, was constructed, and its biological properties were analyzed. The results show that deletion of genes L7L-L11L did not affect replication of the virus in vitro. Virulence of SY18△L7-11 was significantly reduced, as 11 of the 12 pigs survived for 28 days after intramuscular inoculation with a low dose (10(3) TCID(50)) or a high dose (10(6) TCID(50)) of SY18ΔL7-11. All 11 surviving pigs were completely protected against challenge with the parental ASFV SY18 on 28 days postinoculation (dpi). Transient fever and/or irregularly low levels of genomic DNA in the blood were monitored in some pigs after inoculation. No ASF clinical signs or viremia were monitored after challenge. Antibodies to ASFV were induced in all pigs from 14 to 21 days postinoculation. IFN-γ was detected in most of the inoculated pigs, which is usually inhibited in ASFV-infected pigs. Overall, the results demonstrate that SY18ΔL7-11 is a candidate for further constructing safer vaccine(s), with better joint deletions of other gene(s) related to virulence.
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spelling pubmed-79151382021-03-01 Deletion of the L7L-L11L Genes Attenuates ASFV and Induces Protection against Homologous Challenge Zhang, Jingyuan Zhang, Yanyan Chen, Teng Yang, Jinjin Yue, Huixian Wang, Lidong Zhou, Xintao Qi, Yu Han, Xun Ke, Junnan Wang, Shuchao Yang, Jinmei Miao, Faming Zhang, Shoufeng Zhang, Fei Wang, Ying Li, Min Hu, Rongliang Viruses Article African swine fever (ASF), caused by the African swine fever virus (ASFV), is a major epidemic disease endangering the swine industry. Although a number of vaccine candidates have been reported, none are commercially available yet. To explore the effect of unknown genes on the biological characteristics of ASFV and the possibility of a gene-deleted isolate as a vaccine candidate, the strain SY18ΔL7-11, with deletions of L7L–L11L genes from ASFV SY18, was constructed, and its biological properties were analyzed. The results show that deletion of genes L7L-L11L did not affect replication of the virus in vitro. Virulence of SY18△L7-11 was significantly reduced, as 11 of the 12 pigs survived for 28 days after intramuscular inoculation with a low dose (10(3) TCID(50)) or a high dose (10(6) TCID(50)) of SY18ΔL7-11. All 11 surviving pigs were completely protected against challenge with the parental ASFV SY18 on 28 days postinoculation (dpi). Transient fever and/or irregularly low levels of genomic DNA in the blood were monitored in some pigs after inoculation. No ASF clinical signs or viremia were monitored after challenge. Antibodies to ASFV were induced in all pigs from 14 to 21 days postinoculation. IFN-γ was detected in most of the inoculated pigs, which is usually inhibited in ASFV-infected pigs. Overall, the results demonstrate that SY18ΔL7-11 is a candidate for further constructing safer vaccine(s), with better joint deletions of other gene(s) related to virulence. MDPI 2021-02-08 /pmc/articles/PMC7915138/ /pubmed/33567491 http://dx.doi.org/10.3390/v13020255 Text en © 2021 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Zhang, Jingyuan
Zhang, Yanyan
Chen, Teng
Yang, Jinjin
Yue, Huixian
Wang, Lidong
Zhou, Xintao
Qi, Yu
Han, Xun
Ke, Junnan
Wang, Shuchao
Yang, Jinmei
Miao, Faming
Zhang, Shoufeng
Zhang, Fei
Wang, Ying
Li, Min
Hu, Rongliang
Deletion of the L7L-L11L Genes Attenuates ASFV and Induces Protection against Homologous Challenge
title Deletion of the L7L-L11L Genes Attenuates ASFV and Induces Protection against Homologous Challenge
title_full Deletion of the L7L-L11L Genes Attenuates ASFV and Induces Protection against Homologous Challenge
title_fullStr Deletion of the L7L-L11L Genes Attenuates ASFV and Induces Protection against Homologous Challenge
title_full_unstemmed Deletion of the L7L-L11L Genes Attenuates ASFV and Induces Protection against Homologous Challenge
title_short Deletion of the L7L-L11L Genes Attenuates ASFV and Induces Protection against Homologous Challenge
title_sort deletion of the l7l-l11l genes attenuates asfv and induces protection against homologous challenge
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7915138/
https://www.ncbi.nlm.nih.gov/pubmed/33567491
http://dx.doi.org/10.3390/v13020255
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