Cargando…
In Vivo Demonstration of the Superior Replication and Infectivity of Genotype 2.1 with Respect to Genotype 3.4 of Classical Swine Fever Virus by Dual Infections
In Taiwan, the prevalent CSFV population has shifted from the historical genotype 3.4 (94.4 strain) to the newly invading genotype 2.1 (TD/96 strain) since 1996. This study analyzed the competition between these two virus genotypes in dual infection pigs with equal and different virus populations an...
Autores principales: | , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7238001/ https://www.ncbi.nlm.nih.gov/pubmed/32260208 http://dx.doi.org/10.3390/pathogens9040261 |
_version_ | 1783536441884672000 |
---|---|
author | Huang, Yu-Liang Tsai, Kuo-Jung Deng, Ming-Chung Liu, Hsin-Meng Huang, Chin-Cheng Wang, Fun-In Chang, Chia-Yi |
author_facet | Huang, Yu-Liang Tsai, Kuo-Jung Deng, Ming-Chung Liu, Hsin-Meng Huang, Chin-Cheng Wang, Fun-In Chang, Chia-Yi |
author_sort | Huang, Yu-Liang |
collection | PubMed |
description | In Taiwan, the prevalent CSFV population has shifted from the historical genotype 3.4 (94.4 strain) to the newly invading genotype 2.1 (TD/96 strain) since 1996. This study analyzed the competition between these two virus genotypes in dual infection pigs with equal and different virus populations and with maternally derived neutralizing antibodies induced by a third genotype of modified live vaccine (MLV), to simulate that occurring in natural situations in the field. Experimentally, under various dual infection conditions, with or without the presence of maternal antibodies, with various specimens from blood, oral and fecal swabs, and internal organs at various time points, the TD/96 had consistently 1.51−3.08 log higher loads than those of 94.4. A second passage of competition in the same animals further widened the lead of TD/96 as indicated by viral loads. The maternally derived antibodies provided partial protection to both wild type CSFVs and was correlated with lower clinical scores, febrile reaction, and animal mortality. In the presence of maternal antibodies, pigs could be infected by both wild type CSFVs, with TD/96 dominating. These findings partially explain the CSFV shift observed, furthering our understanding of CSFV pathogenesis in the field, and are helpful for the control of CSF. |
format | Online Article Text |
id | pubmed-7238001 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-72380012020-05-28 In Vivo Demonstration of the Superior Replication and Infectivity of Genotype 2.1 with Respect to Genotype 3.4 of Classical Swine Fever Virus by Dual Infections Huang, Yu-Liang Tsai, Kuo-Jung Deng, Ming-Chung Liu, Hsin-Meng Huang, Chin-Cheng Wang, Fun-In Chang, Chia-Yi Pathogens Article In Taiwan, the prevalent CSFV population has shifted from the historical genotype 3.4 (94.4 strain) to the newly invading genotype 2.1 (TD/96 strain) since 1996. This study analyzed the competition between these two virus genotypes in dual infection pigs with equal and different virus populations and with maternally derived neutralizing antibodies induced by a third genotype of modified live vaccine (MLV), to simulate that occurring in natural situations in the field. Experimentally, under various dual infection conditions, with or without the presence of maternal antibodies, with various specimens from blood, oral and fecal swabs, and internal organs at various time points, the TD/96 had consistently 1.51−3.08 log higher loads than those of 94.4. A second passage of competition in the same animals further widened the lead of TD/96 as indicated by viral loads. The maternally derived antibodies provided partial protection to both wild type CSFVs and was correlated with lower clinical scores, febrile reaction, and animal mortality. In the presence of maternal antibodies, pigs could be infected by both wild type CSFVs, with TD/96 dominating. These findings partially explain the CSFV shift observed, furthering our understanding of CSFV pathogenesis in the field, and are helpful for the control of CSF. MDPI 2020-04-03 /pmc/articles/PMC7238001/ /pubmed/32260208 http://dx.doi.org/10.3390/pathogens9040261 Text en © 2020 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 Huang, Yu-Liang Tsai, Kuo-Jung Deng, Ming-Chung Liu, Hsin-Meng Huang, Chin-Cheng Wang, Fun-In Chang, Chia-Yi In Vivo Demonstration of the Superior Replication and Infectivity of Genotype 2.1 with Respect to Genotype 3.4 of Classical Swine Fever Virus by Dual Infections |
title | In Vivo Demonstration of the Superior Replication and Infectivity of Genotype 2.1 with Respect to Genotype 3.4 of Classical Swine Fever Virus by Dual Infections |
title_full | In Vivo Demonstration of the Superior Replication and Infectivity of Genotype 2.1 with Respect to Genotype 3.4 of Classical Swine Fever Virus by Dual Infections |
title_fullStr | In Vivo Demonstration of the Superior Replication and Infectivity of Genotype 2.1 with Respect to Genotype 3.4 of Classical Swine Fever Virus by Dual Infections |
title_full_unstemmed | In Vivo Demonstration of the Superior Replication and Infectivity of Genotype 2.1 with Respect to Genotype 3.4 of Classical Swine Fever Virus by Dual Infections |
title_short | In Vivo Demonstration of the Superior Replication and Infectivity of Genotype 2.1 with Respect to Genotype 3.4 of Classical Swine Fever Virus by Dual Infections |
title_sort | in vivo demonstration of the superior replication and infectivity of genotype 2.1 with respect to genotype 3.4 of classical swine fever virus by dual infections |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7238001/ https://www.ncbi.nlm.nih.gov/pubmed/32260208 http://dx.doi.org/10.3390/pathogens9040261 |
work_keys_str_mv | AT huangyuliang invivodemonstrationofthesuperiorreplicationandinfectivityofgenotype21withrespecttogenotype34ofclassicalswinefevervirusbydualinfections AT tsaikuojung invivodemonstrationofthesuperiorreplicationandinfectivityofgenotype21withrespecttogenotype34ofclassicalswinefevervirusbydualinfections AT dengmingchung invivodemonstrationofthesuperiorreplicationandinfectivityofgenotype21withrespecttogenotype34ofclassicalswinefevervirusbydualinfections AT liuhsinmeng invivodemonstrationofthesuperiorreplicationandinfectivityofgenotype21withrespecttogenotype34ofclassicalswinefevervirusbydualinfections AT huangchincheng invivodemonstrationofthesuperiorreplicationandinfectivityofgenotype21withrespecttogenotype34ofclassicalswinefevervirusbydualinfections AT wangfunin invivodemonstrationofthesuperiorreplicationandinfectivityofgenotype21withrespecttogenotype34ofclassicalswinefevervirusbydualinfections AT changchiayi invivodemonstrationofthesuperiorreplicationandinfectivityofgenotype21withrespecttogenotype34ofclassicalswinefevervirusbydualinfections |