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Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis
Small ruminant lentiviruses (SRLV) cause a multisystemic chronic disease affecting animal production and welfare. SRLV infections are spread across the world with the exception of Iceland. Success in controlling SRLV spread depends largely on the use of appropriate diagnostic tools, but the existenc...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705272/ https://www.ncbi.nlm.nih.gov/pubmed/23611847 http://dx.doi.org/10.3390/v5041175 |
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author | Ramírez, Hugo Reina, Ramsés Amorena, Beatriz de Andrés, Damián Martínez, Humberto A. |
author_facet | Ramírez, Hugo Reina, Ramsés Amorena, Beatriz de Andrés, Damián Martínez, Humberto A. |
author_sort | Ramírez, Hugo |
collection | PubMed |
description | Small ruminant lentiviruses (SRLV) cause a multisystemic chronic disease affecting animal production and welfare. SRLV infections are spread across the world with the exception of Iceland. Success in controlling SRLV spread depends largely on the use of appropriate diagnostic tools, but the existence of a high genetic/antigenic variability among these viruses, the fluctuant levels of antibody against them and the low viral loads found in infected individuals hamper the diagnostic efficacy. SRLV have a marked in vivo tropism towards the monocyte/macrophage lineage and attempts have been made to identify the genome regions involved in tropism, with two main candidates, the LTR and env gene, since LTR contains primer binding sites for viral replication and the env-encoded protein (SU ENV), which mediates the binding of the virus to the host’s cell and has hypervariable regions to escape the humoral immune response. Once inside the host cell, innate immunity may interfere with SRLV replication, but the virus develops counteraction mechanisms to escape, multiply and survive, creating a quasi-species and undergoing compartmentalization events. So far, the mechanisms of organ tropism involved in the development of different disease forms (neurological, arthritic, pulmonary and mammary) are unknown, but different alternatives are proposed. This is an overview of the current state of knowledge on SRLV genetic variability and its implications in tropism as well as in the development of alternative diagnostic assays. |
format | Online Article Text |
id | pubmed-3705272 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-37052722013-07-09 Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis Ramírez, Hugo Reina, Ramsés Amorena, Beatriz de Andrés, Damián Martínez, Humberto A. Viruses Review Small ruminant lentiviruses (SRLV) cause a multisystemic chronic disease affecting animal production and welfare. SRLV infections are spread across the world with the exception of Iceland. Success in controlling SRLV spread depends largely on the use of appropriate diagnostic tools, but the existence of a high genetic/antigenic variability among these viruses, the fluctuant levels of antibody against them and the low viral loads found in infected individuals hamper the diagnostic efficacy. SRLV have a marked in vivo tropism towards the monocyte/macrophage lineage and attempts have been made to identify the genome regions involved in tropism, with two main candidates, the LTR and env gene, since LTR contains primer binding sites for viral replication and the env-encoded protein (SU ENV), which mediates the binding of the virus to the host’s cell and has hypervariable regions to escape the humoral immune response. Once inside the host cell, innate immunity may interfere with SRLV replication, but the virus develops counteraction mechanisms to escape, multiply and survive, creating a quasi-species and undergoing compartmentalization events. So far, the mechanisms of organ tropism involved in the development of different disease forms (neurological, arthritic, pulmonary and mammary) are unknown, but different alternatives are proposed. This is an overview of the current state of knowledge on SRLV genetic variability and its implications in tropism as well as in the development of alternative diagnostic assays. MDPI 2013-04-23 /pmc/articles/PMC3705272/ /pubmed/23611847 http://dx.doi.org/10.3390/v5041175 Text en © 2013 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Review Ramírez, Hugo Reina, Ramsés Amorena, Beatriz de Andrés, Damián Martínez, Humberto A. Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis |
title | Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis |
title_full | Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis |
title_fullStr | Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis |
title_full_unstemmed | Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis |
title_short | Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis |
title_sort | small ruminant lentiviruses: genetic variability, tropism and diagnosis |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705272/ https://www.ncbi.nlm.nih.gov/pubmed/23611847 http://dx.doi.org/10.3390/v5041175 |
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