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...

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Published in:Viruses
Main Authors: Hugo Ramírez, Ramsés Reina, Beatriz Amorena, Damián Andrés, Humberto Martínez
Format: Text
Language:English
Published: Multidisciplinary Digital Publishing Institute 2013
Subjects:
VMV
Online Access:https://doi.org/10.3390/v5041175
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spelling ftmdpi:oai:mdpi.com:/1999-4915/5/4/1175/ 2023-08-20T04:07:29+02:00 Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis Hugo Ramírez Ramsés Reina Beatriz Amorena Damián Andrés Humberto Martínez agris 2013-04-23 application/pdf https://doi.org/10.3390/v5041175 EN eng Multidisciplinary Digital Publishing Institute https://dx.doi.org/10.3390/v5041175 https://creativecommons.org/licenses/by/3.0/ Viruses; Volume 5; Issue 4; Pages: 1175-1207 SRLV CAEV VMV genetic variability tropism diagnosis Text 2013 ftmdpi https://doi.org/10.3390/v5041175 2023-07-31T20:32:20Z 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. Text Iceland MDPI Open Access Publishing Viruses 5 4 1175 1207
institution Open Polar
collection MDPI Open Access Publishing
op_collection_id ftmdpi
language English
topic SRLV
CAEV
VMV
genetic variability
tropism
diagnosis
spellingShingle SRLV
CAEV
VMV
genetic variability
tropism
diagnosis
Hugo Ramírez
Ramsés Reina
Beatriz Amorena
Damián Andrés
Humberto Martínez
Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis
topic_facet SRLV
CAEV
VMV
genetic variability
tropism
diagnosis
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 Text
author Hugo Ramírez
Ramsés Reina
Beatriz Amorena
Damián Andrés
Humberto Martínez
author_facet Hugo Ramírez
Ramsés Reina
Beatriz Amorena
Damián Andrés
Humberto Martínez
author_sort Hugo Ramírez
title Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis
title_short 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_sort small ruminant lentiviruses: genetic variability, tropism and diagnosis
publisher Multidisciplinary Digital Publishing Institute
publishDate 2013
url https://doi.org/10.3390/v5041175
op_coverage agris
genre Iceland
genre_facet Iceland
op_source Viruses; Volume 5; Issue 4; Pages: 1175-1207
op_relation https://dx.doi.org/10.3390/v5041175
op_rights https://creativecommons.org/licenses/by/3.0/
op_doi https://doi.org/10.3390/v5041175
container_title Viruses
container_volume 5
container_issue 4
container_start_page 1175
op_container_end_page 1207
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