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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ftdoajarticles:oai:doaj.org/article:793cede7f772419597bf79a97fef9bde 2023-05-15T16:51:14+02:00 Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis Humberto A. Martínez Ramsés Reina Beatriz Amorena Damián de Andrés Hugo Ramírez 2013-04-01T00:00:00Z https://doi.org/10.3390/v5041175 https://doaj.org/article/793cede7f772419597bf79a97fef9bde EN eng MDPI AG http://www.mdpi.com/1999-4915/5/4/1175 https://doaj.org/toc/1999-4915 doi:10.3390/v5041175 1999-4915 https://doaj.org/article/793cede7f772419597bf79a97fef9bde Viruses, Vol 5, Iss 4, Pp 1175-1207 (2013) SRLV CAEV VMV genetic variability tropism diagnosis Microbiology QR1-502 article 2013 ftdoajarticles https://doi.org/10.3390/v5041175 2022-12-31T13:01:24Z 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. Article in Journal/Newspaper Iceland Directory of Open Access Journals: DOAJ Articles Viruses 5 4 1175 1207 |
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Directory of Open Access Journals: DOAJ Articles |
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ftdoajarticles |
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English |
topic |
SRLV CAEV VMV genetic variability tropism diagnosis Microbiology QR1-502 |
spellingShingle |
SRLV CAEV VMV genetic variability tropism diagnosis Microbiology QR1-502 Humberto A. Martínez Ramsés Reina Beatriz Amorena Damián de Andrés Hugo Ramírez Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis |
topic_facet |
SRLV CAEV VMV genetic variability tropism diagnosis Microbiology QR1-502 |
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 |
Article in Journal/Newspaper |
author |
Humberto A. Martínez Ramsés Reina Beatriz Amorena Damián de Andrés Hugo Ramírez |
author_facet |
Humberto A. Martínez Ramsés Reina Beatriz Amorena Damián de Andrés Hugo Ramírez |
author_sort |
Humberto A. Martínez |
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 |
MDPI AG |
publishDate |
2013 |
url |
https://doi.org/10.3390/v5041175 https://doaj.org/article/793cede7f772419597bf79a97fef9bde |
genre |
Iceland |
genre_facet |
Iceland |
op_source |
Viruses, Vol 5, Iss 4, Pp 1175-1207 (2013) |
op_relation |
http://www.mdpi.com/1999-4915/5/4/1175 https://doaj.org/toc/1999-4915 doi:10.3390/v5041175 1999-4915 https://doaj.org/article/793cede7f772419597bf79a97fef9bde |
op_doi |
https://doi.org/10.3390/v5041175 |
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1175 |
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1207 |
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