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...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2013-04-01
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| Series: | Viruses |
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| Online Access: | http://www.mdpi.com/1999-4915/5/4/1175 |
| _version_ | 1819125883601944576 |
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| 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 |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-12-22T07:47:13Z |
| format | Article |
| id | doaj.art-793cede7f772419597bf79a97fef9bde |
| institution | Directory Open Access Journal |
| issn | 1999-4915 |
| language | English |
| last_indexed | 2024-12-22T07:47:13Z |
| publishDate | 2013-04-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj.art-793cede7f772419597bf79a97fef9bde2022-12-21T18:33:36ZengMDPI AGViruses1999-49152013-04-01541175120710.3390/v5041175Small Ruminant Lentiviruses: Genetic Variability, Tropism and DiagnosisHumberto A. MartínezRamsés ReinaBeatriz AmorenaDamián de AndrésHugo RamírezSmall 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.http://www.mdpi.com/1999-4915/5/4/1175SRLVCAEVVMVgenetic variabilitytropismdiagnosis |
| spellingShingle | Humberto A. Martínez Ramsés Reina Beatriz Amorena Damián de Andrés Hugo Ramírez Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis Viruses SRLV CAEV VMV genetic variability tropism 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 | SRLV CAEV VMV genetic variability tropism diagnosis |
| url | http://www.mdpi.com/1999-4915/5/4/1175 |
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