Leader (L) and L* proteins of Theiler's murine encephalomyelitis virus (TMEV) and their regulation of the virus' biological activities
<p>Abstract</p> <p>Theiler's murine encephalomyelitis virus (TMEV) is divided into two subgroups on the basis of their different biological activities. GDVII subgroup strains produce fatal poliomyelitis in mice without virus persistence or demyelination. In contrast, TO subgro...
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Format: | Article |
Language: | English |
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BMC
2006-08-01
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Series: | Journal of Neuroinflammation |
Online Access: | http://www.jneuroinflammation.com/content/3/1/19 |
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author | Asakura Kunihiko Ohara Yoshiro Takano-Maruyama Masumi Okuwa Takako |
author_facet | Asakura Kunihiko Ohara Yoshiro Takano-Maruyama Masumi Okuwa Takako |
author_sort | Asakura Kunihiko |
collection | DOAJ |
description | <p>Abstract</p> <p>Theiler's murine encephalomyelitis virus (TMEV) is divided into two subgroups on the basis of their different biological activities. GDVII subgroup strains produce fatal poliomyelitis in mice without virus persistence or demyelination. In contrast, TO subgroup strains induce demyelinating disease with virus persistence in the spinal cords of weanling mice. Two proteins, whose open reading frames are located in the N-terminus of the polyprotein, recently have been reported to be important for TMEV biological activities. One is leader (L) protein and is processed from the most N-terminus of the polyprotein; its function is still unknown. Although the homology of capsid proteins between DA (a representative strain of TO subgroup) and GDVII strains is over 94% at the amino acid level, that of L shows only 85%. Therefore, L is thought to be a key protein for the subgroup-specific biological activities of TMEV. Various studies have demonstrated that L plays important roles in the escape of virus from host immune defenses in the early stage of infection. The second protein is a 17–18 kDa protein, L*, which is synthesized out-of-frame with the polyprotein. Only TO subgroup strains produce L* since GDVII subgroup strains have an ACG rather than AUG at the initiation site and therefore do not synthesize L*. 'Loss and gain of function' experiments demonstrate that L* is essential for virus growth in macrophages, a target cell for TMEV persistence. L* also has been demonstrated to be necessary for TMEV persistence and demyelination. Further analysis of L and L* will help elucidate the pathomechanism(s) of TMEV-induced demyelinating disease.</p> |
first_indexed | 2024-12-11T03:37:02Z |
format | Article |
id | doaj.art-c3738bdbf48240f483b384a9151c826d |
institution | Directory Open Access Journal |
issn | 1742-2094 |
language | English |
last_indexed | 2024-12-11T03:37:02Z |
publishDate | 2006-08-01 |
publisher | BMC |
record_format | Article |
series | Journal of Neuroinflammation |
spelling | doaj.art-c3738bdbf48240f483b384a9151c826d2022-12-22T01:22:14ZengBMCJournal of Neuroinflammation1742-20942006-08-01311910.1186/1742-2094-3-19Leader (L) and L* proteins of Theiler's murine encephalomyelitis virus (TMEV) and their regulation of the virus' biological activitiesAsakura KunihikoOhara YoshiroTakano-Maruyama MasumiOkuwa Takako<p>Abstract</p> <p>Theiler's murine encephalomyelitis virus (TMEV) is divided into two subgroups on the basis of their different biological activities. GDVII subgroup strains produce fatal poliomyelitis in mice without virus persistence or demyelination. In contrast, TO subgroup strains induce demyelinating disease with virus persistence in the spinal cords of weanling mice. Two proteins, whose open reading frames are located in the N-terminus of the polyprotein, recently have been reported to be important for TMEV biological activities. One is leader (L) protein and is processed from the most N-terminus of the polyprotein; its function is still unknown. Although the homology of capsid proteins between DA (a representative strain of TO subgroup) and GDVII strains is over 94% at the amino acid level, that of L shows only 85%. Therefore, L is thought to be a key protein for the subgroup-specific biological activities of TMEV. Various studies have demonstrated that L plays important roles in the escape of virus from host immune defenses in the early stage of infection. The second protein is a 17–18 kDa protein, L*, which is synthesized out-of-frame with the polyprotein. Only TO subgroup strains produce L* since GDVII subgroup strains have an ACG rather than AUG at the initiation site and therefore do not synthesize L*. 'Loss and gain of function' experiments demonstrate that L* is essential for virus growth in macrophages, a target cell for TMEV persistence. L* also has been demonstrated to be necessary for TMEV persistence and demyelination. Further analysis of L and L* will help elucidate the pathomechanism(s) of TMEV-induced demyelinating disease.</p>http://www.jneuroinflammation.com/content/3/1/19 |
spellingShingle | Asakura Kunihiko Ohara Yoshiro Takano-Maruyama Masumi Okuwa Takako Leader (L) and L* proteins of Theiler's murine encephalomyelitis virus (TMEV) and their regulation of the virus' biological activities Journal of Neuroinflammation |
title | Leader (L) and L* proteins of Theiler's murine encephalomyelitis virus (TMEV) and their regulation of the virus' biological activities |
title_full | Leader (L) and L* proteins of Theiler's murine encephalomyelitis virus (TMEV) and their regulation of the virus' biological activities |
title_fullStr | Leader (L) and L* proteins of Theiler's murine encephalomyelitis virus (TMEV) and their regulation of the virus' biological activities |
title_full_unstemmed | Leader (L) and L* proteins of Theiler's murine encephalomyelitis virus (TMEV) and their regulation of the virus' biological activities |
title_short | Leader (L) and L* proteins of Theiler's murine encephalomyelitis virus (TMEV) and their regulation of the virus' biological activities |
title_sort | leader l and l proteins of theiler s murine encephalomyelitis virus tmev and their regulation of the virus biological activities |
url | http://www.jneuroinflammation.com/content/3/1/19 |
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