Fine-tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis A virus capsid.
Hepatitis A virus (HAV), the prototype of genus Hepatovirus, has several unique biological characteristics that distinguish it from other members of the Picornaviridae family. Among these, the need for an intact eIF4G factor for the initiation of translation results in an inability to shut down host...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2010-03-01
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| Series: | PLoS Pathogens |
| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20221432/?tool=EBI |
| _version_ | 1819045067135909888 |
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| author | Lluís Aragonès Susana Guix Enric Ribes Albert Bosch Rosa M Pintó |
| author_facet | Lluís Aragonès Susana Guix Enric Ribes Albert Bosch Rosa M Pintó |
| author_sort | Lluís Aragonès |
| collection | DOAJ |
| description | Hepatitis A virus (HAV), the prototype of genus Hepatovirus, has several unique biological characteristics that distinguish it from other members of the Picornaviridae family. Among these, the need for an intact eIF4G factor for the initiation of translation results in an inability to shut down host protein synthesis by a mechanism similar to that of other picornaviruses. Consequently, HAV must inefficiently compete for the cellular translational machinery and this may explain its poor growth in cell culture. In this context of virus/cell competition, HAV has strategically adopted a naturally highly deoptimized codon usage with respect to that of its cellular host. With the aim to optimize its codon usage the virus was adapted to propagate in cells with impaired protein synthesis, in order to make tRNA pools more available for the virus. A significant loss of fitness was the immediate response to the adaptation process that was, however, later on recovered and more associated to a re-deoptimization rather than to an optimization of the codon usage specifically in the capsid coding region. These results exclude translation selection and instead suggest fine-tuning translation kinetics selection as the underlying mechanism of the codon usage bias in this specific genome region. Additionally, the results provide clear evidence of the Red Queen dynamics of evolution since the virus has very much evolved to re-adapt its codon usage to the environmental cellular changing conditions in order to recover the original fitness. |
| first_indexed | 2024-12-21T10:22:40Z |
| format | Article |
| id | doaj.art-9a981881a2af4a8f90fcb3e589abe109 |
| institution | Directory Open Access Journal |
| issn | 1553-7366 1553-7374 |
| language | English |
| last_indexed | 2024-12-21T10:22:40Z |
| publishDate | 2010-03-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS Pathogens |
| spelling | doaj.art-9a981881a2af4a8f90fcb3e589abe1092022-12-21T19:07:23ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742010-03-0163e100079710.1371/journal.ppat.1000797Fine-tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis A virus capsid.Lluís AragonèsSusana GuixEnric RibesAlbert BoschRosa M PintóHepatitis A virus (HAV), the prototype of genus Hepatovirus, has several unique biological characteristics that distinguish it from other members of the Picornaviridae family. Among these, the need for an intact eIF4G factor for the initiation of translation results in an inability to shut down host protein synthesis by a mechanism similar to that of other picornaviruses. Consequently, HAV must inefficiently compete for the cellular translational machinery and this may explain its poor growth in cell culture. In this context of virus/cell competition, HAV has strategically adopted a naturally highly deoptimized codon usage with respect to that of its cellular host. With the aim to optimize its codon usage the virus was adapted to propagate in cells with impaired protein synthesis, in order to make tRNA pools more available for the virus. A significant loss of fitness was the immediate response to the adaptation process that was, however, later on recovered and more associated to a re-deoptimization rather than to an optimization of the codon usage specifically in the capsid coding region. These results exclude translation selection and instead suggest fine-tuning translation kinetics selection as the underlying mechanism of the codon usage bias in this specific genome region. Additionally, the results provide clear evidence of the Red Queen dynamics of evolution since the virus has very much evolved to re-adapt its codon usage to the environmental cellular changing conditions in order to recover the original fitness.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20221432/?tool=EBI |
| spellingShingle | Lluís Aragonès Susana Guix Enric Ribes Albert Bosch Rosa M Pintó Fine-tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis A virus capsid. PLoS Pathogens |
| title | Fine-tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis A virus capsid. |
| title_full | Fine-tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis A virus capsid. |
| title_fullStr | Fine-tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis A virus capsid. |
| title_full_unstemmed | Fine-tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis A virus capsid. |
| title_short | Fine-tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis A virus capsid. |
| title_sort | fine tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis a virus capsid |
| url | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20221432/?tool=EBI |
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