Abstract
The infection of a cell by a virus elicits a Cytotoxic T Lymphocyte (CTL) response to viral peptides presented by the Major Histocompatibility Complex class I molecules [6, 20]. Such a CTL response plays a critical role in the host's anti-viral immune response [39]. This role is suggested by studies indicating a drop of viral loads and the relief of the acute infection symptoms following the emergence of virus-specific CTLs [8], as well as by data from CTL depleted animal models [33, 41]. The CTL response is also associated with a rapid selection of viral CTL escape variants [23, 34]. In the last few years we have applied an immunomic methodology combining genomic data and multiple bioinformatic tools to study the anti-viral CTL response [5, 19, 28, 35, 38, 55–57] and found that viruses selectively mutate proteins inducing the highest danger to their survival. We here summarize these results, and propose some general conclusions regarding the selective forces affecting viruses and their human host.
| Original language | American English |
|---|---|
| Title of host publication | Mathematical Methods and Models in Biomedicine |
| Editors | Urszula LedzewiczHeinz, Heinz Schättler, Avner Friedman, Eugene Kashdan |
| Place of Publication | New York |
| Publisher | Springer |
| Pages | 59-83 |
| Number of pages | 25 |
| ISBN (Print) | 978-1-4614-4177-9 |
| State | Published - 2012 |
Publication series
| Name | Lecture Notes on Mathematical Modelling in the Life Sciences |
|---|
Bibliographical note
AbstractThe infection of a cell by a virus elicits a Cytotoxic T Lymphocyte (CTL) response to viral peptides presented by the Major Histocompatibility Complex class I molecules [6, 20]. Such a CTL response plays a critical role in the host's anti-viral immune response [39]. This role is suggested by studies indicating a drop of viral loads and the relief of the acute infection symptoms following the emergence of virus-specific CTLs [8], as well as by data from CTL depleted animal models [33, 41]. The CTL response is also associated with a rapid selection of viral CTL escape variants [23, 34]. In the last few years we have applied an immunomic methodology combining genomic data and multiple bioinformatic tools to study the anti-viral CTL response [5, 19, 28, 35, 38, 55–57] and found that viruses selectively mutate proteins inducing the highest danger to their survival. We here summarize these results, and propose some general conclusions regarding the selective forces affecting viruses and their human host.