Why do Individuals Differ in Viral Susceptibility? A Story Told by Model Organisms
Viral susceptibility and disease progression is determined by host genetic variation that underlies individual differences. Genetic polymorphisms that affect the phenotype upon infection have been well-studied for only a few viruses, such as HIV-1 and Hepatitis C virus. However, even for well-studie...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2017-09-01
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| Series: | Viruses |
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| Online Access: | https://www.mdpi.com/1999-4915/9/10/284 |
| _version_ | 1818307582903713792 |
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| author | Lisa van Sluijs Gorben P. Pijlman Jan E. Kammenga |
| author_facet | Lisa van Sluijs Gorben P. Pijlman Jan E. Kammenga |
| author_sort | Lisa van Sluijs |
| collection | DOAJ |
| description | Viral susceptibility and disease progression is determined by host genetic variation that underlies individual differences. Genetic polymorphisms that affect the phenotype upon infection have been well-studied for only a few viruses, such as HIV-1 and Hepatitis C virus. However, even for well-studied viruses the genetic basis of individual susceptibility differences remains elusive. Investigating the effect of causal polymorphisms in humans is complicated, because genetic methods to detect rare or small-effect polymorphisms are limited and genetic manipulation is not possible in human populations. Model organisms have proven a powerful experimental platform to identify and characterize polymorphisms that underlie natural variations in viral susceptibility using quantitative genetic tools. We summarize and compare the genetic tools available in three main model organisms, Mus musculus, Drosophila melanogaster, and Caenorhabditis elegans, and illustrate how these tools can be applied to detect polymorphisms that determine the viral susceptibility. Finally, we analyse how candidate polymorphisms from model organisms can be used to shed light on the underlying mechanism of individual variation. Insights in causal polymorphisms and mechanisms underlying individual differences in viral susceptibility in model organisms likely provide a better understanding in humans. |
| first_indexed | 2024-12-13T07:00:41Z |
| format | Article |
| id | doaj.art-a125cc62caad404bb40d72632d893eab |
| institution | Directory Open Access Journal |
| issn | 1999-4915 |
| language | English |
| last_indexed | 2024-12-13T07:00:41Z |
| publishDate | 2017-09-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj.art-a125cc62caad404bb40d72632d893eab2022-12-21T23:55:56ZengMDPI AGViruses1999-49152017-09-0191028410.3390/v9100284v9100284Why do Individuals Differ in Viral Susceptibility? A Story Told by Model OrganismsLisa van Sluijs0Gorben P. Pijlman1Jan E. Kammenga2Laboratory of Nematology, Wageningen University, 6708 PB Wageningen, The NetherlandsLaboratory of Virology, Wageningen University, 6708 PB Wageningen, The NetherlandsLaboratory of Nematology, Wageningen University, 6708 PB Wageningen, The NetherlandsViral susceptibility and disease progression is determined by host genetic variation that underlies individual differences. Genetic polymorphisms that affect the phenotype upon infection have been well-studied for only a few viruses, such as HIV-1 and Hepatitis C virus. However, even for well-studied viruses the genetic basis of individual susceptibility differences remains elusive. Investigating the effect of causal polymorphisms in humans is complicated, because genetic methods to detect rare or small-effect polymorphisms are limited and genetic manipulation is not possible in human populations. Model organisms have proven a powerful experimental platform to identify and characterize polymorphisms that underlie natural variations in viral susceptibility using quantitative genetic tools. We summarize and compare the genetic tools available in three main model organisms, Mus musculus, Drosophila melanogaster, and Caenorhabditis elegans, and illustrate how these tools can be applied to detect polymorphisms that determine the viral susceptibility. Finally, we analyse how candidate polymorphisms from model organisms can be used to shed light on the underlying mechanism of individual variation. Insights in causal polymorphisms and mechanisms underlying individual differences in viral susceptibility in model organisms likely provide a better understanding in humans.https://www.mdpi.com/1999-4915/9/10/284model organismsgenetic variationviral susceptibilityGWASQTLinbred populations |
| spellingShingle | Lisa van Sluijs Gorben P. Pijlman Jan E. Kammenga Why do Individuals Differ in Viral Susceptibility? A Story Told by Model Organisms Viruses model organisms genetic variation viral susceptibility GWAS QTL inbred populations |
| title | Why do Individuals Differ in Viral Susceptibility? A Story Told by Model Organisms |
| title_full | Why do Individuals Differ in Viral Susceptibility? A Story Told by Model Organisms |
| title_fullStr | Why do Individuals Differ in Viral Susceptibility? A Story Told by Model Organisms |
| title_full_unstemmed | Why do Individuals Differ in Viral Susceptibility? A Story Told by Model Organisms |
| title_short | Why do Individuals Differ in Viral Susceptibility? A Story Told by Model Organisms |
| title_sort | why do individuals differ in viral susceptibility a story told by model organisms |
| topic | model organisms genetic variation viral susceptibility GWAS QTL inbred populations |
| url | https://www.mdpi.com/1999-4915/9/10/284 |
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