The genomic signature of human rhinoviruses A, B and C.

Human rhinoviruses are single stranded positive sense RNA viruses that are presented in more than 50% of acute upper respiratory tract infections. Despite extensive studies on the genetic diversity of the virus, little is known about the forces driving it. In order to explain this diversity, many re...

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Main Authors: Spyridon Megremis, Philippos Demetriou, Heidi Makrinioti, Alkistis E Manoussaki, Nikolaos G Papadopoulos
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS ONE
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23028561/pdf/?tool=EBI
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spelling doaj-dfa6a3e9329d4240870b4d649771265c2021-03-04T00:19:14ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0179e4455710.1371/journal.pone.0044557The genomic signature of human rhinoviruses A, B and C.Spyridon MegremisPhilippos DemetriouHeidi MakriniotiAlkistis E ManoussakiNikolaos G PapadopoulosNikolaos G PapadopoulosHuman rhinoviruses are single stranded positive sense RNA viruses that are presented in more than 50% of acute upper respiratory tract infections. Despite extensive studies on the genetic diversity of the virus, little is known about the forces driving it. In order to explain this diversity, many research groups have focused on protein sequence requirements for viable, functional and transmissible virus but have missed out an important aspect of viral evolution such as the genomic ontology of the virus. This study presents for the first time the genomic signature of 111 fully sequenced HRV strains from all three groups HRV-A, HRV-B and HRV-C. We observed an HRV genome tendency to eliminate CpG and UpA dinucleotides, coupling with over-representation of UpG and CpA. We propose a specific mechanism which describes how rapid changes in the HRV genomic sequence can take place under the strict control of conservation of the polypeptide backbone. Moreover, the distribution of the observed under- and over-represented dinucleotides along the HRV genome is presented. Distance matrice tables based on CpG and UpA odds ratios were constructed and viewed as heatmaps and distance trees. None of the suppressions can be attributed to codon usage or in RNA secondary structure requirements. Since viral recognition is dependent on RNA motifs rich in CpG and UpA, it is possible that the overall described genome evolution mechanism acts in order to protect the virus from host recognition.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23028561/pdf/?tool=EBI
collection DOAJ
language English
format Article
sources DOAJ
author Spyridon Megremis
Philippos Demetriou
Heidi Makrinioti
Alkistis E Manoussaki
Nikolaos G Papadopoulos
Nikolaos G Papadopoulos
spellingShingle Spyridon Megremis
Philippos Demetriou
Heidi Makrinioti
Alkistis E Manoussaki
Nikolaos G Papadopoulos
Nikolaos G Papadopoulos
The genomic signature of human rhinoviruses A, B and C.
PLoS ONE
author_facet Spyridon Megremis
Philippos Demetriou
Heidi Makrinioti
Alkistis E Manoussaki
Nikolaos G Papadopoulos
Nikolaos G Papadopoulos
author_sort Spyridon Megremis
title The genomic signature of human rhinoviruses A, B and C.
title_short The genomic signature of human rhinoviruses A, B and C.
title_full The genomic signature of human rhinoviruses A, B and C.
title_fullStr The genomic signature of human rhinoviruses A, B and C.
title_full_unstemmed The genomic signature of human rhinoviruses A, B and C.
title_sort genomic signature of human rhinoviruses a, b and c.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2012-01-01
description Human rhinoviruses are single stranded positive sense RNA viruses that are presented in more than 50% of acute upper respiratory tract infections. Despite extensive studies on the genetic diversity of the virus, little is known about the forces driving it. In order to explain this diversity, many research groups have focused on protein sequence requirements for viable, functional and transmissible virus but have missed out an important aspect of viral evolution such as the genomic ontology of the virus. This study presents for the first time the genomic signature of 111 fully sequenced HRV strains from all three groups HRV-A, HRV-B and HRV-C. We observed an HRV genome tendency to eliminate CpG and UpA dinucleotides, coupling with over-representation of UpG and CpA. We propose a specific mechanism which describes how rapid changes in the HRV genomic sequence can take place under the strict control of conservation of the polypeptide backbone. Moreover, the distribution of the observed under- and over-represented dinucleotides along the HRV genome is presented. Distance matrice tables based on CpG and UpA odds ratios were constructed and viewed as heatmaps and distance trees. None of the suppressions can be attributed to codon usage or in RNA secondary structure requirements. Since viral recognition is dependent on RNA motifs rich in CpG and UpA, it is possible that the overall described genome evolution mechanism acts in order to protect the virus from host recognition.
url https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23028561/pdf/?tool=EBI
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