Abstract

We studied the molecular evolution of the capsid gene in all genotypes (genotypes 1–9) of human norovirus (NoV) genogroup I. The evolutionary time scale and rate were estimated by the Bayesian Markov chain Monte Carlo (MCMC) method. We also performed selective pressure analysis and B-cell linear epitope prediction in the deduced NoV GI capsid protein. Furthermore, we analysed the effective population size of the virus using Bayesian skyline plot (BSP) analysis. A phylogenetic tree by MCMC showed that NoV GI diverged from the common ancestor of NoV GII, GIII, and GIV approximately 2,800 years ago with rapid evolution (about 10−3 substitutions/site/year). Some positive selection sites and over 400 negative selection sites were estimated in the deduced capsid protein. Many epitopes were estimated in the deduced virus capsid proteins. An epitope of GI.1 may be associated with histo-blood group antigen binding sites (Ser377, Pro378, and Ser380). Moreover, BSP suggested that the adaptation of NoV GI strains to humans was affected by natural selection. The results suggested that NoV GI strains evolved rapidly and date back to many years ago. Additionally, the virus may have undergone locally affected natural selection in the host resulting in its adaptation to humans.

Highlights

  • IntroductionWe studied the molecular evolution of the capsid gene in all genotypes (genotypes 1–9) of human norovirus (NoV) genogroup I

  • We studied the molecular evolution of the capsid gene in all genotypes of human norovirus (NoV) genogroup I

  • The evolutionary rate of them was significantly different (p < 0 .05, Kruskal-Wallis test). These results suggested that an ancestor NoV GI strain diverged from the ancestor of NoV GII, GIII, and GIV strains and it could be dated back to 1570–4390 years ago, corresponding to 95% highest posterior densities (HPDs) (Fig. 1)

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Summary

Introduction

We studied the molecular evolution of the capsid gene in all genotypes (genotypes 1–9) of human norovirus (NoV) genogroup I. Many epitopes were estimated in the deduced virus capsid proteins. BSP suggested that the adaptation of NoV GI strains to humans was affected by natural selection. NoV shows strong infectivity leading to large epidemics of acute gastroenteritis in various countries including Japan[2,3,4]. The capsid protein may be an essential determinant of the antigenicity of the non-enveloped virus[12]. It plays pivotal roles in viral adsorption/entry and leads to the generation of neutralising antibodies[13,14,15,16]. NoV evolution has been investigated considerably, but most studies have focused on NoV GII17–19

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