Abstract

The current COVID-19 pandemic creates the biggest health and economic challenges to the world. However, not much knowledge is available about this coronavirus, SARS-CoV-2, because of its novelty. Indeed, it necessarily knows the fate of proteins generated by SARS-CoV-2. Anyway, before a large-scale study on proteins from SARS-CoV-2, it would be better to conduct a small-scale study on a well-known protein from influenza A viruses, because both are positive-sense RNA viruses. Thus, we applied a simple method of amino-acid pair probability to analyze 94 neuraminidases of influenza A viruses for better understanding of their fate. The results demonstrate three features of these neuraminidases: (i) the N1 neuraminidases are more susceptible to mutations, which is the current state of the neuraminidases; (ii) the N1 neuraminidases have undergone more mutations in the past, which is the history of the neuraminidases; and (iii) the N1 neuraminidases have a larger potential towards future mutations, which is the future of the neuraminidases. Moreover, our study reveals two clues on the mutation tendency, i.e. the mutations represent a degeneration process, and chickens, ducks and geese are rendered more susceptive to mutation. We hope to apply this approach to study the proteins from SARS-CoV-2 in near future.

Highlights

  • Influenza A viruses have led several pandemics in humans and animals [1]

  • The results demonstrate three features of these neuraminidases: (i) the N1 neuraminidases are more susceptible to mutations, which is the current state of the neuraminidases; (ii) the N1 neuraminidases have undergone more mutations in the past, which is the history of the neuraminidases; and (iii) the N1 neuraminidases have a larger potential towards future mutations, which is the future of the neuraminidases

  • We hope to apply this approach to study the proteins from SARS-CoV-2 in near future

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Summary

Introduction

Influenza A viruses have led several pandemics in humans and animals [1]. The most famous pandemic is the Spanish flu, which led to a great loss of life and devastating impact on world economy before the ending of World War I [2, 3]. The huge genetic variability exists in the influenza A viruses, either by continuous and gradual mutation or by reassortment of gene segments between viruses, or both [3, 11]. Regarding the host-mediated variation of influenza A viruses, it has been so far proposed, at least, two mechanisms. The first mechanism focuses on the pressure of the antibody whereas the second mechanism emphases the selective pressure for the appearance of host cell variant with altered receptor binding specificities [18]

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