Role of the host genetic variability in the influenza A virus susceptibility.

Ana Carolina Arcanjo; Giovanni Mazzocco; Silviene Fabiana de Oliveira; Dariusz Plewczynski; Jan P Radomski

doi:10.18388/abp.2014_1858

Ana Carolina Arcanjo Laboratório de Genética, Departamento de Genética e Morfologia, Instituto de Ciências Biológicas, Universidade de Brasília, Brasília, DF, Brazil.;
Giovanni Mazzocco Interdisciplinary Center for Mathematical and Computational Modeling, Warsaw University, Warsaw, Poland and Institute of Computer Science, Polish Academy of Sciences, Warsaw, Poland.;
Silviene Fabiana de Oliveira Laboratório de Genética, Departamento de Genética e Morfologia, Instituto de Ciências Biológicas, Universidade de Brasília, Brasília, DF, Brazil and The Jackson Laboratory for Genomic Medicine, c/o University of Connecticut Health Center; Farmington, CT USA.;
Dariusz Plewczynski Interdisciplinary Center for Mathematical and Computational Modeling, Warsaw University, Warsaw, Poland; The Jackson Laboratory for Genomic Medicine, c/o University of Connecticut Health Center; Farmington, CT USA; Yale University, New Haven, CT, USA and Center for Innovative Research, Medical University of Bialystok, Poland.;
Jan P Radomski Interdisciplinary Center for Mathematical and Computational Modeling, Warsaw University, Warsaw, Poland and Institute of Biotechnology and Antibiotics, Warsaw, Poland.;

DOI: https://doi.org/10.18388/abp.2014_1858

Abstract

The aftermath of influenza infection is determined by a complex set of host-pathogen interactions, where genomic variability on both viral and host sides influences the final outcome. Although there exists large body of literature describing influenza virus variability, only a very small fraction covers the issue of host variance. The goal of this review is to explore the variability of host genes responsible for host-pathogen interactions, paying particular attention to genes responsible for the presence of sialylated glycans in the host endothelial membrane, mucus, genes used by viral immune escape mechanisms, and genes particularly expressed after vaccination, since they are more likely to have a direct influence on the infection outcome.