Abstract
The influenza virus continually evolves because of the high mutation rate, resulting in dramatic changes in its pathogenicity and other biological properties. This study aimed to evaluate the evolution of certain essential properties, understand the connections between them, and find the molecular basis for the manifestation of these properties. To that end, 21 A(H1N1)pdm09 influenza viruses were tested for their pathogenicity and toxicity in a mouse model with a ts/non-ts phenotype manifestation and HA thermal stability. The results demonstrated that, for a strain to have high pathogenicity, it must express a toxic effect, have a non-ts phenotype, and have a thermally stable HA. The ancestor A/California/07/2009 (H1N1)pdm influenza virus expressed the non-ts phenotype, after which the cycling trend of the ts/non-ts phenotype was observed in new strains of A(H1N1)pdm09 influenza viruses, indicating that the ratio of the ts phenotype will increase in the coming years. Of the 21 tested viruses, A/South Africa/3626/2013 had the high pathogenicity in the mouse model. Sequence alignment analysis showed that this virus has three unique mutations in the polymerase complex, two of which are in the PB2 gene and one that is in the PB1 gene. Further study of these mutations might explain the distinguishing pathogenicity.
Highlights
The influenza virus is a worldwide disease that affects up to 5–15% of the global population
We focused on the evolution of these characteristics and the contribution of each of these to the viral pathogenicity; we attempted to explain the relationships between the viral properties and determine how they are connected to the evolution of the viral genome
A comparative analysis of modern A(H1N1)pdm09 influenza viruses, according to their essential biological characteristics and how are they associated with changes at the molecular level, was conducted
Summary
The influenza virus is a worldwide disease that affects up to 5–15% of the global population. The mortality from influenza-associated respiratory disease is estimated to be more than half a million each year, and that number significantly increases when a new strain emerges to cause a pandemic [1]. The last pandemic was influenza A(H1N1) in 2009–2010, which is estimated to have caused about 400,000 deaths in 2009 alone [5]. Influenza is an RNA virus that is part of the Orthomyxoviruses family, which is divided into four subfamilies: A, B, C, and D. Influenza A is divided into several subtypes depending on the combination of the hemagglutinin protein (HA), which has 18 subtypes, and the neuraminidase protein (NA), which has 11 subtypes [6]. This study will focus on the evolution of the H1N1pdm pandemic of the virus
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