Abstract
Influenza A is a significant public health threat, partially because of its capacity to readily exchange gene segments between different host species to form novel pandemic strains. An understanding of the fundamental factors providing species barriers between different influenza hosts would facilitate identification of strains capable of leading to pandemic outbreaks and could also inform vaccine development. Here, we describe the difference in predicted RNA secondary structure stability that exists between avian, swine and human coding regions. The results predict that global ordered RNA structure exists in influenza A segments 1, 5, 7 and 8, and that ranges of free energies for secondary structure formation differ between host strains. The predicted free energy distributions for strains from avian, swine, and human species suggest criteria for segment reassortment and strains that might be ideal candidates for viral attenuation and vaccine development.
Highlights
Influenza A is a (2)sense RNA virus of significant public health concern
Pandemics are believed to arise because the genome consists of eight single-stranded RNA segments that can reassort from multiple host species to form novel strains to which humans have little or no prior immunity [2]
This work demonstrates that Genome-scale Ordered RNA Structure (GORS) exists in (+)RNA segments 1, 5, 7, and 8 of Influenza A virus (Figures 1, 5, 6, and 8)
Summary
Influenza A is a (2)sense RNA virus of significant public health concern. More concerning is the ability of Influenza A to cause pandemics. Pandemics are believed to arise because the genome consists of eight single-stranded RNA segments that can reassort from multiple host species to form novel strains to which humans have little or no prior immunity [2]. The 2009 ‘‘Swine-flu’’ pandemic is thought to involve reassortment of genes from avian, swine, and human strains [3]. Because swine cells have surface glycoproteins that are recognized by both avian and human HA protein, they have been proposed as a ‘‘mixing vessel’’ for reassortment [4,5]. It is believed that there is a natural species barrier largely preventing direct transmission between avian and human strains [6]. Several studies have identified different aspects of influenza A that restrict host replication range [7,8,9,10], but fundamental factors that differentiate host influenza strains are not well defined
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