Abstract
We present the near complete virus genome sequences with phylogenetic and network analyses of potential transmission networks of a total of 18 Australian cases of human parechovirus type 3 (HPeV3) infection in infants in the period from 2012–2015. Overall the results support our previous finding that the Australian outbreak strain/lineage is a result of a major recombination event that took place between March 2012 and November 2013 followed by further virus evolution and possibly recombination. While the nonstructural coding region of unknown provenance appears to evolve significantly both at the nucleotide and amino acid level, the capsid encoding region derived from the Yamagata 2011 lineage of HPeV3 appears to be very stable, particularly at the amino acid level. The phylogenetic and network analyses performed support a temporal evolution from the first Australian recombinant virus sequence from November 2013 to March/April 2014, onto the 2015 outbreak. The 2015 outbreak samples fall into two separate clusters with a possible common ancestor between March/April 2014 and September 2015, with each cluster further evolving in the period from September to November/December 2015.
Highlights
The picornaviruses are small, single-stranded positive sense RNA viruses causing disease in animals and humans and include the human parechoviruses (HPeV)
HPeV type 1 (HPeV1) and 2 were initially classified as echoviruses 22 and 23 in the genus Enterovirus, but reclassified in 1998/99 into their own genus based on nucleotide and biological features including a lack of host cell protein synthesis shut-off during replication[2,3,4,5,6]
human parechovirus type 3 (HPeV3) appears to cause more severe disease in young infants compared to the other HPeV types and is the most common type identified in cerebrospinal fluid (CSF) samples from young infants with central nervous system (CNS) infection and/or sepsis-like presentation[22]
Summary
Generation sequencing (NGS) was performed on RNA extracted from the clinical samples (Table 1) as well as on available virus isolates. The comparison between clinical samples and corresponding virus isolates served two purposes It further supports the very high accuracy of the NGS generated sequences indicated by comparing different sample types mentioned above. Only indirectly related to our analyses presented here and to our knowledge not reported in the literature, the Yamagata 2011 lineage viruses reported[38,39,40] and deposited in GenBank contain what appear to be two different clusters most likely derived by recombination at approximately nucleotide 5000 (equivalent to nucleotide 4300 in the deposited Yamagata 2011 lineage viruses as they only included the coding regions) These two clusters are represented by GenBank Accession number AB759207 in one of the two clusters and AB759204 and AB759205 in another. We inadvertently based our initial NGS panel on AB7592071 and this particular panel coincidentally resulted in high quality sequence for sample CS-HP-16018 up to approximately nucleotide 5000, consistent with this sample, from March 2012, being of full Yamagata 2011 lineage, but really matched most closely to the AB759204/AB759205
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