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The Indian leafwing butterfly Kallima paralekta (Horsfield, 1829) (Nymphalidae) is an Asian forest-dwelling, leaf-mimic. Genome skimming by Illumina sequencing permitted assembly of a complete circular mitogenome of 15,200 bp from K. paralekta consisting of 79.5% AT nucleotides, 22 tRNAs, 13 protein-coding genes, two rRNAs and a control region in the typical butterfly gene order. Kallima paralekta COX1 features an atypical CGA start codon, while ATP6, COX1, COX2 , ND4 , ND4L, and ND5 exhibit incomplete stop codons completed by 3' A residues added to the mRNA. Phylogenetic reconstruction places K. paraleckta within the monophyletic genus Kallima , sister to Mallika in the subfamily Nymphalinae. These data support the monophyly of tribe Kallimini and contribute to the evolutionary systematics of the Nymphalidae., Competing Interests: No potential conflict of interest was reported by the author(s)., (© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.)

Influenza viruses are a continual public health concern resulting in 3-5 million severe infections annually despite intense vaccination campaigns and messaging. Secondary bacterial infections, including Staphylococcus aureus , result in increased morbidity and mortality during seasonal epidemics and pandemics. While coinfections can result in deleterious pathologic consequences, including alveolar-capillary barrier disruption, the underlying mechanisms are poorly understood. We have characterized host- and pathogen-centric mechanisms contributing to influenza-bacterial coinfections in a primary cell coculture model of the alveolar-capillary barrier. Using 2009 pandemic influenza (pH1N1) and methicillin-resistant S. aureus (MRSA), we demonstrate that coinfection resulted in dysregulated barrier function. Preinfection with pH1N1 resulted in modulation of adhesion- and invasion-associated MRSA virulence factors during lag phase bacterial replication. Host response modulation in coinfected alveolar epithelial cells were primarily related to TLR- and inflammatory response-mediated cell signaling events. While less extensive in cocultured endothelial cells, coinfection resulted in changes to cellular stress response- and TLR-related signaling events. Analysis of cytokine expression suggested that cytokine secretion might play an important role in coinfection pathogenesis. Taken together, we demonstrate that coinfection pathogenesis is related to complex host- and pathogen-mediated events impacting both epithelial and endothelial cell regulation at the alveolar-capillary barrier.