Human Anti-Influenza A Virus HA (Ca2 region) monoclonal antibody, clone GF28

Congregation of different migratory and resident bird species on aquatic ecosystems during winter migration increases contact rates and enhances influenza A virus (IAV) transmission. However, scarce research has been focused on the resident bird's contribution to the viral ecology at a local scale. The Mexican duck (Anas diazi) is an endemic endangered anatid from Mexico. This resident species shares aquatic habitats with migratory birds in the wetlands of Central Mexico. Therefore, here we describe the phylogenetic analysis of an IAV (A/Mexican duck/EstadodeMexico; Lerma/UIFMVZ377/2016(H5N2)) isolated in this species, during spatiotemporal concurrence with migratory anatids in the winter season. All eight gene sequences were obtained by nextgeneration sequencing. Maximum Likelihood trees were constructed using MEGA-X, with General Time Reversible + Invariant (GTR+I), Subtree Pruning and Regrafting (SPR) heuristic method, and 1000 bootstrap replicates. Similarities with six different IAV subtypes were observed through a BLAST search: H6N5, H7N7, H5N2, H4N6, H9N2, and H11N9, detected in wild ducks during 2015 in the Pacific, Central and Mississippi flyways stop sites across the United States of America and Canada. The molecular identification of this reassortant H5N2 IAV highlights the importance of resident species as a reservoir host and its potential participation in the maintenance and transmission of IAV in wetlands surrounded by rural areas.

Pattern recognition receptors (PRRs) are key elements in the innate immune response. Formyl peptide receptor (FPR) 2 is a PRR that, in addition to proinflammatory, pathogen-derived compounds, also recognizes the anti-inflammatory endogenous ligand annexin A1 (ArixA1). Because the contribution of this signaling axis in viral infections is undefined, we investigated AnxA1-mediated FPR2 activation on influenza A virus (IAV) infection in the murine model. AnxA1-treated mice displayed significantly attenuated pathology upon a subsequent IAV infection with significantly improved survival, impaired viral replication in the respiratory tract, and less severe lung damage. The AnxA1-mediated protection against IAV infection was not caused by priming of the type I LEN response but was associated with an increase in the number of alveolar macrophages (AMs) and enhanced pulmonary expression of the AM-regulating cytokine granulocyte-M-CSF (GM-CSF). Both AnxA1-mediated increase in AM levels and GM-CSF production were abrogated when mouse (m)FPR2 signaling was antagonized but remained up-regulated in mice genetically deleted for mFPR1, an mFPR2 isoform also serving as AnxA1 receptor. Our results indicate a novel protective function of the AnxA1-FPR2 signaling axis in IAV pathology via GM-CSF-associated maintenance of AMs, expanding knowledge on the potential use of proresolving mediators in host defense against pathogens.