Highly pathogenic avian influenza H5N1 virus infections in pinnipeds and seabirds in Uruguay: Implications for bird-mammal transmission in South America

Abstract

The highly pathogenic avian influenza viruses of clade 2.3.4.4b have caused unprecedented deaths in South American wild birds, poultry, and marine mammals. In September 2023, pinnipeds and seabirds appeared dead on the Uruguayan Atlantic coast. Sixteen influenza virus strains were characterized by real-time reverse transcription PCR and genome sequencing in samples from sea lions (Otaria flavescens), fur seals (Arctocephalus australis), and terns (Sterna hirundinacea). Phylogenetic and ancestral reconstruction analysis showed that these strains have pinnipeds most likely as the ancestral host, representing a recent introduction of clade 2.3.4.4b in Uruguay. The Uruguayan and closely related strains from Peru (sea lions) and Chile (sea lions and a human case) carry mammalian adaptative residues 591K and 701N in the viral polymerase basic protein 2 (PB2). Our findings suggest that clade 2.3.4.4b strains in South America may have spread from mammals to mammals and seabirds, revealing a new transmission route.

Keywords: South America; avian influenza; mammal adaptation; sea mammals; transmission.

Figure 1.

Bayesian phylogenetic reconstruction of concatenated segments, including timing estimates of the most recent common ancestors of specific Uruguayan clades and ancestral state reconstruction of countries, hosts, and presence/absence of two PB2 mutations known to increase the infection in mammalian cells. (A) Discrete phylogeographic analysis of South American countries. Country colors denote specific countries, asterisks are posterior probability support above 90, and numbers indicate distinct Uruguayan clades. (B) tMRCA of the six selected clades highlighted in (A). (C) Discrete ancestral host reconstruction and associated ancestral state reconstruction posterior probabilities of each trait (ASR PP). (D) Discrete ancestral reconstruction of PB2 mammal adaptation double mutation and associated ASR PP values.