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Sanchez-Rodriguez, F.

Publications and source records attributed to Sanchez-Rodriguez, F..

2 recordsLinked to original sources

Highly pathogenic avian influenza (HPAI) in South America, 2022-2025: temporality, affected species, and the southwards expansion to the Antarctic region.

The H5N1 highly pathogenic avian influenza (HPAI) virus has caused severe global losses, reaching South America in 2022 and Antarctica in 2024. Here we synthesize outbreak reports submitted to the World Organization for Animal Health (WOAH) by South American countries and document the viruss unprecedented expansion into Antarctica, affecting wild birds, wild mammals, and domestic poultry. More than 6 million domestic birds died or were culled, mostly from commercial operations. Of the 11 South American countries that reported H5N1 to WOAH, 10 reported infections in wild birds, spanning 104 species, 59.62% of which are migratory and predominantly non-trans-equatorial. Marine mammal cases occurred after wild bird detections, with the South American sea lion (Otaria flavescens) most affected, and several Antarctic bird species with migratory behavior were also reported in South America. To complement outbreak data, we examined available genomic sequences through phylogenetic and time-calibrated Bayesian analyses, which revealed multiple introduction events, viral diversity across regions, and evidence of interspecies transmission dynamics. These findings highlight the extensive ecological reach of H5N1 in the Southern Hemisphere and underscore the urgent need for a One Health approach that strengthens wildlife and backyard-poultry surveillance while fostering coordinated regional action to control and prevent further spread of HPAI. IMPORTANCEThe arrival of H5N1 highly pathogenic avian influenza (HPAI) in South America has caused severe mortality in wild birds, marine mammals, and domestic poultry, and has recently expanded into Antarctica. Understanding how the virus entered and spread across the continent is essential for preparedness and response. Using phylogenetic and time-calibrated analyses, we identify three independent introductions into South America, estimate their temporal windows of entry, and document repeated spillover across species, including into marine mammals and humans. These findings provide novel resolution beyond previous reports and highlight the extensive inter-country connectivity of circulating viruses. The unprecedented detection of HPAI in Antarctica further illustrates the ecological risks posed by ongoing southward spread. Together, this analysis underscores the urgent need for integrated One Health surveillance that bridges wildlife, domestic animal, and human health systems to mitigate the future impacts of HPAI in the region.

microbiology↗

The subunit 3 of the SUPERKILLER (SKI) complex mediates miR172-directed cleavage of Nodule Number Control 1 (NNC1) to modulate nodulation in Medicago truncatula

Legumes and rhizobia establish a nitrogen-fixing symbiosis that involves the formation of a lateral root organ, the nodule, and the infection process that allows intracellular accommodation of rhizobia within nodule cells. This process involves significant gene expression changes regulated at the transcriptional and post-transcriptional levels. We have previously shown that a transcript encoding the subunit 3 of the Superkiller Complex (SKI), which guides mRNAs to the exosome for 3'-to-5' degradation, is required for nodule formation and bacterial persistence within the nodule, as well as the induction of early nodulation genes (e.g., MtENOD40) during the Medicago truncatula-Sinorhizobium meliloti symbiosis. Here, we reveal through transcript degradome and small RNA sequencing analysis that knockdown of MtSKI3 impairs the miR172-directed endonucleolytic cleavage of the mRNA encoding Nodule Number Control 1 (MtNNC1), an APETALA2 transcription factor that negatively modulates nodulation. Knockdown of MtNNC1 enhances nodule number, bacterial infection, and the induction of MtENOD40 upon inoculation with S. meliloti whereas overexpression of a miR172-resistant form of MtNNC1 significantly reduces nodule formation. This work identifies miR172 cleavage of MtNNC1 and its control by MtSKI3, a component of the 3'-to-5'mRNA degradation pathway, as a new regulatory hub controlling indeterminate nodulation.

plant biology↗