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Jorquera, R.

Publications and source records attributed to Jorquera, R..

2 recordsLinked to original sources

Detection of clade 2.3.4.4b H5N1 high pathogenicity avian influenza virus in a sheep in Great Britain, 2025

Clade 2.3.4.4b H5N1 high pathogenicity avian influenza virus (HPAIV) continues to pose a significant global threat, affecting wild and domestic avian populations, and mammalian species. In early 2024, H5N1 HPAIV was detected in dairy cattle in the United States of America, where it has continued to circulate, with sporadic detections also reported in other ruminant species. The detection of high viral loads in milk from infected cattle, has resulted in several human infections, underscoring the zoonotic potential of these viruses. In response, several countries have intensified surveillance in non-avian species to evaluate the potential for undetected viral circulation in captive mammals. In Great Britain, bulk milk tank testing of cattle and targeted surveillance of captive mammalian species on an infected premises is undertaken in accordance with the outcome of a rapid risk assessment undertaken to determine the epidemiological links between the poultry and captive mammals. A result of this testing was the first recorded detection of clade 2.3.4.4b H5N1 HPAIV in a sheep in March 2025, identified on an infected poultry premises in Great Britain. An initial seropositive result in a single ewe triggered further investigation, confirming serological positivity across repeated sampling and the presence of viral RNA in milk samples. This detection was confined to a single animal and was likely attributable to proximity to infected poultry and a presumed heavily contaminated environment. The implications of this ruminant detection are discussed in the context of interspecies transmission and surveillance strategies.

microbiology↗

FAM162A is Crucial for Mitochondrial Structure, Dynamics, and Bioenergetics, Driving Cellular Protection and Longevity

IntroductionFAM162A is a mitochondrial protein evolutionarily conserved across taxa and ubiquitously expressed in various tissues. It is known for its role in hypoxia-induced apoptosis. However, paradoxically, FAM162A is overexpressed in cancer, where its pro-apoptotic function seems overridden, suggesting an alternative role associated with mitochondrial function and cell survival. Additionally, its precise localization and topology remain controversial. ObjectivesTo assess the role of FAM162A in mitochondrial structure, dynamics, and bioenergetics and its impact on cell viability, while establishing its precise localization, orientation, and topology. Additionally, to generate a transgenic Drosophila model overexpressing human FAM162A to evaluate its effects on organismal survival under normal and stress conditions. MethodsLocalization, orientation, and topology were determined by protease protection assays in COS7 cells. Loss-and gain-of-function experiments were performed to assess mitochondrial function and turnover by confocal microscopy, immunoblots and Seahorse technology. A transgenic Drosophila model overexpressing human FAM162A was generated to evaluate organismal survival under normal and stress conditions. ResultsFAM162A is essential for maintaining mitochondrial ultrastructure and bioenergetics, thereby influencing cell viability and stress resistance. Localization studies revealed that FAM162A resides predominantly in the inner mitochondrial membrane, particularly within the cristae, where it modulates the fusion protein OPA1. Transgenic Drosophila overexpressing human FAM162A exhibited increased lifespan and locomotor activity under both normal and heat stress conditions. ConclusionFAM162A emerges as a crucial player in maintaining mitochondrial integrity and bioenergetics. Its functional role, potentially mediated through interaction with OPA1, impacts mitochondrial health, stress resistance, cellular viability, and organismal longevity.

cell biology↗