In late 2014, a H5N8 highly pathogenic avian influenza (HPAI) virus, clade 2.3.4.4, spread by migratory waterfowl into North America reassorting with low pathogenicity AI viruses to produce a H5N2 HPAI virus. Since domestic waterfowl are common backyard poultry frequently in contact with wild waterfowl, the infectivity, transmissibility, and pathogenicity of the United States H5 HPAI index viruses (H5N8 and H5N2) was investigated in domestic ducks and geese. Ducks infected with the viruses had an increase in body temperature but no or mild clinical signs. Infected geese did not show increase in body temperature and most only had mild clinical signs; however, some geese presented severe neurological signs. Ducks became infected and transmitted the viruses to contacts when inoculated with high virus doses [(10 and 10 50% embryo infective dose (EID)], but not with a lower dose (10 EID). Geese inoculated with the H5N8 virus became infected regardless of the virus dose given, and transmitted the virus to direct contacts. Only geese inoculated with the higher doses of the H5N2 and their contacts became infected, indicating differences in infectivity between the two viruses and the two waterfowl species. Geese shed higher titers of virus and for a longer period of time than ducks. In conclusion, the H5 HPAI viruses can infect domestic waterfowl and easily transmit to contact birds, with geese being more susceptible to infection and disease than ducks. The disease is mostly asymptomatic, but infected birds shed virus for several days representing a risk to other poultry species.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5463389 | PMC |
http://dx.doi.org/10.1186/s13567-017-0435-4 | DOI Listing |
Alzheimers Dement
December 2024
Xiangya Hospital, Central South University, Changsha, Hunan, China.
Background: Single nucleotide polymorphism (SNP)-based genetic studies have identified many risk genes for Alzheimer's disease (AD), but only explain part of the heritability. Structural variation (SVs) may account for some of this otherwise unexplained heritability. In this study, we sequenced 1,519 AD patients and 2,010 controls using 30X whole-genome sequencing (WGS).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Harvard Medical School and Brigham & Women's Hospital, Boston, MA, USA.
SORL1 (SORLA, LR11) is a large (2214 residue), multi-domain type 1 integral membrane protein that is the product of the SORL1 gene. In neurons, where it is highly expressed, SORL1 functions as both a substrate of and a cargo receptor for the retromer multi protein complex that is a master regulator of protein trafficking out of the early endosome. The SORL1-Vps26b retromer, in particular, is dedicated to the recycling of cell surface proteins, including APP and AMPA receptor subunit GLUA1, back to the plasma membrane.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Background: The microtubule-associated protein tau is the most commonly misfolded protein in neurodegenerative disorders including Alzheimer's disease and other related tauopathies. These neurological illnesses are hypothesized to share a common mechanism of disease progression, where pathogenic aggregates or 'seeds' of the tau protein function as templates promoting misfolding of functional, soluble tau protein. Under this premise, therapeutic strategies that modulate the seeding cascade, have high potential to interfere with the disease process.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Queen Mary University of London, London, United Kingdom.
Background: Various explanations have been proposed for how hearing impairment might be associated with increased risk of dementia. Several theories have proposed direct links with Alzheimer's disease (AD) neuropathology, either due to shared aetiology (i.e.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Case Western Reserve University, Cleveland, OH, USA.
Background: Pathological tau forms from Alzheimer's disease (AD) brains act as seeds, replicating in cells and forming tau aggregates in a template-like manner. The exploration of this prion-like pathogenic mechanism has predominantly occurred in transgenic mice and cell systems that overexpress tau protein and its truncated forms with pro-aggregation mutations. However, these systems do not entirely capture the propagation kinetics and template conformational changes of various tau seeds.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!