The phenotype-genotype problem is a fundamental problem of biology where an organism's genotype (genetic information) predicts its phenotype (observable characteristic). Viral fitness, defined as the reproductive capacity of a virus compared to a standard, is a continuous phenotype. We construct models to predict viral fitness as a function of mutation away from the standard wildtype virus. Data of this nature are difficult to analyse because there are potentially many more parameters than observations. We treat this issue as a regression problem using a prior with both a shrinkage component and a variable selection component. The key to practical implementation of the model is the prior specification for the regression coefficients. We use results from the scientific literature to construct several informative exchangeable within subsets priors (ESP). We use prior model selection (PMS) to select among our priors. Two novel graphics present results from five models each with 71 predictors.
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http://dx.doi.org/10.1002/sim.2595 | DOI Listing |
Viruses
January 2025
Clinical Center for Biotherapy, Zhongshan Hospital, Fudan University, Shanghai 200433, China.
This study aimed to create a new recombinant virus by modifying the EV-A71 capsid protein, serving as a useful tool and model for studying human Enteroviruses. We developed a new screening method using EV-A71 pseudovirus particles to systematically identify suitable insertion sites and tag types in the VP1 capsid protein. The pseudovirus's infectivity and replication can be assessed by measuring postinfection luciferase signals.
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January 2025
Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
The tripartite-motif protein 56 (TRIM56) is a RING-type E3 ubiquitin ligase whose functions were recently beginning to be unveiled. While the physiological role(s) of TRIM56 remains unclear, emerging evidence suggests this protein participates in host innate defense mechanisms that guard against viral infections. Interestingly, TRIM56 has been shown to pose a barrier to viruses of distinct families by utilizing its different domains.
View Article and Find Full Text PDFMicrobiol Res
January 2025
State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China. Electronic address:
Bacteriophages as viral predators can restrict host strains and shape the bacterial community. Conversely, bacteria also adopt diverse strategies for phage defense. Pseudomonas syringae pv.
View Article and Find Full Text PDFVet Microbiol
January 2025
Key Laboratory of Avian Bioproducts Development, College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China; Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonosis, College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China; Key Laboratory of Prevention and Control of Biological Hazard Factors (Animal Origin) for Agri-food Safety and Quality, Ministry of Agriculture of China (26116120), College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China.
Currently, there is increasing spillover of highly pathogenic H5N1 avian influenza virus (AIV) to mammals, raising a concern of pandemic threat about this virus. Although the function of PA protein of the influenza virus is well understood, the understanding of how phosphorylation regulates this protein and influenza viral life cycle is still limited. We previously identified PA S225 as the phosphorylation site in the highly pathogenic H5N1 AIV.
View Article and Find Full Text PDFEMBO Mol Med
January 2025
Sabri Ülker Center for Metabolic Research, Department of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Host metabolic fitness is a critical determinant of infectious disease outcomes. Obesity, aging, and other related metabolic disorders are recognized as high-risk disease modifiers for respiratory infections, including coronavirus infections, though the underlying mechanisms remain unknown. Our study highlights fatty acid-binding protein 4 (FABP4), a key regulator of metabolic dysfunction and inflammation, as a modulator of SARS-CoV-2 pathogenesis, correlating strongly with disease severity in COVID-19 patients.
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