Recent progress has provided clear evidence that many RNA-viruses form cytoplasmic biomolecular condensates mediated by liquid-liquid phase separation to facilitate their replication. In contrast, seemingly contradictory data exist for herpesviruses, which replicate their DNA genomes in nuclear membrane-less replication compartments (RCs). Here, we review the current literature and comment on nuclear condensate formation by herpesviruses, specifically with regard to RC formation. Based on data obtained with human cytomegalovirus (human herpesvirus 5), we propose that liquid and homogenous early RCs convert into more heterogeneous RCs with complex properties over the course of infection. We highlight how the advent of DNA replication leads to the maturation of these biomolecular condensates, likely by adding an additional DNA scaffold.
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http://dx.doi.org/10.3390/v14050960 | DOI Listing |
Mechanical properties of the nucleus are remodeled not only by extracellular forces transmitted to the nucleus but also by internal modifications, such as those induced by viral infections. During herpes simplex virus type 1 infection, the viral regulation of essential nuclear functions and growth of the nuclear viral replication compartments are known to reorganize nuclear structures. However, little is known about how this infection-induced nuclear deformation changes nuclear mechanobiology.
View Article and Find Full Text PDFJ Theor Biol
January 2025
Center for Computational and Theoretical Biology, University of Wuerzburg, Klara-Oppenheimer-Weg 32, Wuerzburg, 97074, Germany; Department of Theoretical Biology, Max Planck Institute for Evolutionary Biology, August-Thienemann-Str. 2, Ploen, 24306, Germany.
Real-world processes often exhibit temporal separation between actions and reactions - a characteristic frequently ignored in many modelling frameworks. Adding temporal aspects, like time delays, introduces a higher complexity of problems and leads to models that are challenging to analyse and computationally expensive to solve. In this work, we propose an intermediate solution to resolve the issue in the framework of evolutionary game theory.
View Article and Find Full Text PDFSci Rep
January 2025
School of Biological Sciences, University of California San Diego, La Jolla, CA, 92093, USA.
As nucleus-forming phages become better characterized, understanding their unifying similarities and unique differences will help us understand how they occupy varied niches and infect diverse hosts. All identified nucleus-forming phages fall within the Chimalliviridae family and share a core genome of 68 unique genes including chimallin, the major nuclear shell protein. A well-studied but non-essential protein encoded by many nucleus-forming phages is PhuZ, a tubulin homolog which aids in capsid migration, nucleus rotation, and nucleus positioning.
View Article and Find Full Text PDFNeuroinformatics
January 2025
Blue Brain Project, EPFL, Chemin des mines 9, 1202, Geneva, Switzerland.
Long-range axons are fundamental to brain connectivity and functional organization, enabling communication between different brain regions. Recent advances in experimental techniques have yielded a substantial number of whole-brain axonal reconstructions. While previous computational generative models of neurons have predominantly focused on dendrites, generating realistic axonal morphologies is more challenging due to their distinct targeting.
View Article and Find Full Text PDFVaccines (Basel)
December 2024
Infectious Diseases and Immunity in Global Health Program, Research Institute of the McGill University Health Centre, Montreal, QC H4A 3J1, Canada.
HIV causes intense polyclonal activation of B cells, resulting in increased numbers of spontaneously antibody-secreting cells in the circulation and hypergammaglobulinemia. It is accompanied by significant perturbations in various B cell subsets, such as increased frequencies of immature/transitional B cells, activated memory B cells, atypical memory B cells, short-lived plasmablasts and regulatory B cells, as well as by decreased frequencies of resting memory and resting naïve B cells. Furthermore, both memory and antigen-inexperienced naïve B cells show exhausted and immune-senescent phenotypes.
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