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Negative-sense RNA viruses (NSVs) carrying a non-segmented genome encompass a broad group of viruses responsible for numerous human diseases such as rabies, mumps, measles, respiratory illness and encephalitis. Viruses replicate intracellular and interact with various host proteins to evade the immune response and persist within the host. A salient trait of NSVs is their ability to form cytoplasmic inclusion bodies (IBs) which are believed to serve as pivotal sites for viral replication. The formation of viral IBs is a complex process involving the recruitment of viral RNA and its proteins along with cellular components. These different constituents of IBs fulfil diverse roles depending on the structure and composition which remains specific to each virus. Therefore, understanding the viral strategies underlying IB formation is imperative. Numerous studies have explored the relationship between virus-induced IBs and host cell factors. This review aims to summarize how cellular factors participate in the formation of distinct viral IBs among non-segmented NSVs.
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http://dx.doi.org/10.1186/s12985-025-02784-w | DOI Listing |
Crit Rev Immunol
January 2025
Department of Pharmacy, Birla Institute of Technology and Science (BITS) Pilani, Hyderabad Campus, Dist. Medchal,500078, Telangana State, India.
Caseinolytic protease P (ClpP) is a highly conserved serine protease that plays a pivotal role in protein homeostasis and quality control in bacteria, mitochondria of mammalian cells, and plant chloroplasts. As the proteolytic core of the ATP-dependent Clp protease complex, ClpP partners with regulatory ATPases (e.g.
View Article and Find Full Text PDFPLoS Pathog
September 2025
Institut de Chimie des Substances Naturelles, CNRS, Université Paris-Saclay, Gif-sur-Yvette, France.
Respiratory syncytial virus (RSV), the most common cause of bronchiolitis and pneumonia in infants, elicits a remarkably weak innate immune response. This is partly due to type I interferon (IFN) antagonism by the non-structural RSV NS1 protein. It was recently suggested that NS1 could modulate host transcription via an interaction with the MED25 subunit of the Mediator complex.
View Article and Find Full Text PDFPLoS Pathog
September 2025
Department of Molecular Biology, Princeton University, Princeton, New Jersey, United States of America.
Hepatitis C virus (HCV) exhibits a narrow species tropism, causing robust infections only in humans and experimentally inoculated chimpanzees. While many host factors and restriction factors are known, many more likely remain unknown, which has limited the development of mouse or other small animal models for HCV. One putative restriction factor, the black flying fox orthologue of receptor transporter protein 4 (RTP4), was previously shown to potently inhibit viral genome replication of several ER-replicating RNA viruses.
View Article and Find Full Text PDFPLoS One
September 2025
Chilean Invasive Mycosis Network, Santiago, Chile.
Background: Invasive mold diseases (IMDs) are a severe complication of immunocompromised subjects and an emerging problem among severely ill, apparently immunocompetent patients. The aim of this study was to describe the epidemiological and clinical features of IMDs in Chile.
Methods: Prospective study of IMD cases in children and adults from 11 reference hospitals in Chile from May 2019 to May 2021.
J Vis Exp
August 2025
Department of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa; Department of Radiation Oncology, Holden Comprehensive Cancer Center, University of Iowa; Geminii, Inc.
Non-small cell lung cancer (NSCLC) continues to be the number one cause of cancer-related death for both women and men worldwide. More information needs to be gathered to understand the interactions between cancer cells, the immune system, the microenvironment within each tumor, and the host tissue to develop more effective treatment modalities. Reported here is a simple, repeatable method for inducing cancer within the mouse lung, allowing for the monitoring of tumor growth from early to late-stage disease.
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