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Avian Reovirus: From Molecular Biology to Pathogenesis and Control.
Viruses
December 2024
Southeast Poultry Research Laboratory, U.S. National Poultry Research Center, United States Department of Agriculture-Agricultural Research Service (USDA-ARS), Athens, GA 30605, USA.
Avian reoviruses (ARVs) represent a significant economic burden on the poultry industry due to their widespread prevalence and potential pathogenicity. These viruses, capable of infecting a diverse range of avian species, can lead to a variety of clinical manifestations, most notably tenosynovitis/arthritis. While many ARV strains are asymptomatic, pathogenic variants can cause severe inflammation and tissue damage in organs such as the tendons, heart, and liver.
View Article and Find Full Text PDFViral Oncogenesis: Synergistic Role of Genome Integration and Persistence.
Viruses
December 2024
Laboratory of Virology, National Institute for Infectious Diseases "Lazzaro Spallanzani" (IRCCS), 00149 Rome, Italy.
Persistence is a strategy used by many viruses to evade eradication by the immune system, ensuring their permanence and transmission within the host and optimizing viral fitness. During persistence, viruses can trigger various phenomena, including target organ damage, mainly due to an inflammatory state induced by infection, as well as cell proliferation and/or immortalization. In addition to immune evasion and chronic inflammation, factors contributing to viral persistence include low-level viral replication, the accumulation of viral mutants, and, most importantly, maintenance of the viral genome and reliance on viral oncoprotein production.
View Article and Find Full Text PDFThe 'Oma's of the Gammas-Cancerogenesis by γ-Herpesviruses.
Viruses
December 2024
Division of Virology, ICMR-National Institute of Translational Virology and AIDS Research, Pune 411026, MH, India.
Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), which are the only members of the gamma(γ) herpesviruses, are oncogenic viruses that significantly contribute to the development of various human cancers, such as Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's lymphoma, Kaposi's sarcoma, and primary effusion lymphoma. Oncogenesis triggered by γ-herpesviruses involves complex interactions between viral genetics, host cellular mechanisms, and immune evasion strategies. At the genetic level, crucial viral oncogenes participate in the disruption of cell signaling, leading to uncontrolled proliferation and inhibition of apoptosis.
View Article and Find Full Text PDFDHX15 and Rig-I Coordinate Apoptosis and Innate Immune Signaling by Antiviral RNase L.
Viruses
December 2024
Department of Biological Sciences, University of Toledo, 2801 West Bancroft Street, Toledo, OH 43606, USA.
During virus infection, the activation of the antiviral endoribonuclease, ribonuclease L (RNase L), by a unique ligand 2'-5'-oilgoadenylate (2-5A) causes the cleavage of single-stranded viral and cellular RNA targets, restricting protein synthesis, activating stress response pathways, and promoting cell death to establish broad antiviral effects. The immunostimulatory dsRNA cleavage products of RNase L activity (RL RNAs) recruit diverse dsRNA sensors to activate signaling pathways to amplify interferon (IFN) production and activate inflammasome, but the sensors that promote cell death are not known. In this study, we found that DEAH-box polypeptide 15 (DHX15) and retinoic acid-inducible gene I (Rig-I) are essential for apoptosis induced by RL RNAs and require mitochondrial antiviral signaling (MAVS), c-Jun amino terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) for caspase-3-mediated intrinsic apoptosis.
View Article and Find Full Text PDFThe Role of vIL-6 in KSHV-Mediated Immune Evasion and Tumorigenesis.
Viruses
December 2024
Department of Dermatology, School of Medicine, University of California Davis, Sacramento, CA 95817, USA.
Kaposi's sarcoma-associated herpesvirus (KSHV) is a double-stranded DNA gamma herpesvirus. Like other herpesviruses, KSHV establishes a latent infection with limited gene expression, while KSHV occasionally undergoes the lytic replication phase, which produces KSHV progenies and infects neighboring cells. KSHV genome encodes 80+ open reading frames.
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