The Flavivirus genus (Flaviviridae family) contains a number of important human pathogens, including dengue and Zika viruses, which have the potential to cause severe disease. In order to efficiently establish a productive infection in mammalian cells, flaviviruses have developed key strategies to counteract host immune defences, including the type I interferon response. They employ different mechanisms to control interferon signal transduction and effector pathways, and key research generated over the past couple of decades has uncovered new insights into their abilities to actively decrease interferon antiviral activity. Given the lack of antivirals or prophylactic treatments for many flaviviral infections, it is important to fully understand how these viruses affect cellular processes to influence pathogenesis and disease outcome. This review will discuss the strategies mosquito-borne flaviviruses have evolved to antagonise type I interferon mediated immune responses.
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http://dx.doi.org/10.1111/cmi.12737 | DOI Listing |
Trends Mol Med
December 2024
Cancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Philadelphia, PA, USA. Electronic address:
Genetic and epigenetic defects of the p53 system have previously been associated with resistance to CDK4/6 inhibitors in women with HR breast cancer. Recent data from Kudo et al. demonstrate that CDK2-targeting agents may offer an effective strategy to circumvent such resistance by enforcing cellular senescence downstream of RBL2 dephosphorylation.
View Article and Find Full Text PDFJ Ethnopharmacol
December 2024
Department of Pathogenic Biology and Immunology, College of Integrated Chinese and Western Medicine (College of Life Science), Anhui University of Chinese Medicine, Hefei, China; Institute of Integrated Traditional Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, China; Anhui Province Key Laboratory of Chinese Medicinal Formula, Hefei, China. Electronic address:
Ethnopharmacological Relevance: Vulvovaginal candidiasis (VVC) is a relatively common fungal infectious disease in the female reproductive tract. The pathogenesis of VVC not only involves Candida albicans (C. albicans) infection, but also the improper immune response of the vaginal mucosal immune system to the fungus.
View Article and Find Full Text PDFJ Cell Mol Med
December 2024
Department of Orthopedics, Shenshan Medical Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Shanwei, Guangdong, P. R. China.
Mitochondrial programmed cell death (PCD) plays a critical role in the pathogenesis of diabetic foot ulcers (DFU). In this study, we performed a comprehensive transcriptome analysis to identify potential hub genes and key cell types associated with PCD and mitochondria in DFU. Using intersection analysis of PCD- and mitochondria-related genes, we identified candidate hub genes through protein-protein interaction and random forest analysis.
View Article and Find Full Text PDFCurr Issues Mol Biol
December 2024
Foodborne Toxin Detection and Prevention Research Unit, Western Regional Research Center, Agricultural Research Service, United States Department of Agriculture, Albany, CA 94710, USA.
Abrin, a toxin of the rosary pea plant (), has been implicated as causing an autoimmune demyelinating disease in humans, but the exact mechanisms responsible for the induction of these demyelinating conditions are still unknown. Certain superantigen microbial toxins such as Staphylococcus enterotoxin type A, type D, type E or streptococcal pyrogenic exotoxin type C also lead to various diseases including autoimmune disorders of the nervous system. Here, the effect of abrin toxin on the immune reaction was studied in human CD4 T-cell lines, and its inhibition of protein synthesis in kidney cells.
View Article and Find Full Text PDFCurr Res Microb Sci
November 2024
CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Institute of Oceanology; CAS Center for Ocean Mega-Science, Chinese Academy of Sciences, Qingdao, China.
RIG-I and MDA5 are members of RIG-I-like receptors (RLRs) that detect viral RNA within the cytoplasm and subsequently initiate antiviral immune responses. Necroptosis is a form of programmed cell death (PCD) executed by mixed lineage kinase domain-like (MLKL), which, upon phosphorylation by receptor-interacting protein kinase 3 (RIPK3), causes necrotic cell death. To date, no link between RLRs and necroptosis has been observed during bacterial infection.
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