Genetic recombination in RNA viruses was discovered many years ago for poliovirus (PV), an enterovirus of the Picornaviridae family, and studied using PV or other picornaviruses as models. Recently, recombination was shown to be a general phenomenon between different types of enteroviruses of the same species. In particular, the interest for this mechanism of genetic plasticity was renewed with the emergence of pathogenic recombinant circulating vaccine-derived polioviruses (cVDPVs), which were implicated in poliomyelitis outbreaks in several regions of the world with insufficient vaccination coverage. Most of these cVDPVs had mosaic genomes constituted of mutated poliovaccine capsid sequences and part or all of the non-structural sequences from other human enteroviruses of species C (HEV-C), in particular coxsackie A viruses. A study in Madagascar showed that recombinant cVDPVs had been co-circulating in a small population of children with many different HEV-C types. This viral ecosystem showed a surprising and extensive biodiversity associated to several types and recombinant genotypes, indicating that intertypic genetic recombination was not only a mechanism of evolution for HEV-C, but an usual mode of genetic plasticity shaping viral diversity. Results suggested that recombination may be, in conjunction with mutations, implicated in the phenotypic diversity of enterovirus strains and in the emergence of new pathogenic strains. Nevertheless, little is known about the rules and mechanisms which govern genetic exchanges between HEV-C types, as well as about the importance of intertypic recombination in generating phenotypic variation. This review summarizes our current knowledge of the mechanisms of evolution of PV, in particular recombination events leading to the emergence of recombinant cVDPVs.
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http://dx.doi.org/10.3390/v3081460 | DOI Listing |
Front Oncol
January 2025
Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Introduction: Small cell lung cancer (SCLC) is characterized by significant heterogeneity and plasticity, contributing to its aggressive progression and therapy resistance. Autophagy, a conserved cellular process, is implicated in many cancers, but its role in SCLC remains unclear.
Methods: Using a genetically engineered mouse model ( ; ; GFP-LC3-RFP-LC3△G), we tracked autophagic flux to investigate its effects on SCLC biology.
World J Oncol
February 2025
Comprehensive Breast Health Center, Department of Surgery, Taipei Veterans General Hospital, Taipei 112201, Taiwan.
Background: While mutations in the gene play important roles in human breast carcinogenesis, gene alterations are recognized as actionable mutations for clinical cancer treatment. We aimed to elucidate the role of PIK3R1 in cell proliferation on breast carcinoma and to correlate the PIK3R1 expression with patients' outcome using human tumor tissue arrays.
Methods: Using human BT-474 (estrogen receptor (ER)+/human epidermal growth factor receptor 2 (HER2)-high) breast carcinoma cell line as model, the role of PIK3R1 in cell proliferation was elucidated by knock-down of the gene (ΔPIK3R1) in this cell line.
Tzu Chi Med J
August 2024
Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.
Schizophrenia (SCZ) is a chronic psychotic disorder that profoundly alters an individual's perception of reality, resulting in abnormal behavior, cognitive deficits, thought distortions, and disorientation in emotions. Many complicated factors can lead to SCZ, and investigations are ongoing to understand the neurobiological underpinnings of this condition. Presynaptic Netrin G1 and its cognate partner postsynaptic Netrin-G-Ligand-1 (NGL-1) have been implicated in SCZ.
View Article and Find Full Text PDFHum Mol Genet
January 2025
Department of Facial Plastic and Reconstructive Surgery, ENT Institute, Eye & ENT Hospital, Fudan University, No. 83 Fenyang Road, Xuhui District, Shanghai 200031, China.
Waardenburg syndrome type 2 (WS2) is an autosomal dominant disorder characterized by congenital sensorineural hearing loss, blue iris, and abnormal pigmentation of the hair and skin. WS2 is genetically heterogeneous, often resulting from pathogenic mutations in SOX10 gene. We identified a novel heterozygous frameshift mutation in SOX10 (NM_006941.
View Article and Find Full Text PDFClin Epigenetics
January 2025
School of Forensic Medicine, China Medical University, Shenyang, People's Republic of China.
Enriched environment (EE), as a non-pharmacological intervention, has garnered considerable attention for its potential to ameliorate neurodegenerative diseases (NDs). This review delineated the impact of EE on the biological functions associated with NDs, emphasizing its role in enhancing neural plasticity, reducing inflammation, and bolstering cognitive performance. We discussed the molecular underpinnings of the effects of EE, including modulation of key signaling pathways such as extracellular regulated kinase 1/2 (ERK1/2), mitogen-activated protein kinases (MAPK), and AMPK/SIRT1, which were implicated in neuroprotection and synaptic plasticity.
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