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Altered LY6E and TRIM6 expression in PBMCs correlated with HBsAg clearance and response to Peg-IFN-α treatment in HBeAg-negative chronic hepatitis B patients.
Virol J
March 2025
Department of Infectious Diseases, Chongqing Key Laboratory of Infectious Diseases and Parasitic Diseases, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Background: Pegylated interferon alpha (Peg-IFN-α) has the potential to eradicate hepatitis B surface antigen (HBsAg). This study aimed to investigate whether the expression levels of lymphocyte antigen 6 family member E (LY6E) and tripartite motif-containing protein 6 (TRIM6) mRNAs in peripheral blood mononuclear cells (PBMCs) of hepatitis B e antigen (HBeAg)-negative chronic hepatitis B virus (HBV) patients is associated with the response to Peg-IFN-α treatment and HBsAg clearance.
Methods: In this prospective study, HBeAg-negative chronic HBV patients treated with Peg-IFN-α were followed for 48 weeks.
Antibiotic resistance and viral co-infection in children diagnosed with pneumonia caused by Mycoplasma pneumoniae admitted to Russian hospitals during October 2023-February 2024.
BMC Infect Dis
March 2025
Scientific Research Institute for Systems Biology and Medicine, Federal Service on Consumer Rights Protection and Human Well-Being Surveillance, Moscow, Russia.
Background: Mycoplasma pneumoniae (MP) is a common bacterial respiratory infection that can cause pneumonia, particularly in children. Previously published data have highlighted the high incidence of viral co-infections and the problem of increasing macrolide resistance in MP worldwide.
Aims: (1) to estimate the impact of viral infections circulating in a local population on the spectrum of co-infection in hospitalized children with Mycoplasma pneumoniae pneumonia (MPP), (2) to determine if there are differences in resistance mutation rate for samples from hospitals of Russia located in the European and Far East, (3) to describe genomic characteristics of MP from Russian patients during the MPP outbreaks in the fall-winter of 2023-2024.
A single-nucleus and spatial transcriptomic atlas of the COVID-19 liver reveals topological, functional, and regenerative organ disruption in patients.
Genome Biol
March 2025
Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Background: The molecular underpinnings of organ dysfunction in severe COVID-19 and its potential long-term sequelae are under intense investigation. To shed light on these in the context of liver function, we perform single-nucleus RNA-seq and spatial transcriptomic profiling of livers from 17 COVID-19 decedents.
Results: We identify hepatocytes positive for SARS-CoV-2 RNA with an expression phenotype resembling infected lung epithelial cells, and a central role in a pro-fibrotic TGFβ signaling cell-cell communications network.
Macrophage-derived SPP1 exacerbate myocardial injury by interacting with fibroblasts in viral myocarditis.
Biol Direct
March 2025
Department of Pediatric Cardiology, Cheeloo Colledge of Medicine, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China.
Background: Viral myocarditis (VMC) is an inflammatory myocardial condition triggered by viral infections which involves pathogenic-related damage and immune-mediated damage. However, the precise immunopathogenic mechanisms underlying VMC remain elusive.
Methods: We performed single-cell RNA sequencing on mouse hearts during the acute phase of CVB3-induced VMC.
Critical role of ferroptosis in viral infection and host responses.
Virology
March 2025
Institute for Animal Health & UK-China Centre of Excellence for Research on Avian Diseases, Henan Academy of Agricultural Sciences, Zhengzhou, 450002, People's Republic of China; Laboratory of Functional Microbiology and Animal Health, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, 471003, People's Republic of China. Electronic address:
Ferroptosis is an iron-dependent form of programmed cell death that plays a crucial role in regulating intracellular redox homeostasis and lipid metabolism, and in combating viral infections. Viruses have persistently evolved and adapted synergistically with their hosts over a long period and, to some extent, have been able to utilize ferroptosis to promote viral replication. Herein, we summarize the characteristics, mechanisms, and regulatory networks of ferroptosis and provide an overview of the key regulatory steps of ferroptosis involved in viral infection, together with the changes in host indicators and key regulatory signaling pathways.
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