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Epstein-Barr virus BALF0/1 subverts the Caveolin and ERAD pathways to target B cell receptor complexes for degradation.
Proc Natl Acad Sci U S A
January 2025
Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.
Epstein-Barr virus (EBV) establishes persistent infection, causes infectious mononucleosis, is a major trigger for multiple sclerosis and contributes to multiple cancers. Yet, knowledge remains incomplete about how the virus remodels host B cells to support lytic replication. We previously identified that EBV lytic replication results in selective depletion of plasma membrane (PM) B cell receptor (BCR) complexes, composed of immunoglobulin and the CD79A and CD79B signaling chains.
View Article and Find Full Text PDFMulticenter Analysis of Acute Retinal Necrosis: Clinical Characteristics, Viral Pathogens, and Diagnostic Predictive Factors.
Ocul Immunol Inflamm
January 2025
Ocular inflammation and infection division, Department of Ophthalmology, Phramongkutklao College of Medicine, Bangkok, Thailand.
Purpose: This multicenter study aimed to investigate the clinical characteristics and factors associated with specific viral pathogens in patients with acute retinal necrosis (ARN).
Methods: A retrospective multicenter cohort study included ARN patients who underwent aqueous or vitreous polymerase chain reaction (PCR) testing. Multivariable mixed-effects Poisson regression was used to identify factors associated with viral pathogens.
Ofatumumab successfully treats myelin oligodendrocyte glycoprotein antibody-associated disease accompanied by Epstein-Barr viral infection: a case series.
Front Immunol
January 2025
Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) caused by pathogenic immunoglobulin G antibodies to myelin oligodendrocyte glycoprotein is a rare demyelinating disease of the central nerve system (CNS). The clinical phenotypes of MOGAD include acute disseminated encephalomyelitis, optic neuritis, and transverse myelitis. At present, the mechanism underlying the disease is unknown.
View Article and Find Full Text PDFDeciphering the Differences Between Epstein-Barr Virus-Associated and Negative Gastric Cancer in the Prospect of CDKN2A Genomic Alterations and Lymphoid Infiltration.
Cancer Med
January 2025
Department of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Sir Y.K. Pao Cancer Center, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, China.
Background: Gastric cancer (GC) is a major health concern worldwide. One important contributing factor is the presence of the Epstein-Barr virus (EBV). However, the molecular pattern of how EBV participates in the malignant transition process remains unclear.
View Article and Find Full Text PDFIntrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment.
Nat Commun
January 2025
Dept. of Microbiology and Immunology, Center for Microbial Pathogenesis and Host Inflammatory Responses, and Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Gammaherpesviruses are DNA tumor viruses that establish lifelong latent infections in lymphocytes. For viruses such as Epstein-Barr virus and murine gammaherpesvirus 68, this is accomplished through a viral gene-expression program that promotes cellular proliferation and differentiation, especially of germinal center B cells. Intrinsic host mechanisms that control virus-driven cellular expansion are incompletely defined.
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