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The measles virus matrix F50S mutation from a lethal case of subacute sclerosing panencephalitis promotes receptor-independent neuronal spread.
J Virol
December 2024
Mayo Clinic Graduate School of Biomedical Sciences, Mayo Clinic, Rochester, Minnesota, USA.
Subacute sclerosing panencephalitis (SSPE) is a lethal neurological disorder occurring several years after measles. Reconstruction of the evolution of the measles virus (MeV) genome in an SSPE case suggested that the matrix (M) protein mutation M-F50S, when added to other mutations, drove neuropathogenesis. However, whether and how M-F50S would promote spread independently from other mutations was in question.
View Article and Find Full Text PDFA zebrafish-based in vivo model of Zika virus infection unveils alterations of the glutamatergic neuronal development and NS4A as a key viral determinant of neuropathogenesis.
PLoS Pathog
December 2024
Centre Armand-Frappier Santé Biotechnologie, Institut National de la Recherche Scientifique, Laval, Québec, Canada.
Infection of pregnant women by Zika virus (ZIKV) is associated with severe neurodevelopmental defects in newborns through poorly defined mechanisms. Here, we established a zebrafish in vivo model of ZIKV infection to circumvent limitations of existing mammalian models. Leveraging the unique tractability of this system, we gained unprecedented access to the ZIKV-infected brain at early developmental stages.
View Article and Find Full Text PDFImproving antibody-mediated protection against HSV infection by eliminating interactions with the viral Fc receptor gE/gI.
bioRxiv
November 2024
Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, NH 03756, USA.
Herpes simplex virus (HSV) encodes surface glycoproteins that are host defense evasion molecules, allowing the virus to escape immune clearance. In addition to their role in neuropathogenesis and cell-cell spread, glycoproteins E and I (gE/gI) form a viral Fc receptor (vFcR) for most subclasses and allotypes of human IgG and promote evasion of humoral immune responses. While monoclonal antibodies (mAbs) protect mice from neonatal HSV (nHSV) infections, the impact of the vFcR on mAb-mediated protection by binding to IgG is unknown.
View Article and Find Full Text PDFEnterovirus D68: Genomic and Clinical Comparison of 2 Seasons of Increased Viral Circulation and Discrepant Incidence of Acute Flaccid Myelitis-Maryland, USA.
Open Forum Infect Dis
November 2024
Division of Medical Microbiology, Department of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Article Synopsis
- Enterovirus D68 (EV-D68) is linked to severe respiratory illness and acute flaccid myelitis (AFM), with 2022 showing increased infections but no rise in AFM cases unlike in 2018, which had a significant surge in AFM.
- A study of 351 EV-D68 cases mainly involved children under 5, revealing that infections in 2018 led to more hospitalizations compared to 2022, and identified specific viral genomic changes associated with severe outcomes.
- The findings emphasize the need for ongoing viral genomic surveillance to better understand the connections between genomic changes, immune responses, and the severity of diseases like AFM.
Dengue virus NS1 hits hard at the barrier integrity of human cerebral microvascular endothelial cells via cellular microRNA dysregulations.
Tissue Barriers
November 2024
Molecular Biology Unit, Faculty of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
Dengue virus (DENV) infections are commonly reported in the tropical and subtropical regions of the world. DENV is reported to exploit various strategies to cross the blood-brain barrier. The NS1 protein of DENV plays an important role in viral neuropathogenesis, resulting in endothelial hyperpermeability and cytokine-induced vascular leak.
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