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Updated: Jun 19, 2026

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
Vascular and glomerular manifestations of viral hepatitis B and C: a review
1Department of Pathology, University Health Network/University of Toronto, 200 Elizabeth Street, Toronto, ON M5G 2C4, Canada. oyedele.adeyi@uhn.on.ca
Abstract:
Secondary vasculopathies have varied etiologies that include paraneoplastic processes (eg, migratory thrombophlebitis, urticarial vasculitis); direct invasion by tumors (eg, superior and inferior vena cava syndrome); metabolic diseases (eg, diabetes mellitus); and infections, among others. The infective causes of vasculitides could result from direct involvement of vessels by a vasculo-tropic agent (eg, mucor infection); adjacent inflammation nonspecifically affecting nearby vessels; or from infection-induced immune-mediated vasculitis. Viruses represent a major group in the development of the latter, and many human viruses have been reported to cause vasculitis. The vasculitic lesions secondary to hepatitis B and hepatitis C viruses largely fall within the spectrum of immune-mediated secondary vascular injury and are discussed in this review.
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