Cellular and Molecular Biology



Role of oxidative damage in the pathogenesis of viral infections of the nervous system

T. Valyi-Nagy1 and T.S. Dermody2,3,4

Department of 1Pathology, University of Illinois at Chicago, College of Medicine, Chicago, Illinois and Departments of 2Microbiology and Immunology and 3Pediatrics and 4Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, Tennessee

Offprint requests to: Terence S. Dermody, Lamb Center for Pediatric Research, D7235 MCN, Vanderbilt University School of Medicine, Nashville, TN, 37232, USA. e-mail: terry.dermody@vanderbilt.edu

Summary. Oxidative stress, primarily due to increased generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), is a feature of many viral infections. ROS and RNS modulate the permissiveness of cells to viral replication, regulate host inflammatory and immune responses, and cause oxidative damage to both host tissue and progeny virus. The lipid-rich nervous system is particularly susceptible to lipid peroxidation, an autocatalytic process that damages lipid-containing structures and yields reactive by-products, which can covalently modify and damage cellular macromolecules. Oxidative injury is a component of acute encephalitis caused by herpes simplex virus type 1 and reovirus, neurodegenerative disease caused by human immunodeficiency virus and murine leukemia virus, and subacute sclerosing panencephalitis caused by measles virus. The extent to which oxidative damage plays a beneficial role for the host by limiting viral replication is largely unknown. An enhanced understanding of the role of oxidative damage in viral infections of the nervous system may lead to therapeutic strategies to reduce tissue damage during viral infection without impeding the host antiviral response. Histol Histopathol 20, 957-967 (2005)

Key words: Brain, Lipid peroxidation, Nervous system, Oxidative damage, Oxidative stress, Viral pathogenesis, Virus

DOI: 10.14670/HH-20.957