Publication: Role of oxidative damage in the pathogenesis
of viral infections of the nervous system
Authors
Valyi-Nagy, T. ; Dermody, T.S.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
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.
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