Endogenous Retroviruses in Pathogenesis of Autoimmunity

April 11, 2001

Editorial J Rheumatol vol 28, no 3, March 2001.

Viral infections often lead to inflammatory syndromes where arthralgias or

arthritis may represent a major manifestation.

Considerable evidence indicates that viruses may also be involved in

pathogenesis of autoimmune rheumatic diseases. Based on the hypothesis that

molecular interactions between the host genome and environmental factors are

critical for autoimmunity, endogenous retroviruses (ERV) are of particular

importance.

They belong to the larger family of retrotransposable elements that make up

as much as 40% of the human genome. ERV may have originated from exogenous

retroviruses that integrated into the genome and became trapped owing to

mutations of essential genes.

Human ERV have generally been found to be defective proviruses. They

represent a large reservoir of viral genes that may be activated by

mutations caused by radiation or chemicals, or recombination with exogenous

retroviruses.

While exogenous retroviruses are infectious, with a replication cycle that

requires integration of proviral DNA into host cell DNA, ERV are transmitted

genetically in a classical mendelian fashion through the germline as

proviral DNA. Expression of ERV can influence the outcome of infections in

different ways both beneficial and detrimental to the host. These include

provision of genes for recombination with exogenous viruses, interference

with virion assembly, blocking cellular receptors for viral entry, and

modulation of immune responses to exogenous viruses.

ERV may lead to autoimmunity directly, by encoding autoantigens, or

indirectly, by affecting the expression of genes regulating immune responses

and tolerance.

The entire editorial can be found at:

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