Virus-induced autoantibody response to a transgenic viral antigen

Article Abstract:

The production of autoantibodies (antibodies made against a component of the body that is mistakenly recognized as foreign) and the role of autoantibodies in the development of autoimmune diseases is not fully understood. It is thought that pathogenic organisms may trigger the autoimmune response. The mechanisms for the normal state of unresponsiveness against body components are also not fully understood. B lymphocytes, which mature and produce the antibody molecules, may be aborted or killed during development, inactivated, or suppressed. To evaluate the unresponsiveness of B cells, transgenic mice (mice receiving foreign DNA at the embryo stage) were given the gene encoding the cell membrane-associated glycoprotein of the vesicular stomatitis virus (VSV-G). These transgenic mice expressed the VSV-G as a protein that was not recognized as foreign. Autoantibodies to VSV-G could not be induced by the injection of the protein into the mice. However, an immune response was induced by infection of the transgenic mice with the whole virus. It is thought that the B cells must take up and modify the antigen, in this case the VSV-G protein, to allow interaction with helper T cells, which are necessary for the production of an immune response. These data show that for B cells to be inactive, helper T cells must also be inactive. Helper T cells against foreign bodies are needed to break the inactivity of B cells. A direct physical interaction of T and B cells must occur for tolerance to be broken, and for an immune response to occur. This study increases the understanding of how viruses can trigger autoimmunity against the body's own components. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, Autoimmune diseases, Viruses, Autoimmunity, Genetically modified mice

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Original antigenic sin impairs cytotoxic T lymphocyte responses to viruses bearing variant epitopes

Article Abstract:

Mice primed with lymphocytic choriomeningitis virus-WE strain respond to a subsequent infection by WE-derived cytotoxic T lymphocyte (CTL) epitope variants with a CTL response directed towards the initial epitope, rather than towards the new variant epitope. This finding extends the concept of original antigenic sin to CTLs. Original antigenic sin by CTL produces impaired clearance of variant viruses infecting the same individual. This may boost the immune escape of mutant viruses evolving in an individual host.

Viral antigens

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A non-retroviral RNA virus persists in DNA form

Article Abstract:

Genetic research has established that virus-specific genome patterns of the non-cytopathic segmented ribonucleic acid (RNA) virus lymphocytic choriomeningitis exist as deoxyribonucleic acid (DNA) strands in mice after more than 200 days following infection. The exogenous RNA virus interacts with endogenous retroviral via a new pathological route which may be useful in DNA vaccine development.

Virus diseases, RNA viruses

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