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[Virus and autoimmune disease. An excursion exemplified by autoimmune hepatitis]
Leber, Magen, Darm
|January 1, 1992
Summary
Viruses infect lymphocytes, but not all dying cells show HIV. Autoimmune responses, potentially protective, may combat viral infections and contribute to autoimmune hepatitis pathogenesis.
Area of Science:
- Immunology
- Virology
- Pathogenesis
Background:
- Viruses, particularly human immune deficiency virus (HIV), are known to infect and cause deletion of lymphocytes, primarily CD4+ helper T-cells.
- The presence of HIV in only a fraction of dying lymphocytes suggests that other viral and non-viral cytotoxic mechanisms contribute to lymphocyte destruction.
Discussion:
- Autoimmune phenomena are increasingly recognized as playing a role in lymphocyte deletion and disease pathogenesis.
- Storch's hypothesis on viral infection of lymphocytes causing autoimmune hepatitis is supported by new findings, indicating involvement of multiple viruses.
Key Insights:
- Autoimmunity directed against viruses might be a physiological, protective mechanism against exogenous and endogenous factors.
- The role of autoantibodies and immune cells in autoimmune diseases can be pathogenic, protective, or indifferent.
Outlook:
- Further research into "autogenes" analogous to oncogenes may elucidate the development of autoimmune diseases.
- Understanding the complex interplay between viral infections, autoimmunity, and lymphocyte homeostasis is crucial for developing targeted therapies.