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Is the acetylcholine receptor a rabies virus receptor?
Science (New York, N.Y.)
|January 8, 1982
Summary
Rabies virus infection in muscle cells correlates with acetylcholine receptors. Blocking these receptors with specific toxins reduced viral infection, suggesting they are key entry points for rabies virus.
Area of Science:
- Neurovirology
- Cellular Biology
- Molecular Neuroscience
Background:
- Rabies virus infects the nervous system, causing a fatal disease.
- The initial sites of viral entry and spread in peripheral tissues are not fully understood.
- Acetylcholine receptors are crucial for neuromuscular transmission.
Purpose of the Study:
- To investigate the role of acetylcholine receptors in rabies virus infection.
- To determine if acetylcholine receptors act as entry points for rabies virus in muscle cells.
Main Methods:
- Localization of rabies virus on mouse diaphragms and cultured chick myotubes.
- Treatment of cultured myotubes with alpha-bungarotoxin and d-tubocurarine prior to viral exposure.
- Assessment of viral infection rates in treated and untreated myotubes.
Main Results:
- Rabies virus distribution in muscle tissues mirrored acetylcholine receptor locations.
- Pre-treatment with alpha-bungarotoxin and d-tubocurarine significantly decreased rabies virus infection in myotubes.
- These findings indicate a specific interaction between rabies virus and acetylcholine receptors.
Conclusions:
- Acetylcholine receptors likely serve as receptors for rabies virus.
- Viral binding to acetylcholine receptors at neuromuscular junctions may facilitate localized concentration.
- This concentration mechanism could promote viral uptake by peripheral nerves and subsequent transport to the central nervous system.