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Effect of E2 envelope glycoprotein cytoplasmic domain mutations on Sindbis virus pathogenesis
B Levine1, H H Jiang, L Kleeman
1Department of Medicine, Columbia University College of Physicians & Surgeons, New York, New York 10032, USA.
Journal of Virology
|February 1, 1996
Summary
The E2 cytoplasmic domain influences Sindbis virus (SV) neurovirulence and persistent infection. Specific residues like tyrosine or serine are not essential for viral replication in the mouse brain.
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- The E2 envelope glycoprotein's cytoplasmic domain is crucial for Sindbis virus assembly.
- Its specific role in Sindbis virus encephalitis pathogenesis remains largely uncharacterized.
Purpose of the Study:
- To investigate the role of the E2 cytoplasmic domain in Sindbis virus pathogenesis.
- To determine the impact of mutations within this domain on viral neurovirulence and infection persistence.
Main Methods:
- Construction of six recombinant Sindbis viruses with site mutations in the E2 cytoplasmic domain.
- Utilizing the neurovirulent TE12 strain as a background.
- Infection studies in suckling and weanling scid mice.
Main Results:
- The E2 cytoplasmic domain is a key determinant of Sindbis virus growth and neurovirulence in suckling mice.
- This domain also influences persistent infection in weanling scid mice.
- Tyrosine, serine, or threonine residues are not essential for viral replication in the mouse brain or antibody-mediated restriction.
Conclusions:
- The E2 cytoplasmic domain plays a significant role in Sindbis virus pathogenesis, affecting neurovirulence and persistence.
- Specific amino acid residues within the domain are not critical for all aspects of viral replication or immune evasion.