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The Semliki Forest virus E2 gene as a virulence determinant
M G Santagati1, J A Määttä, P V Itäranta
1Turku Immunology Centre, University of Turku, Finland.
The Journal of General Virology
|January 1, 1995
Summary
The Semliki Forest virus variant A774 (SFV A7) shows high genetic similarity to the prototype strain L10. Amino acid changes in the E2 glycoprotein of SFV A7 contribute to its reduced virulence in mice.
Area of Science:
- Virology
- Molecular Biology
- Genetics
Background:
- Semliki Forest virus (SFV) is an alphavirus with both virulent and avirulent strains.
- Understanding the genetic basis of SFV virulence is crucial for developing effective control strategies.
Purpose of the Study:
- To determine the nucleotide and amino acid sequences of key genes in the avirulent SFV A774 (SFV A7) strain.
- To investigate the role of specific genetic alterations, particularly in the E2 glycoprotein, in SFV attenuation.
Main Methods:
- Nucleotide sequencing of SFV A7 genes (capsid, E3, E2, 6K) and comparison with SFV L10.
- Construction of a recombinant virus (CME2) by replacing the E2 gene of virulent SFV4 with that of SFV A7.
- In vitro replication studies in mouse brain cell lines (MBA 13).
- In vivo virulence studies in BALB/c mice via intraperitoneal injection.
Main Results:
- SFV A7 shares high nucleotide identity (97-98%) with SFV L10.
- SFV A7 exhibits distinct amino acid substitutions in capsid, E3, and E2 proteins compared to L10.
- The recombinant virus CME2, containing the SFV A7 E2 gene, replicated similarly to SFV4 in vitro.
- CME2 infection caused mild or asymptomatic disease in mice, unlike the lethal effect of SFV4, indicating attenuation.
Conclusions:
- Amino acid differences in the E2 glycoprotein are strongly implicated in the attenuation of SFV A7.
- The E2 glycoprotein plays a significant role in determining the virulence of Semliki Forest virus strains.