Table 3.
Protein | AA position | AA change | Number of Population Samples | Virus variants |
---|---|---|---|---|
VP3 | 204 | A > V | 8 | WT 372 299 |
VP4 | 17 | N > D | 6 | WT 372 299 |
VP4 | 20 | G > S | 6 | WT 372 299 |
3D | 452 | S > P | 6 | WT 372 299 |
3B | 6 | V > L | 5 | WT 372 |
VP2 | 138 | D > N | 4 | WT 299 |
VP4 | 21 | N > D | 4 | WT 372 |
VP4 | 15 | R > G | 4 | 372 299 |
2B | 11 | N > D | 4 | 372 299 |
VP4 | 23 | I > T | 4 | 372 299 |
Implementing our method on one of the CVB wild-type samples, and recording the changes throughout the passages (1, 60 and 120), the positions demonstrating the highest increase in variant allele rate was detected. Out of the top 10 most changing positions, only four were non-structural, one synonymous in the viral protease (3C) one nonsynonymous in 2B and two non-synonymous in the viral polymerase (3D). The polymerase variants were then recognized as variants already known to modulate viral replication fidelity.