To evaluate the effects of F protein genetic variations from the globally dominant HRSV genotypes ON1 and BA9 on viral replication dynamics and pathogenicity.
Approach:
Recombinant Virus Generation: Two recombinant HRSV strains were generated by replacing the F gene in the Long-BAC backbone with F genes from clinical isolates BJ19-03 (ON1) and SY21-03 (BA9).
Phenotypic Assessment: The phenotypes of the recombinant viruses were assessed in cellular and animal models.
Key Findings:
Both recombinant viruses showed attenuated replication kinetics compared to the parental Long-BAC strain.
Peak viral titers were delayed by at least 12 hours post-infection.
In vivo, both recombinant viruses caused less severe disease than Long-BAC, with rLong-SY2103-BF displaying greater pathogenicity than rLong-BJ1903-AF.
Interpretation:
The findings indicate that both recombinant viruses exhibit reduced replication capacity and less severe pathogenic phenotypes compared to the Long-BAC parental strain.
Limitations:
The study does not establish direct clinical correlations due to confounding factors such as host immune status.
Conclusion:
The study provides insights into the genetic variations of HRSV and their effects on viral behavior.
