Abstract
First, we thank Marie-Anne Rameix-Welti for the thoughtful comments on our recent paper (1). The M2-1 protein from respiratory syncytial virus (RSV) has for many years been rather enigmatic in allowing researchers to probe its structure and function, with details slow to emerge. In Selvaraj et al. (2), we suggested a model that posited that the requirement of M2-1 in RSV transcription involved binding of an M2-1 …
Highlights
As described above, the model we proposed has some notable gaps, but we view it as a starting point and hope the gaps may soon be closed following careful experimentation
The M2-1 protein from respiratory syncytial virus (RSV) has for many years been rather enigmatic in allowing researchers to probe its structure and function, with details slow to emerge
In Selvaraj et al. (2), we suggested a model that posited that the requirement of M2-1 in RSV transcription involved binding of an M2-1 tetramer to every viral mRNA transcript via its poly(A) tail, and one option we explored was that this interaction was maintained for the lifetime of the mRNA
Summary
The model we proposed has some notable gaps, but we view it as a starting point and hope the gaps may soon be closed following careful experimentation. We thank Marie-Anne Rameix-Welti for the thoughtful comments on our recent paper (1).
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