Downregulation of Cell Surface Major Histocompatibility Complex Class I Expression Is Mediated by the Left-End Transcription Unit of Fowl Adenovirus 9
Round 1
Reviewer 1 Report
The MS by Griffin et al discusses the effect of the fowl adenovirus left genomic end on MHCI expression. Thorough research was conducted to shed light on the possible mechanisms, and the achieved conclusions seem to be supported by the results.
A major request would be to enhance figure quality. The figures are either saved at a low resolution or at a high compression, which makes them often hard to interpret. Especially figure legends are written using minuscule letters.
Further questions, recommended edits and comments are available in the edited, attached, downloadable MS, please include those in your answer as well.
Comments for author File: 
Comments.pdf
Author Response
Please see the attachment with point-by-point responses followed by the responses to the comments embedded in the manuscript.
Author Response File: Author Response.pdf
Reviewer 2 Report
The Authors investigated an interesting topic and the findings are of practical application in poultry industry and farming.
The manuscript was properly structured and results well properly reported.
However, some minor changes could be made before a possible acceptance of the paper.
Here, I am reporting some suggestions aiming to further improve the paper:
Pay attention to the minor remarks:
line 38 : please change" species" for "types"
So, I recommend the acceptance of the manuscript
Author describe the degree of specificity for FAdV-9-induced downregulation of MHC , and were examined the expression of the cell surface personated of the transferrin receptor (TfR), a membrane glycoprotein expressed at low levels that is nonetheless commonly used as a specificity control for MHC-I surface analyses.
This is the first study to report the effects of FAdVs on the downregulation of surface expression of MHC-I molecules. The data presented by authors suggests that one of the mechanisms for reduced MHC-I during infection is an FE1-driven process that results in intracellular sequestration of MHC-I that could be attributed to a generalized block in the se- cretory pathway. This work provides the foundation for further studies on FAdV pathogenesis and development of next-generation FAdV-based vaccines with increased efficiency.
Author Response
We thank the reviewers very much for their constructive comments. The manuscript has benefited by addressing these suggestions and comments, and we hope that our reply to the comments has satisfactorily addressed these concerns.
Reviewer #2:
The Authors investigated an interesting topic and the findings are of practical application in poultry industry and farming.
The manuscript was properly structured and results well properly reported.
However, some minor changes could be made before a possible acceptance of the paper.
Here, I am reporting some suggestions aiming to further improve the paper:
Pay attention to the minor remarks:
line 38 : please change" species" for "types"
Thank you for identifying this error. We have corrected the text accordingly.
So, I recommend the acceptance of the manuscript
Author describe the degree of specificity for FAdV-9-induced downregulation of MHC , and were examined the expression of the cell surface personated of the transferrin receptor (TfR), a membrane glycoprotein expressed at low levels that is nonetheless commonly used as a specificity control for MHC-I surface analyses.
This is the first study to report the effects of FAdVs on the downregulation of surface expression of MHC-I molecules. The data presented by authors suggests that one of the mechanisms for reduced MHC-I during infection is an FE1-driven process that results in intracellular sequestration of MHC-I that could be attributed to a generalized block in the se- cretory pathway. This work provides the foundation for further studies on FAdV pathogenesis and development of next-generation FAdV-based vaccines with increased efficiency.
