Asset Details
Do you wish to reserve the book?
Knockout of signal peptide peptidase in the eye reduces HSV-1 replication and eye disease in ocularly infected mice
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Knockout of signal peptide peptidase in the eye reduces HSV-1 replication and eye disease in ocularly infected mice
Do you wish to request the book?
Knockout of signal peptide peptidase in the eye reduces HSV-1 replication and eye disease in ocularly infected mice
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Knockout of signal peptide peptidase in the eye reduces HSV-1 replication and eye disease in ocularly infected mice
2022
Overview
We previously reported that knocking out signal peptide peptidase (SPP), a glycoprotein K (gK) binding partner, in mouse peripheral sensory neurons reduced latency-reactivation in infected mice without affecting primary virus replication or eye disease. Since virus replication in the eye plays an essential role in eye disease, we generated a conditional knockout mouse lacking SPP expression in the eye by crossing Pax6 (paired box 6)-Cre mice that have intact Pax6 expression with SPP flox/flox mice. Significantly less SPP protein expression was detected in the eyes of Pax6-SPP -/- mice than in WT control mice. HSV-1 replication in the eyes of Pax6-SPP -/- mice was significantly lower than in WT control mice. Levels of gB, gK, and ICP0 transcripts in corneas, but not trigeminal ganglia (TG), of Pax6-SPP -/- infected mice were also significantly lower than in WT mice. Corneal scarring and angiogenesis were significantly lower in Pax6-SPP -/- mice than in WT control mice, while corneal sensitivity was significantly higher in Pax6-SPP -/- mice compared with WT control mice. During acute viral infection, absence of SPP in the eye did not affect CD4 expression but did affect CD8α and IFNγ expression in the eye. However, in the absence of SPP, latency-reactivation was similar in Pax6-SPP -/- and WT control groups. Overall, our results showed that deleting SPP expression in the eyes reduced primary virus replication in the eyes, reduced CD8α and IFNγ mRNA expression, reduced eye disease and reduced angiogenesis but did not alter corneal sensitivity or latency reactivation to HSV-1 infection. Thus, blocking gK binding to SPP in the eye may have therapeutic potential by reducing both virus replication in the eye and eye disease associated with virus replication.
Publisher
Public Library of Science,Public Library of Science (PLoS)
