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The Cyclin-Dependent Kinase 5 Inhibitor Peptide Inhibits Herpes Simplex Virus Type 1 Replication.

Sci Rep. 2019 Feb 04;9(1):1260
Adrian Man 1 , Mark Slevin 2 , Eugen Petcu 3 , Cornel Fraefel 4
Adrian Man 1 , Mark Slevin 2 , Eugen Petcu 3 , Cornel Fraefel 4

[No authors listed]

Author information
  • 1 Department of Microbiology, University of Medicine and Pharmacy of Tîrgu Mureș, Târgu Mureș, Romania.
  • 2 School of Healthcare Science, Manchester Metropolitan University, Manchester, UK. M.A.Slevin@mmu.ac.uk.
  • 3 Griffith University, Gold Coast, Brisbane, Australia.
  • 4 Institute of Virology, University of Zurich, Zurich, Switzerland.

摘要


In order to evaluate the influence of CDK5 inhibitory peptide (CIP) on Human alphaherpesvirus 1 (HSV-1) replication, we constructed two recombinant adeno-associated-virus 2 (rAAV2) vectors encoding CIP fused with cyan-fluorescent-protein (CFP), with or without nuclear localization signal. A third vector encoding non-fused CIP and CFP was also constructed. HeLa and HEK 293T cells were infected with the rAAV-CIP vectors at multiplicity of infection (MOI) of 5000, in the absence or presence of a recombinant HSV-1 that encodes a yellow-fluorescent-protein (rHSV48Y; MOI = 1). Cells co-infected with rHSV48Y and rAAV vectors that did not express the CIP gene (rAAV-CFP-Neo) served as controls. At 24 h after infection, the effect of CIP on rHSV48Y replication was assessed by PCR, qRT-PCR, Western-blot, flow-cytometry, epifluorescence and confocal microscopy. We show that in cultures co-infected with rAAV-CFP-Neo, 27% of the CFP-positive cells present rHSV48Y replication compartments. By contrast, in cultures co-infected with CIP-encoding rAAV2 vectors and rHSV48Y only 6-20% of the cells positive for CIP showed rHSV48Y replication compartments, depending on the CIP variant. Flow-cytometry showed that less than 40% of the rHSV48Y/rAAV-CIP, and more than 75% of rHSV48Y/rAAV-CFP-Neo co-infected cells were positive for both transgene products. The microscopy and flow-cytometry data support the hypothesis that CIP is inhibiting HSV-1 replication.