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Peptide versus gene therapy: Cathelicidin LL ‐37 and HSV ‐1 corneal infection
Author(s) -
Griffith M.,
Lee C.J.,
Buznyk O.
Publication year - 2015
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2015.0188
Subject(s) - cathelicidin , herpes simplex virus , transfection , virology , peptide , virus , microbiology and biotechnology , in vitro , biology , cell culture , chemistry , antimicrobial peptides , biochemistry , genetics
Summary We compared the performance of biosynthetic corneal implants based on collagen‐phosphorylcholine (Coll‐ MPC ) with anti–Herpes Simplex Virus ( HSV )‐1 activity achieved by sustained release of the cathelicidin LL ‐37 from incorporated nanoparticles, to cell‐based delivery of the peptide from human corneal epithelial cells ( HCEC s) transfected to produce endogenous LL ‐37. LL ‐37 released from the implants blocked HSV ‐1 infection of HCEC s by interfering with viral binding. However, in pre‐infected HCEC s, LL ‐37 delayed but could not prevent viral spreading nor clear viruses from the infected cells. HCEC s transfected with the LL ‐37 to confer viral resistance expressed and secreted the peptide. Secreted LL ‐37 inhibited viral binding in vitro but was insufficient to protect cells completely from HSV ‐1 infection. Nevertheless, secreted LL ‐37 reduced both the incidence of plaque formation and plaque size. LL ‐37 released from composite nanoparticle‐hydrogel corneal implants and HCEC ‐produced peptide, both showed anti– HSV ‐1 activity by blocking binding. While both slowed down virus spread, neither was able on its own to completely inhibit the viruses.