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02352 THETA-DEFENSINS PROTECT CELLS FROM INFECTION BY HERPES SIMPLEX VIRUS Yasin, Bushra*, Theta (q) ) defensins are cyclic octadecapeptides that are encoded by ?-defensin (DEFT) genes. Intact DEFT genes exist in various non-human primates, including Old World monkeys (rhesus and pigtail macaques), lesser apes, and orangutans. Three rhesus ?-defensin peptides (RTD-1, -2, and 3) were purified from the leukocytes and bone marrow of rhesus macaques. However, although the human genome contains at least six different DEFT genes, all of them contain a premature stop codon that stops translation. Thus, ?-defensin peptides are not present in human neutrophils. Retrocyclins 1, -2, and -3 are ?-defensins that could be expressed in human leukocytes if the human DEFT gene sequences lacked the premature stop codon. Previous studies have shown that retrocyclin-1 protected human cells from infection by T and M-tropic strains of HIV-1. Herpes simplex virus (HSV) is also a sexually-transmitted viral pathogen, and herpes infections may predispose to infection by HIV-1. We tested the ability of 20 synthetic ?-defensins to protect ME-180 cervical epithelial cells from infection by HSV-1 and HSV-2 using an MTT assay. The peptides included RTDs 1-3 and retrocyclins 1-3. We also tested 14 retrocyclin analogs, including the retro, enantio and retroenantio forms of retrocyclin-1. Peptides and viruses were co-incubated for 2 h before being added to target cell monolayers. Cells were then incubated at 37oC. for 72 h and viral infection and cytotoxicity were assessed. To study the mechanisms of retrocyclin action, we examined the binding of retrocyclin-2 to the HSV-2 glycoprotein gB2 in surface plasmon resonance studies. Temperature shift experiments were employed to determine whether q-defensins blocked viral attachment, penetration, and nuclear transport. To delineate the steps inhibited by theta-defensins, synchronized infections were induced and monitored to examine transport of the tegument protein VP 16 to the nucleus or expression of the immediate early gene product, ICP4. Retrocyclin-2 provided 100% protection from HSV-2 without causing cytotoxicity or requiring pre-incubation with the virus. Retrocyclin-2 additionally blocked viral attachment and markedly diminished HSV-2 nuclear translocation of VP 16 and ICP4 expression. Human ?-defensins HNP 1-3 also protected human cells from HSV-2 but had little effect on binding. Also, retrocyclin-2 bound to immobilized glycoprotein gB2 with high affinity (KD, 13.3 nM) but did not bind to enzymatically deglycosylated gB2. Given its small size (18 residues), minimal cytotoxicity, and effectiveness in inactivating both HSV-2 and HIV-1, retrocyclin-2 provides an intriguing prototype for topical viral microbicide development. Dr. Bushra Yasin |
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