The Peptide A-3302-B Isolated from a Marine Bacterium Micromonospora sp. Inhibits HSV-2 Infection by Preventing the Viral Egress from Host Cells
- Int J Mol Sci. 2022 Jan 15;23(2):947. doi: 10.3390/ijms23020947.
- 1. Chulabhorn Research Institute, Kamphaeng Phet 6 Road, Laksi, Bangkok 10210, Thailand.
- 2. Department of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, 10043 Orbassano, Italy.
- 3. Institute of Microbiology, ETH Zurich, Vladimir-Prelog-Weg 4, 8093 Zurich, Switzerland.
- 4. Institute of Marine Science, Burapha University, Chonburi 20130, Thailand.
- 5. Program in Chemical Sciences, Chulabhorn Graduate Institute, Chulabhorn Royal Academy, Kamphaeng Phet 6 Road, Laksi, Bangkok 10210, Thailand.
- 6. Center of Excellence on Environmental Health and Toxicology (EHT), OPS, Ministry of Higher Education, Science, Research and Innovation, Bangkok 10210, Thailand.
- 7. Department of Clinical and Biological Sciences, Neuroscience Institute of the "Cavalieri Ottolenghi" Foundation (NICO), University of Turin, 10043 Orbassano, Italy.
Herpesviruses are highly prevalent in the human population, and frequent reactivations occur throughout life. Despite Antiviral drugs against herpetic infections, the increasing appearance of drug-resistant viral strains and their adverse effects prompt the research of novel antiherpetic drugs for treating lesions. Peptides obtained from natural sources have recently become of particular interest for Antiviral therapy applications. In this work, we investigated the Antiviral activity of the peptide A-3302-B, isolated from a marine bacterium, Micromonospora sp., strain MAG 9-7, against herpes simplex virus type 1, type 2, and human cytomegalovirus. Results showed that the peptide exerted a specific inhibitory activity against HSV-2 with an EC50 value of 14 μM. Specific Antiviral assays were performed to investigate the mechanism of action of A-3302-B. We demonstrated that the peptide did not affect the expression of Viral Proteins, but it inhibited the late events of the HSV-2 replicative cycle. In detail, it reduced the cell-to-cell virus spread and the transmission of the extracellular free virus by preventing the egress of HSV-2 progeny from the infected cells. The dual Antiviral and previously reported anti-inflammatory activities of A-3302-B, and its effect against an acyclovir-resistant HSV-2 strain are attractive features for developing a therapeutic to reduce the transmission of HSV-2 infections.
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