Role of Differences in Respiratory Syncytial Virus F and G Glycoproteins on Susceptibility to Inactivation by Antimicrobial Peptides LL-37 and Human Beta-Defensins.
Latsko. Karina N KN; Jacob. Andrew T AT; Junod. Nathan A NA; Haas. Caitlin E CE; Castiglia. Katelyn R KR; Kastelitz. Sydney R SR; Huffman. Elise R ER; Trombley. Michael P MP; Stobart. Christopher C CC
Key Findings
- LL‑37 inactivates RSV in a dose‑dependent, strain‑independent manner.
- Human beta‑defensin‑3 (hBD‑3) also shows dose‑dependent, strain‑independent RSV inactivation.
- hBD‑1 and hBD‑4 show variable antiviral activity depending on the viral F and G proteins.
Practical Outcomes
- For biohackers, boosting LL‑37 levels (e.g., through vitamin D supplementation or safe peptide use) might add a layer of protection against RSV, especially during cold‑season outbreaks. However, LL‑37 is not an over‑the‑counter product and its safety at antiviral doses is not fully established, so any self‑experimentation should be approached cautiously and preferably under professional guidance.
Summary
The study shows that the natural antimicrobial peptide LL‑37 can kill the RSV virus in a dose‑dependent way, no matter which strain of the virus is used. One of the human beta‑defensins (hBD‑3) does the same, while two others (hBD‑1 and hBD‑4) work inconsistently across strains. This suggests LL‑37 and certain defensins could help stop RSV infections or be used as a treatment.
Abstract
Antimicrobial peptides are proteins that have been found to be an important factor in the natural immune response to a variety of pathogens. Respiratory syncytial virus (RSV) is a respiratory pathogen with the capability to cause serious upper and lower respiratory infections in infants and children and is a major viral cause of infant mortality. There is currently no functional vaccine for the virus, as recent efforts have been hindered by the virus's low immunogenicity, its ability to effectively mutate, and underlying instabilities of potential vaccines. Previous studies have shown that antimicrobial peptides may affect viral replication and spread of RSV. Our study evaluates the susceptibility of chimeric strains of RSV that express different fusion (F) and attachment (G) proteins to susceptibilities to inactivation by LL-37 and human beta-defensins (hBDs) hBD-1, hBD-3, and hBD-4. We show that LL-37 and hBD-3 result in dose-dependent, strain-independent inactivation of RSV, whereas treatment with either hBD-1 or hBD-4 appears more variable between strains. This suggests a potential role of the viral structural proteins in mitigating the inhibitory effects of the peptides. This study provides the first evidence of the sensitivity of RSV to several hBDs and indicates a role of LL-37 and beta-defensins in both limiting establishment of natural RSV infections and in the therapeutic treatment of severe RSV disease.
Study Information
pubmed
2022
2022-08-09T00:00:00.000Z
10.1089/vim.2022.0063
3
37