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Searching for FIP treatments

Liu IJ, Tsai WT, Hsieh LE, et al. Peptides corresponding to the predicted heptad repeat 2 domain of the feline coronavirus spike protein are potent inhibitors of viral infection. PLoS One 2013;8:e82081. [free, full text article]

Feline infectious peritonitis, caused by feline coronavirus (FCoV), is a lethal immune-mediated disease and currently no therapy with proven efficacy is available. Many projects are searching for agents to treat or prevent this disease, including studies funded by Winn Feline Foundation. Already numerous antiviral drugs have been tested for their ability to inhibit FCoV replication, including carbohydrate-binding agents, cathepsin inhibitors, protease inhibitors, nitric oxide, siRNA and interferons. 

Viral spike protein heptad repeat (HR) peptides are another type of antiviral drug that has shown to efficiently block entry of the virus into cells and inhibit viral replication in in vitro studies in another deadly corona virus; namely, severe acute respiratory syndrome corona virus (SARS-CoV) in humans. Therefore, in this study, researchers from Taiwan investigated the efficacy of five analogous overlapping peptides based on the putative heptad repeat 2 (HR2) sequence of the FCoV spike protein.

Spike protein HR2 efficacy and toxicity were tested using two different cytotoxicity assays against feline cell cultures. One of the peptides, FP5, demonstrated inhibition of viral replication by approximate 97% for concentrations below 20 mM. Since FIP is considered an immune-mediated disease, the researchers further combined FP5 with human interferon-a, and a significant synergistic antiviral effect was observed.

This preliminary study suggests that FP5 peptide combined with human interferon-a may be a valuable addition in the treatment and prevention of FIP. Follow-up with clinical studies are warranted in order to determine whether these two combined agents are clinically efficacious and safe. [GO]

See also:
Tanaka Y, Sato Y, Sasaki T. Suppression of coronavirus replication by cyclophilin inhibitors. Viruses 2013;5:1250-1260. [free, full text article]