A small peptide from scorpion venom has slowed two unrelated viruses in laboratory tests. A team led from Hubei University of Technology in Wuhan, China, tested the peptide, called BmKDfsin3, against the tick-borne SFTS virus and against herpes simplex virus 1, the virus behind cold sores. The results were published in Microbiology Spectrum on 28 October by Sun, Luo and colleagues.
The work is at a very early stage, but the combination of results makes it interesting: the two viruses are built differently and cause very different diseases, and the peptide affected both.
A peptide with a track record
BmKDfsin3 is a defensin, a type of small, disulphide-bonded peptide the immune system of many animals uses to fight infection. It comes from the venom of the scorpion Mesobuthus martensii and is made of 38 amino acids, held in shape by three disulphide bonds.
It has been studied before. In 2020, a group at the State Key Laboratory of Virology at Wuhan University reported that BmKDfsin3 reduced hepatitis C virus in liver cells, acting at the stage when the virus attaches to the cell and, more strongly, after it had entered. They suggested the effect may be linked to a signalling route called the p38 pathway.
Two very different viruses
SFTSV, the virus that causes severe fever with thrombocytopenia syndrome, is an RNA virus spread by ticks. Herpes simplex virus 1, or HSV-1, is a DNA virus that causes cold sores. The two have different genetic material and spread in different ways, so a single peptide affecting both stands out.
What the peptide did in cells
In human lung cells, BmKDfsin3 slowed both viruses, and the effect was stronger at higher doses. It mostly worked after the viruses had already got inside the cells, rather than stopping them from entering.
The team found evidence that the peptide acts in two ways at once. It blocks the p38 pathway that the viruses rely on to replicate, and it boosts the cells' own interferon defences, the first line of antiviral response.
Low toxicity so far
The peptide showed low toxicity to cells, to red blood cells and to mice.
How early this is
So far this is cell work plus a safety check in mice. The study does not show that the peptide protects an infected animal, let alone a person. The next steps would be tests in infected animals, work to understand how the two mechanisms fit together, and replication by other laboratories. For now, BmKDfsin3 is a useful lead for researchers studying antiviral peptides.