
A research team in Spain has demonstrated that dermcidin, an antimicrobial peptide naturally produced by the body, exhibits antiviral activity against the influenza virus. In fact, the study shows that baseline levels of dermcidin are up to 6x higher in individuals who do not develop flu-like symptoms.
Dermcidin is an antimicrobial peptide produced by eccrine sweat glands and secreted onto the skin as part of a human’s innate immune system. It acts as a crucial, constitutive barrier against pathogens, effectively killing bacteria and fungi on the skin surface. Now, researchers have discovered another use for it: fending off the flu.
During their study, published in PNAS, a research team from Universidad Miguel Hernandez de Elche noted that dermcidin binds to hemagglutinin—a protein essential for the influenza virus to enter the cell—at a key region involved in the fusion process. This interaction induces a change in the viral protein that impairs the flu virus’s ability to fuse with the cell membrane and, therefore, commence infection.
In this way, dermcidin inactivates the virus before it can infect the cell through a previously unknown mechanism. This mode of action contrasts with that of most antivirals, which target neuraminidase—a different viral protein. That’s a different, but related, problem as resistance is growing due to continued reliance on neuraminidase targeting.
“By acting on regions of the virus that hardly change between subtypes—known as highly conserved regions—dermcidin could contribute to defense against different variants of the influenza virus,” said lead study author María Ferrer, head of the Antimicrobial Peptides and Glycobiology group at Fisabio.
According to the study results, baseline levels of dermcidin are up to 6x higher in people who do not develop flu-like symptoms, compared with susceptible individuals. Additionally, the researchers discovered that during a respiratory infection, dermcidin concentration increases significantly.
The researchers also found that dermcidin is present not only in sweat but also in the main entry points for respiratory viruses, including the nose, saliva and tears.
“Altogether, these findings reinforce the idea that dermcidin is part of the innate immune system’s first line of defense against this type of infection,” said Paula Corell, the study’s first author and member of the team.
The researchers say the same mode of action dermcidin takes to inactivate the influenza virus could be extended to other respiratory viruses, such as measles and coronaviruses associated with the common cold.
“These results show that our own bodies have natural mechanisms capable of curbing viral infection, which opens the door to the development of new, more effective antivirals,” said study co-author Álex Mira, head of the Oral Microbiome group at Fisabio.
These study findings open new research paths for the development of antivirals based on the body’s own natural molecules, which would not only enhance effectiveness against various respiratory viruses but also help limit emerging and growing resistance.
Next, the research team says they will investigate whether dermcidin may also play an immunomodulatory role, helping regulate the immune system’s response to infection.