Dermcidin: Natural Protection Against Influenza Viruses
The protein dermcidin, produced by sweat glands, can inhibit the replication of the influenza virus and other respiratory infections. Higher concentrations of this substance are associated with greater resistance to illness and the absence of pronounced symptoms.
Salus
An antimicrobial peptide produced by sweat glands exhibits antiviral activity and, in particular, can suppress the replication of the influenza virus. Studies have shown that some people naturally have higher concentrations of this substance in their bodily fluids, which allows them to experience milder or even asymptomatic cases of influenza.
Properties of Dermcidin
Dermcidin is a protein synthesized by sweat glands and encoded by the DCD gene. About 25 years ago, it was discovered that dermcidin possesses both antibacterial and antifungal properties. Due to its constant presence in sweat and, consequently, on the skin’s surface, dermcidin plays a crucial role in protecting the body from bacterial and fungal infections as part of the innate immune system.
Antiviral Activity
Recent research has demonstrated that dermcidin’s protective function extends not only to bacteria and fungi but also to viruses. It has been established that this protein can block the replication of pathogens responsible for acute respiratory viral infections (ARVI), including influenza virus, measles virus, and coronavirus OC43. Respiratory viruses enter the body through the upper respiratory tract, affecting the mucous membranes of the nose, sinuses, throat, larynx, trachea, bronchi, and lungs.
Experimental Data
In laboratory conditions (in vitro), dermcidin effectively suppressed all tested strains of influenza A virus, as well as the measles virus and coronavirus OC43. In experiments on laboratory mice (in vivo), dermcidin prevented the spread of influenza A virus within the animals’ bodies.
Mechanism of Action
Dermcidin has been found to employ a novel antiviral mechanism. The protein binds to hemagglutinin—a key influenza virus protein necessary for the virus to enter cells. This interaction alters the structure of hemagglutinin, disrupting the virus’s ability to fuse with the cell membrane and initiate infection. As a result, the virus is inactivated before it can penetrate the cell.
This mechanism differs from that of most antiviral drugs against influenza, which block another viral protein—neuraminidase. Structural differences in neuraminidase among various strains allow the virus to evade the effects of these drugs, reducing their effectiveness. In contrast, dermcidin binds to a highly conserved region of hemagglutinin that remains virtually unchanged between strains, providing protection against different variants of the influenza virus. It is believed that a similar mechanism may also apply to other respiratory viruses, such as the measles virus and coronaviruses.
Dermcidin Concentration and Resistance to Infections
Dermcidin is found not only in sweat but also in other bodily fluids secreted at the main entry points for respiratory viruses—such as nasal secretions, saliva, and tears. During ARVI, the concentration of dermcidin in these fluids increases significantly. In people who are resistant to ARVI and do not experience typical symptoms, the baseline level of dermcidin in bodily fluids was found to be six times higher than in those susceptible to respiratory viral infections.
Application Prospects
The data obtained confirm that dermcidin is part of the first line of innate immune defense against respiratory viral infections. The protein is considered a promising candidate for the development of new strategies to combat such diseases.
