German researchers have uncovered the molecular mechanism whereby virus infections cause cardiac arrhythmia.
Experts at the Max Delbruck Center for Molecular Medicine (MDC) Berlin-Buch say that they have discovered that the receptor that the virus uses to infect heart cells is normally necessary for regular heartbeat in mice.
Writing about their observations in the Journal of Experimental Medicine, the researchers say that arrhythmia occurs in the absence of the receptor.
They are of the view that both the virus infection and the autoimmune disease can block the receptor, which in turn disrupts the heart's normal rhythm.
The team points out that, for the heart to beat correctly and to pump blood through the body, specialized heart fibres generate electric signals that control the heartbeat.
According to them, an irregularity in such signals may give rise to cardiac arrhythmia, and a receptor called Coxsackievirus-Adenovirus-Receptor (CAR) plays an important role in it.
For determining what role does CAR play in a healthy organism, the researchers switched off the CAR-gene in adult mice, which rendered the animals unable to produce the receptor and gave rise to cardiac arrhythmia.
"That is an interesting observation because these special cell-cell-contacts, the tight junctions, have not been connected to arrhythmia so far," Professor Michael Gotthardt, a team member, said.
The researchers also observed that the transfer of electric signals from the atria to the ventricles did not work properly.
"When CAR is missing, the signal can not be passed on and the heart does not beat properly," Dr. Yu Shi, another researcher, said.
Professor Gotthardt now wants to investigate whether CAR is blocked in patients with arrhythmia.
"However, it does not always have to be connected to a virus infection. The body's own antibodies directed against CAR could cause the disease as well," he said.