“Doctors have plenty of antibiotics to fight bacterial infections but few antiviral drugs. Although these are early days, and we don’t yet know whether all viruses are cleared by this mechanism, we are excited that our discoveries may open multiple avenues for developing new antiviral drugs,” said Dr Leo James, leader of the study at the Laboratory for Molecular Biology in Cambridge.
The body fights infections by unleashing antibodies that stick to viruses as they circulate in the bloodstream. For many years, scientists working on immunity generally believed this made it harder for viruses to get inside healthy cells and spread the illness through the body.
But the new study has shown that for many viruses, antibodies follow the invader inside the cell and co-ordinate an immune attack from within.
Immunologists once believed that antibodies went to work only outside cells. Once a virus had invaded a cell, it was thought to be too late for the immune system to do anything.
Viruses are responsible for influenza, the common cold, smallpox, chickenpox, shingles, herpes, polio, rabies, Ebola, hanta fever, Aids and various forms of cancer.
The new study shows that once inside an infected cell, antibodies attract a protein called TRIM21. This turns on the cell’s equivalent of a waste disposal machine, a large cluster of proteins called a proteasome. The proteasome latches on to TRIM21 and goes to work, dismantling the virus piece by piece, often before the virus has a chance to cause harm. The discovery, which is reported in the journal Proceedings of the National Academy of Sciences, could pave the way for a new generation of antiviral drugs that fight infections by supercharging the body’s own defences.
Future treatments based on this research are expected only to work against a class of viruses that do not shed their protein coats when they invade healthy cells. Those that do would leave the attached antibodies outside the cells, and so not trigger the cell’s own immune attack.