Infection of the thymus by the virus that causes fifth disease — the human parvovirus B19 — can induce thymus overgrowth (hyperplasia) contributing to the development of myasthenia gravis, researchers have found.
Myasthenia gravis is characterized by the increased production of antibodies that prevent the proper function of the AChR protein, which is essential for normal nerve-muscle cell communication.
Although it’s still unclear what causes this disease, thymus overgrowth has been shown to play a role. More than 80 percent of patients with early-onset myasthenia gravis have thymic hyperplasia and 10-15 percent of patients also have thymoma, a benign tumor in the thymus.
The thymus is a small organ responsible for the normal development of immune B- and T-cells, playing a key role in regulation of the immune system.
It’s been proposed that increased thymus inflammation caused by viral infections may contribute to autoimmunity, where the immune system attacks healthy cells in the body. In particular, B19 virus infection has been associated with the production of several autoantibodies — the antibodies that attack the body.
Based on these previous findings, researchers in China proposed evaluating the impact of this virus on the thymus of myasthenia gravis patients.
They analyzed 138 thymus tissue samples, of which 68 were representative of thymic hyperplasia, 58 of thymomas, and 12 were collected from healthy volunteers. Among these, 39 thymic hyperplasia and 23 thymoma samples were from myasthenia gravis patients.
They identified 28 cases of thymic hyperplasia and two cases of thymomas infected with the B19 virus. Of these, 13 were from myasthenia gravis patients. None of the healthy thymus samples were positive for the infection. Interestingly, the frequency of infected thymic hyperplasias was higher in the non-myasthenia gravis group.
When the team looked at the presence of viral proteins — a measure of active infection — they found that thymic hyperplasia with myasthenia gravis samples were more affected than those without the disease (74.36% versus 48.28%). Additionally, the proteins were mainly found in the sites where B-cells are, which could directly impact antibody production.
“Since the presence of viral protein indicates viral replication in tissues, it may also simultaneously imply a causal link with the disease,” the researchers wrote.
They also believe that these “findings revealed a previously unrecognized” cause of thymic hyperplasia-associated myasthenia gravis, “evoking numerous questions that require further investigation.”
They are planning to evaluate the impact of B19 virus infection on B-cell expansion and activation in the context of myasthenia gravis in a future study.