Sarcoidosis is a spontaneous disease of unknown cause. There are no known predisposing risk factors for developing sarcoidosis.
The heightened cellular immune response in the diseased tissue is characterized by significant increases in activated T-lymphocytes with certain characteristic cell-surface antigens, as well as in activated alveolar macrophages. This pronounced, localized cellular response is also accompanied by the appearance in the lung of an array of mediators that are thought to contribute to the disease process; these include interleukin-1, interleukin-2, B-cell growth factor, B-cell differentiation factor, fibroblast growth factor, and fibronectin. Because a number of lung diseases follow respiratory tract infections, ascertaining whether a virus can be implicated in the events leading to sarcoidosis remains an important area of research.
Some recent observations seem to provide suggestive leads on this question. In these studies, the genes of cytomegalovirus (CMV), a common disease-causing virus, were introduced into lymphocytes, and the expression of the viral genes was studied. It was found that the viral genes were expressed both during acute infection of the cells and when the virus was not replicating in the cells. However, this expression seemed to take place only when the T-cells were activated by some injurious event. In addition, the product of a CMV gene was found capable of activating the gene in alveolar macrophages responsible for the production of interleukin-1. Since interleukin-1 levels are found to increase in alveolar macrophages from patients with sarcoidosis, this suggests that certain viral genes can enhance the production of inflammatory components associated with sarcoidosis. Whether these findings implicate viral infections in the disease process in sarcoidosis is unclear.