Acquired and congenital LCMV diseases are both caused by the combination of infection with the virus and the host immune response to the infection. In cases of acquired infection, the virus typically enters the human in an aerosolized form and is deposited in the lung, where initial viral replication occurs. This parenchymal lung infection often manifests as interstitial lung infiltrates and lung edema early in the course of disease. The virus then enters the blood stream and travels to other organs, where further viral replication occurs. Ultimately, LCMV reaches the meninges, choroid plexus, and ventricular ependymal linings, where the virus replicates to high titers and where the inflammatory response produces the characteristic pathology and symptoms of meningitis that give the virus its name.
In acquired LCMV infection, the host immune response is both protective and deleterious. The immune response is protective in the sense that it performs the critically important function of eliminating the virus and protecting against repeat infection. However, the immune response is deleterious in the sense that tissue inflammation underlies the symptoms of disease.