Kenneth P. Johnson

Hydrocephalus as a sequela of experimental myxovirus infections

Abstract Suckling hamsters and mice were inoculated intracerebrally with several human myxoviruses. Mumps virus and parainfluenza-2 (croup-associated) virus were shown to infect ependymal cells in hamsters; this acute infection did not cause clinically apparent disease but resulted in the loss of ependymal cells. Influenza-A virus caused infection of ependymal cells in both hamsters and mice in which antigen developed, but no infectious virus multiplication was found; nevertheless, similar ependymal cell loss ensued. Following this selective destruction of the ependymal cell population by either mechanism, narrowing of the aqueduct of Sylvius evolved in most animals resulting in the development of severe hydrocephalus. The noninflammatory aqueductal stenosis showed several histological similarities to human aqueductal stenosis of obscure etiology. The possibility of acute infections causing noninflammatory yet progressive sequelae is discussed.

Virus-Induced Hydrocephalus: Development of Aqueductal Stenosis in Hamsters after Mumps Infection

Hydrocephalus developed as a sequela of mumps virus infections of suckling hamsters. The initial infection after intracerebral inoculation was limited largely to ependymal cells lining the ventricles. This infection was clinically inapparent but later resulted in a noninflammatory stenosis or occlusion of the aqueduct of Sylvius.

Subacute sclerosing panencephalitis (SSPE) agent in hamsters: III. Induction of defective measles infection in hamster brain☆

Abstract A hamster-adapted SSPE agent was shown to cause a productive infection in weanling hamster brain which changed to a cell-associated or defective infection coincident with the appearance of measles antibodies in serum. Antibodies to measles hemagglutinin, hemolysin and nucleocapsid antigens developed in serum which also contained neutralizing activity for regular measles virus. The agent recovered from brains prior to the appearance of serum antibodies was infectious in cell free media, capable of rapidly destroying Vero cell cultures and able to progressively destroy primary hamster brain cultures. In contrast, the agent recovered from brain after serum antibodies were present was infectious only within cells, destroyed Vero cells ineffectively and spread slowly through primary brain tissue cultures releasing minute amounts of extracellular virus intermittently even though no measles antibodies were present in the culture media. Nevertheless, infected giant cells in the primary brain cultures contained both the HA and HL measles antigens in their cytoplasmic membranes. This in vivo conversion of a productive to a cell-associated cerebral infection appeared to be caused by the host antibody response and may mirror the initial events of human SSPE and possibly other slow or latent measles infections of the CNS.

Subacute sclerosing panencephalitis (SSPE) agent in hamsters: I. Acute giant cell encephalitis in newborn animals

Abstract A viral agent, isolated from brain-derived tissue culture from a patient with subacute sclerosing panencephalitis (SSPE) and adapted to hamsters was used to infect newborn hamsters. Viral replication occurred only after intracerebral inoculation. The agent produced an acute giant cell encephalitis during which virus probably spread from primary periventricular foci to cortical foci via neuronal dendrites. Except for its increased rapidity of effect, the infection was identical to that produced by neuroadapted strains of measles virus in the same host.

Subacute sclerosing panencephalitis (SSPE) agent in hamsters: II. The neuropathology of acute and chronic infections☆

Abstract A human subacute sclerosing panencephalitis (SSPE) virus adapted to the hamster central nervous system produced a chronic form of inclusion cell encephalitis when inoculated intracerebrally into immature hamsters. The pathology produced by this infection was focal, but otherwise had many of the characteristics of SSPE in man, including similar types of inclusion bodies. The same dose of virus produced acute, fatal, giant cell encephalitis in newborn hamsters and an inapparent inclusion cell encephalitis in adults. The pathology of the hamster infection was compared to the human disease and some other experimental animal studies of SSPE.