Natalie E. Cremer

Chronic Progressive Panencephalitis Due to Rubella Virus Simulating Subacute Sclerosing Panencephalitis

Late-onset chronic progressive panencephalitis developed in a 12-year-old boy with congenital rubella syndrome from whose brain rubella virus was isolated. Progressive dementia began at eight, and ataxia, choreiform movements, myoclonic seizures, and fine perimacular pigmentation appeared at 11 years of age. The cerebrospinal fluid was minimally pleocytotic and had a total protein of 156 mg per deciliter, of which 52 per cent was gamma globulin. Electroencephalography demonstrated generalized medium and occasional high-voltage slowing without burst suppression. The antibody titer to rubella virus (hemagglutination inhibition) was 1:8192 in serum and 1:256 in cerebrospinal fluid. Antibody titer to measles virus (complement fixation) was less than 1:8 in serum. Microscopical study of biopsied brain tissue at the age of 11 disclosed panencephalitis similar to subacute sclerosing panencephalitis, but with perivascular deposits and without inclusion bodies. Rubella virus was isolated from the brain by cocultivation with CV-1 cells.

Viruslike particles in muscle from a patient with amyotrophic lateral sclerosis.

An electron microscopic study of muscle and central nervous tissues from a case of amyotrophic lateral sclerosis showed crystalline arrays of 20 to 24 nm viruslike particles in muscle. The particles were located between the myofibrils, adjacent to the Z bands, and near the perinuclear region, but were never seen within the nucleus. Cell cultures from the same muscle specimens showed no such particles. Central nervous system tissues and cultures also failed to show viruslike particles. The cultures were negative by the indirect fluorescent antibody technique with serums from patients with amyotrophic lateral sclerosis. The nature of these particles or their relationship to amyotrophic lateral sclerosis is unknown.

Cyclic expression of antigen and infectious virus in a BHK cell line (0-853) persistently infected with an SSPE strain of measles virus.

Establishment and characteristics of a baby hamster kidney cell line (BHK 0-853) persistently infected with a subacute sclerosing panencephalitis (SSPE) strain of measles virus (Lec strain) is described. The persistent infection was easily and repeatedly established and no special conditions were required. There was a predictable fluctuation in expression of virus intracellular and membrane antigens which varied from greater than 90% to less than 1% of the cells demonstrating these antigens during the first 6 or 7 passages. Thereafter, fluctuation of antigen and infectious virus expression continued in an unpredictable fashion.

Tubular Particles in a Case of Recurrent Lymphocytic Meningitis Followed by Amyotrophic Lateral Sclerosis

A patient suffered recurrent episodes of aseptic lymphocytic meningitis for many years and then developed amyotrophic lateral sclerosis (ALS). Immune-complexes were deposited in the renal glomerular basement membrane and mesangia. The necropsy study revealed both lymphocytic meningitis and ALS. Study of the motor neurons with the electron microscope revealed proliferation of endoplasmic reticulum, small cytoplasmolytic areas and focal neurofibrillar accumulations in axons. Interwoven, serpentine 10–15 nm. tubules first appeared with ER proliferation and, presumably at a later stage, were sometimes present in large masses. These tubules might be virus material but virus cultures, including tissue culture, and animal inoculations have thus far been negative.

Biological Activity of a Monoclonal Antibody to a Measles Virus Haemagglutinin Epitope Detected Late in Infection

A hybrid cell line secreting monoclonal antibody 2H9c (mAb 2H9c) with measles virus haemagglutinin (HA) specificity was produced. The mAb 2H9c was non-reactive in haemagglutination inhibition and neutralization assays. A protein of apparent mol. wt. 79000 was immune-precipitated using a Triton X-100/SDS/sodium deoxycholate detergent buffer and two proteins with mol. wt. of 79000 and 69000 were immune-precipitated using 1% Nonidet P40/sodium deoxycholate buffer in SDS-PAGE assays. Similar results were obtained with other anti-HA monoclonal antibodies, supporting the assumption that mAb 2H9c was directed against the HA polypeptide. The indirect immunofluorescence (IFA) staining pattern of acetone-fixed infected cells with mAb 2H9c differed substantially from that with other HA-specific monoclonal antibodies. Kinetic studies revealed that the reactivity of mAb 2H9c lagged behind other HA-specific monoclonal antibodies by 18 to 36 h post-infection in IFA assays. This suggests that mAb 2H9c may be directed against a binding site that arises late in infection, possibly as a result of a conformational alteration of the HA polypeptide.