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Trypsin- and acetone-treated virions from either of two strains of measles virus grown in Vero cells stimulated the production in guinea pigs of (i) virus-specific antibodies to polypeptide (P) of molecular weight 70,000 (70K) and to the portion of the HA spike embedded in the viral envelope, but not to M protein, and (ii) antibodies to two host cell membrane antigens which were identified as glycoproteins with molecular weights of 108K and 104K. These host cell antigens were present in increased amounts in infected cells and were intimately associated with the virus. Untreated measles virions grown in Vero cells also stimulated the production of antibody to the 108K glycoprotein. The host polypeptides were less antigenic in virus derived from HEp2 cells, which apparently contained less of these antigens.

T-cell control of Epstein-Barr virus (EBV)-infected autologous lymphocytes was examined in 25 multiple sclerosis (MS) patients and in 25 healthy individuals, all seropositive for EBV. By assessing regression of cell transformation, 17 patients and all healthy subjects were scored as “regressors”. Eight MS patients proved to be “nonregressors”, indicating loss of cytotoxic T-cell control. In this group there was apparently a concurrent fall in the mean titer of antibody to Epstein-Barr nuclear antigen.

Summary The haemolysin of measles virus, either in the virion or in infected cells, is functionally and antigenically sensitive to acetone. Absorption of human sera with acetone-treated, measles virus-infected cells removes antibodies to all measles virus structural antigens except haemolysin. The antibody titres of absorbed sera give good correlation in HLI, neutralization and fluorescent antibody staining on unfixed infected cells.

Summary The antigenic determinants of the haemagglutinin and haemolysin antigens of measles virus were located at the surface of HEp2 cells infected with measles virus and on measles virions released from these cells, using immunoelectron microscopy. Antisera specific for haemagglutinin or haemolysin antigen and peroxidase-conjugated antiglobulin were used. Treatment of the infected cells with trypsin removed the virus spikes and prevented binding by the anti-haemagglutinin serum, while the reaction with anti-haemolysin serum was unaltered. This suggests that the antigenic determinants for measles haemagglutinin reside on the spike, while the antigenic determinants for haemolysin reside on, or are close to, the virus membrane.