The Hallé subacute sclerosing panencephalitis (SSPE) measles virus isolate and its plaque-purified progeny were investigated to determine whether any unusual properties could be associated with its ability to cause persistent infection. Three types of plaque-purified progeny were isolated. One population appeared to be similar in biological and biochemical properties to laboratory-adapted measles virus and had the ability to induce syncytia (syn+). A second population (syn−) plaqued more efficiently at 39 °C than at 33 °C, did not cause normal cell fusion at either temperature, and produced particles that interfered with the replication of other measles virus isolates in vivo and in vitro. This syn− virus was further plaquepurified to eliminate the interfering particles, producing the syn− P2 virus. This virus also plaqued more efficiently at 39 °C than at 33 °C, but caused cell fusion only at 39 °C. Both syn− viruses and the parental virus were significantly less virulent in vivo than the syn+ virus and caused a more prolonged infection. Biochemical analysis showed that the syn− P2 population produced particles that banded at two different densities in potassium tartrate gradients; both densities were less than those of the standard laboratory measles virus and the syn+ virus. Although the syn− P2 virus did not cause cell fusion at 33 °C, [35S]methionine labelling demonstrated that the haemolysin/cell fusion protein was present in syn− P2 virions. The production of interfering particles, the inability to cause cell fusion at 33 °C, and the cold-sensitive nature of the syn− population appear to play a role in the ability of the Hallé SSPE virus to establish persistent infection.
HallW. W.,
MartinS. J.,
GouldE. A.1974; Defective interfering particles produced during the replication of measles virus. Medical Microbiology and Immunology 160:155–164
HallW. W.,
LambR. A.,
ChoppinP. W.1979; Measles and subacute sclerosing panencephalitis virus proteins: lack of antibodies to the M protein in patients with subacute sclerosing panencephalitis. Proceedings of the National Academy of Sciences of the United States of America 76:2047–2051
JosephB. S.,
CooperN. R.,
OldstoneM. B. A.1975; Immunologic injury of cultured cells infected with measles virus. I. Role of IgG antibody and the alternative complement pathway. Journal of Experimental Medicine 141:761–774
KratzschV.,
HallW. W.,
NagashimaK.,
Ter MeulenV.1977; Biological and biochemical characterization of a latent subacute sclerosing panencephalitis (SSPE) virus infection in tissue culture. Journal of Medical Virology 1:139–154
LucasA.,
CoulterM.,
AndersonR.,
DalesS.,
FlintoffW.1978; In vivo and in vitro models of demyelinating diseases. II. Persistence and host-regulated thermosensitivity in cells of neural derivation infected with mouse hepatitis and measles viruses. Virology 88:325–337
McKlmmJ.,
RappF.1977b; Variation in ability of measles virus plaque progeny to induce interferon. Proceedings of the National Academy of Sciences of the United States of America 74:3056–3059
MinagawaT.,
SakumaT.,
KuwajimaS.,
YamamotoT. K.,
HdaH.1976; Characterization of measles viruses in establishment of persistent infections in human lymphoid cell line. Journal of General Virology 33:361–379
WechslerS. L.,
FieldsB. N.1978; Differences between the intracellular polypeptides of measles and subacute sclerosing panencephalitis virus. Nature, London 272:458–460
WildT. F.,
DugreR.1978; Establishment and characterization of a subacute sclerosing panencephalitis (measles) virus persistent infection in BGM cells. Journal of General Virology 39:113–124