Callithrix jacchus marmosets infected with Epstein-Barr virus (EBV) with or without concurrent treatment with cyclosporin A (CySA) remained healthy. Five marmosets given virus alone developed lymphocytosis and heterophile antibody. Antibody to EBV capsid antigens (VCA) appeared and remained at titers of 1:40-1:80 from 15 weeks onward. Two animals produced antibody to the R component of early antigens (EA) from six weeks onward. Five CySA-treated EBV-infected marmosets showed no increase in total lymphocyte counts; only two developed heterophile antibody. Four developed persistent antibody to the EA-R component. All developed antibody to VCA, and mean titers were higher than in animals given EBV alone. Antibody to VCA also appeared in animals given EBV into Waldeyer's ring. Because these responses to EBV resemble those of humans, C. jacchus may provide a useful model for exploring the potential of cofactors in inducing EBV-associated malignancy.

The genetic information in a sub-fragment of EBV DNA, designated p31 (containing less than a quarter of the viral genome and derived from a recombinant DNA cosmid library) allows epithelial cells from primary monkey and human kidney cultures to escape senescence under standard tissue culture conditions. A number of epithelial cell lines, designated M1/31, 483/31, 199/31 and HK/31, have been established and characterized following transfection of primary cells with p31 DNA. They share many properties, although morphologically they are not all identical. The cultures are immortalized but not fully transformed or tumorigenic. They appear to be phenotypically stable, although DNA hybridization studies indicate that genotypic alterations, including amplification, occur subsequent to transfection with p31 DNA and the establishment of a continuously proliferating epithelium. All cell lines consistently express high levels of cytokeratin 18 and varying amounts of cytokeratin 7, demonstrating their epithelial origin. From a single marmoset kidney (designated 199) a series of related immortalized cells, with subtle phenotypic differences, have been generated by p31 or sub-fragments of it. Although hallmarks of a "hit-and-run" mechanism are apparent in all of our studies, 2 different techniques (in situ hybridization or selection for cell survival in semi-solid media, followed by nucleic acid hybridization) show that, in late-passaged cultures, a small proportion of the cells still contain some viral DNA. The studies focus on genetic information within the BamHI A and I regions as being relevant to immortalization. The role of the EBV DNA fragment in the genesis of epithelial cell lines is considered.

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SUMMARYPZasmodium berghei yoelii (p.b.y.) was found to cause an acute selflimiting infection in Balb/c mice, lasting for 14 to 18 days. A sharp fall in the primary response to sheep erythrocytes, as measured by the number of haemolytic plaque-forming cells in the spleen, and by the appearance of antibodies in the serum, coincided with high levels of parasitaemia between the 8th and I Ith days of p.b.y. infection. A secondary response to sheep erythrocytes was similarly affected when animals were infected with p. b.y. g days before the second antigen injection. Mice were resistant to reinfection with p.b.y., which produced either transient or no parasitaemia, and no immunodepression.In mice carrying an immunodepressive leukaemogenic virus by vertical transmission, infection with a similar dose of p.b.y. was usually fatal.Murine sarcoma virus (Harvey : m.s.v./H) produces tumours and splenomegaly in newborn mice but very rarely in adults. When injected into adult Balb/c mice at the height of p.b.y. infection, m.s.v./H produced a high incidence of splenomegaly 4 weeks later, although the splenomegaly induced by the plasmodium alone had by then subsided.These results are discussed in relation to Burkitt's (1969) hypothesis of a causal connection between chronic malarial infection and development of Burkitt lymphoma in children.