The DNA-containing Epstein-Barr herpesvirus has been implicated in the etiology of Burkitt's lymphoma, a malignant tumor of children in Africa. Recently, however, particles possessing four biochemical characteristics of RNA tumor viruses have also been identified in these tumors. The fact that both types of viruses are found suggests that an interaction between them niay be playing a role in the etiology of Burkitt The detection of viral-specific RNA in animal tumors by means of molecular hybridization (1) has been a useful tool in relating the etiology of these tumors to oncogenic RNA viruses (2, 3). Recently, radioactive DNA complementary to the RNA of the Rauscher murine leukemia virus was shown to hybridize with the RNA from murine and human leukemias (4), lymphomas (5), and sarcomas (6). Further, radioactive DNA complementary to the RNA of the mouse mammary tumor virus hybridized specifically with the RNA from murine mammary tumors (3) and from human malignant breast tumors (7).Burkitt's disease, a malignant lymphoma first described among African children, has been linked by means of seroepidemiology (8-10), electron microscopy (11), and molecular hybridization (12)

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Adaptation of the Hawaiian strain of dengue virus to growth in the brain of young adult Swiss mice was a gradual process (1). When serial transfers were made with 10 per cent mouse brain suspensions serving as inocula, it required 15 passages before all of the mice became paralyzed. Once paralysis and death occurred regularly, the titer of the virus could be calculated, and after many further passages it increased from an initial value of about 102 to about 10' LD50 per 0.03 gram of brain tissue. Subsequently, following a suggestion by Dr. Gordon Meiklejohn, the mouse-adapted Hawaiian strain was propagated in 3 to 4 day old mice, and this yielded 100-1,000 times higher infectious titers. Furthermore, infected baby mouse brain was found to be a good source of complement-fixing antigen (2). From 1944 to 1946, Sabin and Schlesinger attempted in a number of ways to adapt to mice 3 other strains of dengue virus, i.e. the New Guinea â€oeB―, â€oeC― and â€oeD― strains which were recognized as being immunologically distinct from the Hawaiian type (see (3)). Partial success was obtained when the viruses were inoculated intracerebrally into mice of the dba strain. It was also noted that primary â€oetakes―, i.e. evidence of infection in the form of weakness or paralysis of the extremities, were more apt to follow inoculation of dilute than of undiluted or concentrated virus from human sources (1). Stimulated by the usefulness of the suckling mouse in enhancing the in fectivity of the Hawaiian strain, we decided to attempt reactivation of a series in which the New Guinea â€oeB― strain had been carried through eight successful passages in dba mice. It has been possible to adapt this strain to Swiss baby mice. This process of adaptation has been closely analogous to that reported by Meildejohn et al. (4) for the New Guinea â€oeC― and â€oeD― strains. Since these investigators were unable to obtain similar results with the â€oeB― strain, it is one of the purposes of this communication to round out the present status of known types of dengue virus in relation to pathogenicity for mice and to sero logical group relationship. The second purpose is to describe the gradual ac quisition by the virus of pathogenicity for adult Swiss mice as well, a process which by its nature raises several points of general interest in relation to the problem of viral variation in the course of adaptation to new hosts.

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