A. Introduction

Since type-C retroviruses are known to be involved in naturally occurring leukemias of many animal species [26], a similar viral etiology has been sought in human leukemias. Some of the animal models provide important insight for consideration of human leukemias. For example, while most virus-induced animal leukemias and lymphomas are associated with abundant virus production in the tumor cells, bovine leukemia virus (EL V), the causative agent of bovine leukemias, was not detected until the leukemic cells were cultured in vitro (see review by Miller and Van Der Maaten [13]). This brings out the importance of long-term culture of the appropriate target cells for virus detection and isolation. In 1976, our laboratory reported the discovery of a factor termed T-cell growth factor (TCGF) [ 15]. Following interaction with an antigen, different subsets of mature T cells respond by making and releasing TCG F or making a receptor to TCG F. The TCG F binds to the receptor-bearing T cells and induces cell growth. Addition of exogenous TCGF can maintain growth of activated mature T cells for long periods [6, 26]. When TCGF was added to T cells obtained from patients with mature T -cell leukemias and lymphomas, some cells directly responded without prior activation in vitro [18]. Some of those samples released a retrovirus which we call human T -cell leukemia-Iymphoma virus (HTL V) ([19, 20]; Popovic et al., in preparation). The morphology of HTL V is typically type c. Figure 1 shows an electron micrograph of some HTL V particles. Like all retroviruses, HTL V contains reverse transcriptase, has a high molecular weight RNA genome, and buds from cell membranes. It is distinct from all other known animal retroviruses [9, 16, 22, 23] and to date is the only unequivocal human retrovirus. (The retrovirus later isolated independently in Japan [14, 31] and called ATLV is, in fact, HTL V.) Furthermore, it is specifically associated with certain forms of human leukemia and lymphoma [4]. Here we wish to describe some of the new isolates of HTL V and report on some recent findings on the nature and distribution of HTL V and its transmission to and biological effects on normal T -lymphocytes in vitro.