Burkitt's lymphoma is a highly aggressive B-cell non-Hodgkin lymphoma and is the fastest growing human tumour. The disease is associated with Epstein-Barr virus and was one of the first tumours shown to have a chromosomal translocation that activates an oncogene (c-MYC). Burkitt's lymphoma is the most common childhood cancer in areas where malaria is holoendemic. The incidence is very high in immunosuppressed patients in non-endemic areas, especially when associated with HIV infection. Outcome with intensive chemotherapy has improved and is now excellent in children, but the prognosis is poor in elderly adults. The success of intensive treatment relies on good supportive care. The therapy offered in oncology units in low-income countries is not as aggressive as in centres in high-income countries and outcomes are less successful. Adjuvant monoclonal antibody therapy with rituximab shows promise for improved outcomes and reduced toxic effects in the future.

The complete DNA sequence of the A2 strain of polyoma virus has been determined. It consists of 5,292 base pairs. The sequence is analysed in terms of its coding potential and sites of possible functional significance or structural interest. The polyoma virus genome is compared with those of related tumour viruses, simian virus 40 and BK virus.

A nasopharyngeal carcinoma tumour (designated C15) propagated in nude mice has been used to generate a large cDNA library that we have analysed for Epstein‐Barr virus (EBV) gene expression. No gross alterations exist in viral DNA from C15 relative to other human isolates and the large deletion present in the B95‐8 ‘prototype’ viral strain established in marmoset cells is not found; C15 contains no linear virion DNA. In the cDNA library, of the six EBV nuclear antigens (EBNAs) expressed in latently infected B‐lymphocytes, only clones for EBNA‐1 are found. These data are confirmed by immunoblotting. Sequence analysis shows the EBNA‐1 mRNA splicing pattern in the carcinoma to differ from that observed in B‐lymphocytes. Further, contrary to observations with B‐cell lines, most viral transcription in the tumour is localized onto the ‘rightmost’ region of the conventional EBV physical map. Transcripts identified corresponding to known genes include those for the latent membrane protein (LMP), the alkaline DNA exonuclease and probably the terminal protein; major transcripts are also derived from the BamHI D fragment and the region deleted in B95‐8 EBV DNA. Novel transcripts have also been identified that proceed in an anti‐sense direction to genes encoding functions associated with replication, such as the viral DNA polymerase. They contain a large, hitherto unidentified, open reading frame in the viral genome that is complementary to the putative function known as BALF3 and a smaller open reading frame complementary to BALF5 (the DNA polymerase gene). From the present studies we can conclude that: (i) EBV transcription patterns in the epithelial cells vary markedly from those identified previously in B‐cells, reflecting differential use of promoters or splicing patterns. (ii) Transcription is tightly regulated and restricted in the C15 tumour with many latent genes, notably EBNAs 2‐6, being ‘switched off.’ (iii) A family of cytoplasmic RNAs are transcribed in an antisense direction to a number of existing open reading frames in the EBV genome. (iv) There are a number of mutations in C15 transcripts relative to the B95‐8 genome, some of which could result in amino acid alterations in proteins.

The action of restriction enzymes on (2). Supercoiled viral DNA was purified from the supernatant by phenol extraction, dialysis against 1 M NaCl (pH 7.5), and ethanol precipitation, followed by equilibrium centrifugation in CsCl/ethidium bromide (3). Supercoiled viral DNA was further purified by neutral sucrose density gradient centrifugation (1). Yields of purified product varied from 1 to 5 Mg per 90-mm dish, with specific activity about 4 X 105 cpm/,ug.Enzymes. All the restriction enzymes used, except Hpaii

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