HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hayman, M. J. Search for Related Content PubMed PubMed Citation Articles by Hayman, M. J. Agricola Articles by Hayman, M. J.

Transforming Proteins of Avian Retroviruses

Tumour Virology Laboratory, Imperial Cancer Research Fund, P.O. Box 123, Lincoln's Inn Fields, London WC2A 3PX, U.K.

Introduction. The three virus groups to be considered are the lymphoid leukosis viruses (LLV), the acute leukaemia viruses, also called the defective leukaemia viruses (DLV) since they are all defective for replication, and the avian sarcoma viruses, ASV. Avian retroviruses are divided into these groups on the basis of the spectrum and latency of the neoplasia they induce in vivo (Table 1). Although this method of classification is by no means absolute, there being many overlaps, it does provide an easy basis upon which to consider these viruses. When considering the mechanism of transformation the most important feature of this classification is the latency period. Viruses which transform rapidly, DLV and ASV, appear to do so by virtue of cellular sequences which have been incorporated into the genome which encode a protein(s) that is responsible for transformation. The method by which viruses with a long latency transform cells is poorly understood but it appears to involve more indirect mechanisms.