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p16^INK4A-independence of Epstein–Barr virus-induced cell proliferation and virus latency

¹ School of Life Sciences, University of Sussex, Brighton BN1 9QG, UK
² Department of Dermatology, Leiden University Medical Centre, Leiden, The Netherlands
³ Cancer Research UK London Research Institute, Lincolns Inn Fields, London, UK

Correspondence
Alison J. Sinclair
a.j.sinclair{at}sussex.ac.uk

Epstein–Barr virus (EBV) has the ability to promote cell cycle progression following the initial infection of primary resting B-lymphocytes and to cause cell cycle arrest at the onset of the viral replicative cycle. Various mechanisms have been proposed for the proliferative effects, including the up-regulation of cyclin D2 by the viral EBNA-2 and EBNA-LP proteins, direct binding of EBNA3C to the retinoblastoma protein (pRb), and down-regulation of the p16^INK4A tumour suppressor by the viral LMP1 product. To try to gain insight into the relative importance of these mechanisms, the ability of EBV to immortalize lymphocytes from an individual who is genetically deficient for p16^INK4A was examined. From detailed analyses of the resultant lymphoblastoid cell lines it is concluded that p16^INK4A status has little bearing on EBV's ability to manipulate the cell cycle machinery and a model to accommodate the previously proposed routes taken by EBV to bypass the restriction point is presented.

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