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p16INK4A-independence of Epstein–Barr virus-induced cell proliferation and virus latency

journal contribution
posted on 2023-06-07, 21:49 authored by Michelle J. Hayes, Anna Koundouris, Nelleke Gruis, Wilma Bergman, Gordon G. Peters, Alison Sinclair
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 LIMP1 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.

History

Publication status

  • Published

Journal

Journal of General Virology

ISSN

0022-1317

Publisher

Society for General Microbiology

Issue

6

Volume

85

Page range

1381-1386

Department affiliated with

  • Biochemistry Publications

Full text available

  • No

Peer reviewed?

  • Yes

Legacy Posted Date

2012-02-06

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