File(s) not publicly available
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 SinclairEpstein-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 VirologyISSN
0022-1317Publisher
Society for General MicrobiologyExternal DOI
Issue
6Volume
85Page range
1381-1386Department affiliated with
- Biochemistry Publications
Full text available
- No
Peer reviewed?
- Yes