Gene silencing in HIV-1 latency by polycomb repressive group

Hyeon Guk Kim, Kyung Chang Kim, Tae Young Roh, Jihwan Park, Kyung Min Jung, Joo Shil Lee, Sang Yun Choi, Sung Soon Kim, Byeong Sun Choi

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22 Scopus citations


Background: The persistence of latently Human immunodeficiency virus-1 (HIV-1) infected cellular reservoirs in resting CD4+ T cells is a major obstacle to HIV-1 eradication. The detailed mechanism of HIV-1 latency remains unclear. We investigated histones and their post-translational modification associated with HIV-1 latency in novel HIV-1 latently infected cell lines established previously, NCHA cells. Methods: To examine histones and their modification linked with HIV-1 latency, the expression profiles for core histone proteins and histone deacetylases (HDACs) in NCHA cells were characterized by RT-PCR, ELISA, and western blot. The levels of histone acetylation and methylation at histone H3 Lys9 (H3K9) and Lys 27 (H3K27) in HIV-1 latently infected cells were analyzed by western blot and chromatin immunoprecipitation-sequencing (ChIP-seq). Results: The expression levels for four core histone proteins (H2A, H2B, H3 and H4) and HDACs (HDAC1-8) in NCHA cells were not significantly different from those in their parental cells. Histone H3K9 and H3K27 acetylations in NCHA cells showed no difference in parental and NCHA cells, whereas the levels of di- and tri-methylation were increased in NCHA cells. The expression of EED which is a component of polycomb repressive complex 2 (PRC2), and BMI1 and RING2 which are constituents of PRC1, were upregulated in NCHA cells. In addition, more ubiquitylation at histone H2A was detected in NCHA cells. Conclusions: Our results suggest that tri-methylation of histone H3K27 and H2A ubiquitylation via polycomb group protein may play a crucial role in epigenetic silencing accounting for HIV-1 latency in NCHA cells.

Original languageEnglish
Article number179
JournalVirology Journal
StatePublished - 2011

Bibliographical note

Funding Information:
This work was supported by an intramural grant from the Korea National Institute of Health (Grant Nos. 2007-N51001-00 and 2010-N51001-00) and in part by the World Class University program via the National Research Foundation of Korea, funded by the Ministry of Education, Science and Technology (Grant No. R31-2008-000-10105-0, T-Y. Roh).


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