Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/38997
Title: Epigenetic Modulations in Activated Cells Early after HIV-1 Infection and Their Possible Functional Consequences
Authors: Maricato, Juliana Terzi [UNIFESP]
Furtado, Maria N. [UNIFESP]
Takenaka, Maisa Carla [UNIFESP]
Nunes, Edsel Renata de Morais [UNIFESP]
Fincatti, Patricia [UNIFESP]
Meliso, Fabiana Marcelino [UNIFESP]
Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP]
Jasiulionis, Miriam Galvonas [UNIFESP]
Araripe Sucupira, Maria Cecilia de [UNIFESP]
Diaz, Ricardo Sobhie [UNIFESP]
Janini, Luiz Mário Ramos [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Issue Date: 13-Apr-2015
Publisher: Public Library Science
Citation: Plos One. San Francisco: Public Library Science, v. 10, n. 4, 21 p., 2015.
Abstract: Epigenetic modifications refer to a number of biological processes which alter the structure of chromatin and its transcriptional activity such as DNA methylation and histone post-translational processing. Studies have tried to elucidate how the viral genome and its products are affected by epigenetic modifications imposed by cell machinery and how it affects the ability of the virus to either, replicate and produce a viable progeny or be driven to latency. the purpose of this study was to evaluate epigenetic modifications in PBMCs and CD4(+) cells after HIV-1 infection analyzing three approaches: (i) global DNA-methylation; (ii) qPCR array and (iii) western blot. HIV-1 infection led to methylation increases in the cellular DNA regardless the activation status of PBMCs. the analysis of H3K9me3 and H3K27me3 suggested a trend towards transcriptional repression in activated cells after HIV-1 infection. Using a qPCR array, we detected genes related to epigenetic processes highly modulated in activated HIV-1 infected cells. SETDB2 and RSK2 transcripts showed highest up-regulation levels. SETDB2 signaling is related to transcriptional silencing while RSK2 is related to either silencing or activation of gene expression depending on the signaling pathway triggered down-stream. in addition, activated cells infected by HIV-1 showed lower CD69 expression and a decrease of IL-2, IFN-gamma and metabolism-related factors transcripts indicating a possible functional consequence towards global transcriptional repression found in HIV-1 infected cells. Conversely, based on epigenetic markers studied here, non-stimulated cells infected by HIV-1, showed signs of global transcriptional activation. Our results suggest that HIV-1 infection exerts epigenetic modulations in activated cells that may lead these cells to transcriptional repression with important functional consequences. Moreover, non-stimulated cells seem to increase gene transcription after HIV-1 infection. Based on these observations, it is possible to speculate that the outcome of viral infections may be influenced by the cellular activation status at the moment of infection.
URI: http://repositorio.unifesp.br/handle/11600/38997
ISSN: 1932-6203
Other Identifiers: http://dx.doi.org/10.1371/journal.pone.0119234
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