Previous Article | Next Article ![]()
Journal of Virology, May 2008, p. 4320-4330, Vol. 82, No. 9
0022-538X/08/$08.00+0 doi:10.1128/JVI.01819-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
,
Rienk E. Jeeninga,1
Ben Berkhout,1 and
Dave Speijer2*
Laboratory of Experimental Virology, Department of Medical Microbiology, Center for Infection and Immunity Amsterdam,1 Clinical Proteomics Group, Department of Medical Biochemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands2
Received 19 August 2007/ Accepted 8 February 2008
We performed an extensive two-dimensional differential in-gel electrophoresis proteomic analysis of the cellular changes in human T cells upon human immunodeficiency virus type 1 (HIV-1) infection. We detected 2,000 protein spots, 15% of which were differentially expressed at peak infection. A total of 93 proteins that changed in relative abundance were identified. Of these, 27 were found to be significantly downregulated and 66 were upregulated at peak HIV infection. Early in infection, only a small group of proteins was changed. A clear and consistent program of metabolic rerouting could be seen, in which glycolysis was downregulated and mitochondrial oxidation enhanced. Proteins that participate in apoptotic signaling were also significantly influenced. Apart from these changes, the virus also strongly influenced levels of proteins involved in intracellular transport. These and other results are discussed in light of previous microarray and proteomic studies regarding the impact of HIV-1 infection on cellular mRNA and protein content.
Published ahead of print on 20 February 2008.
Supplemental material for this article may be found at http://jvi.asm.org/.
Present address: Department of Biomolecular Mass Spectrometry, Utrecht University, Sorbonnelaan 16, 3584 CA Utrecht, The Netherlands.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»