Changes in microRNA expression profiles in HIV-1-transfected human cells

MicroRNAs (miRNAs) are small RNAs of 18–25 nucleotides (nt) in length that play important roles in regulating a variety of biological processes. Recent studies suggest that cellular miRNAs may serve to control the replication of viruses in cells. If such is the case, viruses might be expected to evolve the ability to modulate the expression of cellular miRNAs. To ask if expression of HIV-1 genes changes the miRNA profiles in human cells, we employed a high throughput microarray method, termed the RNA-primed Array-based Klenow Enzyme (RAKE) assay. Here, we describe the optimization of this assay to quantify the expression of miRNAs in HIV-1 transfected human cells. We report distinct differences in miRNA profiles in mock-transfected HeLa cells versus HeLa cells transfected with an infectious HIV-1 molecular clone, pNL4-3

Interplay between HIV-1 replication and RNAi effectors

International audiencen.

Obituary: Kuan-Teh Jeang.

Dear colleagues: Our loyal friend Kuan-Teh Jeang, "Teh" to friends and colleagues, passed away unexpectedly at the age of 54 on the evening of January 27, 2013. Great shock and sorrow was apparent in the avalanche of email messages by the very many international colleagues with whom Teh interacted over the years. Many of us came to know Teh as an energetic and gifted scientist for whom we had much respect and affection.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

Premature Activation of the SLX4 Complex by Vpr Promotes G2/M Arrest and Escape from Innate Immune Sensing

SummaryThe HIV auxiliary protein Vpr potently blocks the cell cycle at the G2/M transition. Here, we show that G2/M arrest results from untimely activation of the structure-specific endonuclease (SSE) regulator SLX4 complex (SLX4com) by Vpr, a process that requires VPRBP-DDB1-CUL4 E3-ligase complex. Direct interaction of Vpr with SLX4 induced the recruitment of VPRBP and kinase-active PLK1, enhancing the cleavage of DNA by SLX4-associated MUS81-EME1 endonucleases. G2/M arrest-deficient Vpr alleles failed to interact with SLX4 or to induce recruitment of MUS81 and PLK1. Furthermore, knockdown of SLX4, MUS81, or EME1 inhibited Vpr-induced G2/M arrest. In addition, we show that the SLX4com is involved in suppressing spontaneous and HIV-1-mediated induction of type 1 interferon and establishment of antiviral responses. Thus, our work not only reveals the identity of the cellular factors required for Vpr-mediated G2/M arrest but also identifies the SLX4com as a regulator of innate immunity

Endogenous Retroviruses: Thierry Heidmann wins the 2009 Retrovirology prize

Thierry Heidmann wins the 2009 Retrovirology prize

A trip down memory lane with Retrovirology

Fifteen years ago, Retrovirology was amongst the first open-access journals to be established through Biomed Central, instigated by our late Founding Editor Dr. Kuan-Teh Jeang. Since then, in what seemed like a rather daring move to be paper-free, Retrovirology has witnessed the exponential growth of open access journals that have changed the landscape of scientific publishing and communications. As was pointed out by the staff editors in PLoS Biology [1], the infancy of open access journal was a very different time from our present day, which was before smartphones, prior to most of the digital social media platforms and at a time when we had only begun to learn about the completed DNA sequences from the Human Genome Projec