How Epstein Barr Virus Causes Lymphomas.

Since Epstein-Barr Virus (EBV) was isolated 60 years ago, it has been studied clinically, epidemiologically, immunologically, and molecularly in the ensuing years. These combined studies allow a broad mechanistic understanding of how this ubiquitous human pathogen which infects more than 90% of adults can rarely cause multiple types of lymphomas. We survey these findings to provide a coherent description of its oncogenesis.

Five families of diverse DNA viruses comprehensively restructure the nucleus.

Many viruses have evolved ways to restructure their host cell's nucleus profoundly and unexpectedly upon infection. In particular, DNA viruses that need to commandeer their host's cellular synthetic functions to produce their progeny can induce the condensation and margination of host chromatin during productive infection, a phenomenon known as virus-induced reorganization of cellular chromatin (ROCC). These ROCC-inducing DNA viruses belong to 5 families (herpesviruses, baculoviruses, adenoviruses, parvoviruses, and geminiviruses) that infect a wide range of hosts and are important for human and ecosystem health, as well as for biotechnology.

How Epstein-Barr Virus Induces the Reorganization of Cellular Chromatin.

We have discovered how Epstein-Barr virus (EBV) induces the reorganization of cellular chromatin (ROCC), in which host chromatin is compacted and marginated within the nucleus, with viral DNA replication occurring in the chromatin-free regions. Five families of DNA viruses induce ROCC: herpesviruses, adenoviruses, parvoviruses, baculoviruses, and geminiviruses. These families infect a variety of hosts, including vertebrates, insects, and plants.

Optimal LentiCRISPR-Based System for Sequential CRISPR/Cas9 Screens.

The advent of genome-wide clustered regularly interspaced short palindromic repeats (CRISPR) screening has advanced the understanding of molecular systems within cells. Here, we demonstrate the utility of sequentially performed CRISPR knockout screens that use an existing library to explore a biological question across the human genome, and then the remaining cells are used to examine each gene candidate against one common gene of interest. We call this approach "Many vs One" CRISPR screening, made possible by a modified 7SK promoter in place of the U6 promoter to drive expression of a single guide RNA.