George Khoury Lecture
Organized by NIH scientists to honor the memory of Dr. George Khoury, who was highly regarded as a superb scientist and caring mentor of the postdoctoral fellows in his laboratory. This annual lecture is part of the Wednesday Afternoon Lecture Series. Speakers are selected by a committee led by Dr. Eric Freed.
CANCELLED — Translating Studies of HIV Immunity to SARS-CoV-2
CANCELLED
Human Oncogenic Viruses: Nature, Discovery, and Running Around in Circles
Seven viruses collectively comprise an important cause of cancer, particularly in less developed countries and under conditions of immune suppression. Most of these viruses are common infections for which malignancy is a rare consequence. Viral tumors are by nature biological accidents and tumor viruses are generally ‘non-permissive’ for replication within tumor cells having contracted expression of viral products.
Quasispecies Suppression of Drug Resistance
The spectre of drug resistance renders the development of antivirals difficult, especially in RNA viruses whose genome replication is highly error prone. Karla Kirkegaard's lab has been working to develop principles by which the outgrowth of drug-resistant viruses can be thwarted through the choice of noncanonical antiviral targets.
Getting by with a little help from their friends: how bacteria aid virus infection
Dr. Pfeiffer studies RNA virus evolution, dissemination, pathogenesis, and transmission. Her recent interests include examining the impact of intestinal microbiota on enteric virus infections. Her lab has determined that intestinal bacteria promote replication of several enteric viruses and ongoing work is examining mechanisms and consequences of bacteria-virus interactions.
Sounding the alarm and putting out the fire: new mechanistic insights into inflammation triggered by invasive infection
The Lieberman laboratory has been in the forefront of developing RNAi-based therapeutics and using RNAi for genome-wide screening. They were the first to demonstrate that siRNAs could protect mice from disease. They developed methods to harness RNAi to inhibit herpes and HIV transmission in animal models. They have developed strategies for cell-targeted RNAi to treat viral infection, immune disease, and cancer. They are currently investigating tumor-targeted siRNAs for immunotherapy to activate tumor expression of neoantigens and avoid autoimmune side effects of checkpoint inhibitors.
Thinking about cancer as an infectious disease
Infection causes 1 in 5 cancers worldwide. Many tumor suppressors, such as p53, have dual functions to prevent tumor cell growth and to inhibit viral replication. These molecules may have evolved from a primordial unicellular eukaryotic antiviral defense system that inhibited DNA synthesis and initiated programmed cell death in response to viral infection. Two cancer viruses found by our lab, Kaposi’s sarcoma herpesvirus and Merkel cell polyomavirus, provide examples of how virus targeting in a cell can be used to understand important circuits controlling tumor cell growth.
Hepatitis C and beyond: Never a dull moment
The Rice lab focuses on RNA viruses and is well known for its work on hepatitis C. Besides studies aimed at understanding basic viral replicative processes the lab also probes the interface between viruses and host intrinsic and innate immunity and small non-coding RNAs.
Intrinsic host defenses against HIV-1
The investigation of impeded viral replication in animal cells of particular types or species has uncovered great complexity in the interaction between retroviruses and their hosts. These studies have revealed that cells are equipped with a diverse set of proteins that can directly inhibit the replication of retroviruses, including HIV-1. Genes encoding antiretroviral proteins exhibit unusually high sequence variation, presumably because selection pressures exerted by ancient viral infections have caused them to evolve at an unusually rapid pace.
Chromatin structure and the control of gene expression
The Wu laboratory investigates the biochemical basis for histone H2A.Z exchange using the budding yeast model organism. They have identified the yeast SWR1 ATP-dependent chromatin remodeling complex as the responsible enzyme. In a purified system, SWR1 removes H2A-H2B dimers from nucleosomes and deposits free H2A.Z-H2B dimers in an ATP-dependent manner. Homologous enzymes have since been characterized in mammalian systems. How does SWR1 recognize promoters and enhancers genome-wide?
The page was last updated on Thursday, January 29, 2015 - 2:30pm
