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In eukaryotic cells, the nuclear genome and its transcriptional apparatus is separated from the site of protein synthesis by the nuclear envelope. Thus, a constant flow of proteins and nucleic acids has to cross the nuclear envelope in both directions. This transport in and out of the nucleus is mediated by nuclear pore complexes (NPCs) and occurs in an energy and signal-dependent manner. Thus, nucleocytoplasmic translocation of macro molecules across the nuclear envelope appears to be a highly specific and regulated process. Viruses that replicate their genome in the cell nucleus are therefore forced to develop efficient ways to deal with the intracellulZlr host cell transport machinery. Historically, investigation of Polyomavirus replication allowed identification ofsequences that mediate nuclear import, which led subsequently to our detailed understanding of the cellular factors that are involved in nuclear import. Transport ofmacromolecules in the opposite direction, however, is less well understood. The investigation of retroviral gene expression in recent years pro vided the first insights into the cellular mechanisms that regulate nuclear export. In particular, the detailed dissection of the function of the human immunodeficiency virus type I (HIV-I) Rev trans-activator protein identified CRMI, as a hona fide nuclear export receptor. CRM I appears to be involved in the nucleocytoplasmic translocation of the vast majority of viral and cellular proteins that have subsequently been found to contain a Rev-type leucine-rich nuclear export signal (NES).
For over 25 years the study of retroviruses has underpinned much of what is known about information transfer in cells and the genetic and biochemical mechanisms that underlie cell growth and cancer induction. Emergent diseases such as AIDS and adult T-cell lymphoma have widened even further the community of investigators directly concerned with retroviruses, a development that has highlighted the need for an integrated understanding of their biology and their unique association with host genomes. This remarkable volume satisfies that need. Written by a group of the field's most distinguished investigators, rigorously edited to provide a seamless narrative, and elegantly designed for clarity and readability, this book is an instant classic that demands attention from scientists and physicians studying retroviruses and the disorders in which they play a role.
This comprehensive account of the human herpesviruses provides an encyclopedic overview of their basic virology and clinical manifestations. This group of viruses includes human simplex type 1 and 2, Epstein–Barr virus, Kaposi's Sarcoma-associated herpesvirus, cytomegalovirus, HHV6A, 6B and 7, and varicella-zoster virus. The viral diseases and cancers they cause are significant and often recurrent. Their prevalence in the developed world accounts for a major burden of disease, and as a result there is a great deal of research into the pathophysiology of infection and immunobiology. Another important area covered within this volume concerns antiviral therapy and the development of vaccines. All these aspects are covered in depth, both scientifically and in terms of clinical guidelines for patient care. The text is illustrated generously throughout and is fully referenced to the latest research and developments.
One family of viruses is responsible for the infection of many species of vertebrates. These are the retroviruses whose genomic RNA is used to support genetic information and ensures many essential functions that are required for the formation of an infectious viral particle. These functions depend on structures formed by the folding of the genomic RNA. Structures and Functions of Retroviral RNAs describes the formation of these structures and their specific interactions with nucleic acids and proteins. In light of recent advances in molecular virology, it provides an understanding of the various facets of the retroviral genome. It emphasizes in particular that the study of the structure–function relationship of retroviral RNAs is a driving force behind increased research into HIV-1, the main causal agent of AIDS. Indeed, one of the challenges of pharmacology lies in the exploitation of several targets which allow us to anticipate and stem the emergence of resistance to anti-HIV drugs. The book also presents structures and interactions that may be potential future targets in this regard.
Abstract: Both retroviruses and cellular genes rely on post-transcriptional mechanisms to regulate the timing and abundance of their protein product. The post-transcriptional control element (PCE) has been identified in the 5' untranslated regions of mRNAs from selected retroviruses and the cellular gene JunD. PCE containing mRNAs rely on the DExH/D box helicase RNA helicase A (RHA) to specifically facilitate robust synthesis of their protein product. Study of retroviruses has developed approaches to understand both cellular control of gene expression and the dyregulation that contributes to cancer and immunodeficiency. JunD, a member of the activator protein -1 (AP-1) family of transcription factors, is important for transcriptional regulation of growth control genes. Dysregulation of JunD is implicated in cancer and metabolic disease via defects in cell- proliferation and disease-associated apoptosis and can also modulate viral persistence. Studies described here build on the previous characterization of SNV and JunD PCE function in HIV gag-pol reporter plasmids and investigate the parental SNV provirus. The results presented validate the role of PCE in combination with a newly identified a distal element, designated the I,II element, in regulation of balanced expression and translational utilization of SNV mRNA. A key conclusion is that PCE and the distal I,II element comprise a bipartite element that interacts with RNA helicase A to selectively modulate post-transcriptional expression of the unspliced SNV gag mRNA. This thesis also reviews the current and historical literature of JunD gene regulation. Three core areas are described and intriguing essential issues are discussed: i) transcription regulation by AP-1 complexes containing JunD protein, ii) post-translational modification of JunD by Jun-terminal kinase (Jnk) and protein:protein interactions, and iii) regulation of translation intiation by JunD PCE. Lessons learned from the study of retrovirus genes have produced essential knowledge of the JunD transcription factor and contributed to the characterization of a novel axis of transational control of complex RNAs.
The first book to specifically cover the molecular biology of retroviruses - of immense importance since the high profile of HIV. International contributors provide detailed reviews of the latest knowledge. An excellent text for both medical and non-medical researchers, it also serves as an illuminating introduction for scientists active in other areas.