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Continuous genetic variation and selection of virus subpopulations in the course of RNA virus replications are intimately related to viral disease mechanisms. The central topics of this volume are the origins of the quasispecies concept, and the implications of quasispecies dynamics for viral populations.

In addition, there are in?uences that are extrinsic to potentially auto-reactive lymphocytes, including the function of regulatory cells, d- ferentiation state of antigen-presenting cells, availability of self-antigen, the cytokine and chemokine milieu, as well as the traf?cking patterns involved in generating productive immune interactions.

Cells of the immune system develop in bone marrow and lymphoid organs, but as the cells mature they leave these organs and circulate as single cells. Studies of normal and transformed T cell lines and of T cells from transgenic mice led to comprehensive understanding of the mole- lar basis of antigen-receptor recognition and signaling.

This volume offers an overview of the processes of zoonotic viral emergence, the intricacies of host/virus interactions, and the role of biological transitions and modifying factors.

In addition, there are in?uences that are extrinsic to potentially auto-reactive lymphocytes, including the function of regulatory cells, d- ferentiation state of antigen-presenting cells, availability of self-antigen, the cytokine and chemokine milieu, as well as the traf?cking patterns involved in generating productive immune interactions.

Natural Killer (NK) cells are large granular lymphocytes of the innate immune system. Importantly, NK cells also link the innate and adaptive immune responses, contributing to the initiation of adaptive immune responses and executing adaptive responses using the CD16 FcgRIIIA immunoglobulin Fc receptor.

Measles virus, one of the most contagious of all human viruses, has been largely contained by the development and use of a vaccine that was introduced 50 years ago.

In the last few years the major effect that RNAi has had in invertebrate systems is beginning to take hold in mammalian systems through both single gene knockdown experiments and genome-scale screens. Through the introduction of RNAi, mammalian systems have finally gained admittance to the pantheon of model genetic systems.

This volume explores in detail the molecular biology, genetics and immunology of the bacterium Helicobacter pylori that causes serious gastric diseases such as gastric cancer. The book provides in-depth insights into the mechanisms of H. pylori-induced pathogenicity, gives an overview of how the bacterium colonizes the human gut, how it manages to persist in the body and which factors play a role in the development of H. pylori-induced gastric cancer. Furthermore, the interaction between the Gram-negative bacterium and the human gut microbiome is explored, and clinical management and treatment strategies to combat gastric cancer are discussed.Helicobacter pylori is an extremely successful pathogen that persistently colonizes the gut of about 50% of the world¿s population. H. pylori and its human host share a long co-evolutionary relationship that dates back for at least last 100,000 years and possibly longer. Infection by thisbacterium is a high-risk factor for the development of gastric diseases, including gastric cancer. Gastric cancer is associated with high morbidity and mortality and represents the 5th most common malignant tumour and the 4th leading cause of cancer-related death worldwide. H. pylori is the first bacterium that has been classified as a type-I carcinogen by the International Agency for Research on Cancer (IARC). Recent research progress identified crucial bacterial, host and environmental factors which control H. pylori-induced gastric malignancy. New studies also suggest that specific human germline mutations and other genetic aberrations have an important impact on H. pylori-induced pathology. In this volume, all these recently discovered mechanisms are reviewed in the light of gastric cancer development, and H. pylori epidemiology, virulence factors, immune evasion, pathophysiology, cancer signalling and novel therapeutic protocols are presented. This volume is aimed at researchers in the fields of immunology, genetics, microbiology and medicine who are interested in the detailed mechanisms of the pathogenicity of this carcinogenic stomach bacterium.

The structural and functional importance of the correct patterns of DNA methylation in all parts of a mammalian genome is not well understood. The stability, inheritability, and developmental flexibility of these patterns point to a major role that these patterns appear to play in determining structure and function of the genome.

The purpose of this review is to examine the potential role of molecular mimicry in the pathogenesis of human T-lymphotropic virus type 1 ((HTLV- 1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP)). Comp- hensive reviews on the pathogenic mechanisms of HTLV-1-associated human diseases are available throughout the medical literature (Bangham 2000,, 2003; Barmak et al. 2003; Jacobson 2002; Levin and Jacobson 1997; Nagai and Osame 2003; Osame 2002). Approximately 25 years ago the ?rst human retrovirus, HTLV-1, was isolated (Poeisz et al. 1980). Subsequently, infection with HTLV-1 was shown to cause adult T-cell leukemia (ATL) and HAM/TSP (Gessain et al. 1985; McFarlin and Blattner 1991; Osame et al. 1986; Poeisz et al. 1980; Yoshida et al. 1987). HTLV-1 may infect up to 30% of people in endemic areas and 10-20 million people worldwide (Barmak et al. 2003; Edlich et al. 2000). However, only 1%-5% develop either ATL or HAM/TSP, the remainder being clinically asymptomatic carriers of HTLV-1 (Bangham 2000, 2003; Barmak et al. 2003; Jacobson 2002; Levin and Jacobson 1997; Nagai and Osame 2003; Osame 2002). Why infection with HTLV-1 causes ATL or HAM/TSP in some people while the vast majority of individuals are asymptomatic is largely - known. Some possible factors that may differentiate the asymptomatic from the diseased state include viral strain, human histocompatibility leukocyte antigen (HLA), viral load, and the immune response (Bangham 2000, 2003; Barmak et al. 2003; Jacobson 2002; Levin and Jacobson 1997; Nagai and Osame 2003; Nagai et al. 1998; Niewiesk et al. 1994; Osame 2002).

Apoptosis is a regulated, energy-dependent process by which a cell se- destructs. This mechanism of programmed cell death plays an important role in normal development and control of cell numbers in mature a- mals. Apoptosis was initially defined by morphological criteria to describe the distinctive appearance of dying cells that developed nuclear conden- tion, cell shrinkage, and cytoplasmic blebbing. Initiation of the apoptotic process can come from external or internal stimuli and is highly regulated both by molecules that facilitate and by molecules that inhibit the process. Common features of apoptosis include activation of proteases and - cleases, mitochondrial membrane permeabilization, chromatin disruption, and translocation of phosphatidylserine from the inner to the outer s- face of the plasma membrane. Apoptotic cells attract phagocytes that - gulf the apoptotic bodies and prevent tissue damage in the region. Intense investigation of the cell death process has defined many molecular features of the pathway by which regulation and execution can be exploited by pathogens.

The genus Chlamydia encompasses a number of species of obligate intracellular bacteria, including important human pathogens like the most common bacterial agent of sexually transmitted disease.

This introduction guides readers through different immunological aspects of autophagy as well as the countermeasures used by highly-adapted pathogens to fight autophagy. It includes specifics on the latest in autophagy research in infection and immunity.

It has become apparent that the genomes of many organisms are characterized by unique patterns of DNA methylation which can differ from genome segment to genome segment and cell type to cell type.

This volume summarizes recent advances in understanding the mechanisms of HIV-1 latency, in characterizing residual viral reservoirs, and in developing targeted interventions to reduce HIV-1 persistence during antiretroviral therapy. assays and technical approaches to quantify viral reservoirs in humans and animal models;

This volume discusses the interactions between viruses and their host cells, and explores the roles of host and viral genes and non-coding RNAs in the virus replication cycle.

This volume reviews various facets of Agrobacterium biology, from modern aspects of taxonomy and bacterial ecology to pathogenesis, bacterial cell biology, plant and fungal transformation, natural transgenics, and biotechnology.

This volume summarizes recent advances in understanding the mechanisms of HIV-1 latency, in characterizing residual viral reservoirs, and in developing targeted interventions to reduce HIV-1 persistence during antiretroviral therapy. assays and technical approaches to quantify viral reservoirs in humans and animal models;

coli pathotypes can cause intestinal and extra intestinal infections (e.g. Consequently, there is a pressing need to develop alternative control measures, including the identification of new drug targets and development of vaccines that offer lasting protection.This volume focuses on several types of E.

This volume reviews the current research focused on the functional importance of unfolded protein response (UPR) signaling in the context of health and disease.

This volume offers a comprehensive overview of basic and applied aspects of Staphylococcus aureus, which is one of the most important human pathogens. All chapters were written by respected experts in the field - presenting recent findings on a diverse range of aspects, they are nonetheless interlinked.

The genus Chlamydia encompasses a number of species of obligate intracellular bacteria, including important human pathogens like the most common bacterial agent of sexually transmitted disease.

This volume provides an overview of recent advances in our understanding of the biology of marburg- and ebolaviruses. It focuses on four essential areas: 1) ecology, outbreaks and clinical management, 2) disease, pathogenesis and protection, 3) virus replication inside the cell, and 4) molecular tools for virus study and taxonomy. For 50 years, these viruses have spilled over sporadically and without warning from their wildlife reservoirs, often causing major outbreaks and high fatalities. The consequences can be devastating, with a clear potential for global reach, as demonstrated by the 2013 West African outbreak of Ebola virus, which led to over 28,000 reported cases across three continents and more than 11,000 deaths. Given the international threat posed by these viruses, the pace and scope of basic research have also greatly intensified, ranging from studies of virus emergence, epidemiology, antiviral countermeasures and human disease to detailed mechanistic studies of virus entry, replication, virion assembly and protein structure. Written by internationally respected experts, this book will appeal to a wide audience and be a valuable resource for basic researchers, clinicians and advanced students alike.

This volume focuses on virus-host cell interactions, cellular genes acquired or modulated by viruses, the pathological effects of these interactions, and therapeutic interventions.

This volume highlights the most interesting biomedical and clinical applications of high-dimensional flow and mass cytometry. It reviews current practical approaches used to perform high-dimensional experiments and addresses key bioinformatic techniques for the analysis of data sets involving dozens of parameters in millions of single cells.