Michael B. A. Oldstone - Böcker

More people were killed by smallpox during the twentieth century--over 300 million--than by all of the wars of that period combined. In 1918 and 1919, influenza virus claimed over 50 million lives. A century later, influenza is poised to return, ongoing plagues of HIV/AIDS and hepatitis infect millions, and Ebola, Zika, and West Nile viruses cause new concern and panic.The overlapping histories of humans and viruses are ancient. Earliest cities became both the cradle of civilization and breeding grounds for the first viral epidemics. This overlap is the focus of virologist/immunologist Michael Oldstone in Viruses, Plagues and History. Oldstone explains principles of viruses and epidemics while recounting stories of viruses and their impact on human history. This fully updated second edition includes engrossing new chapters on hepatitis, Zika, and contemporary threats such as the possible return of a catastrophic influenza, and the impact of fear of autism on vaccination efforts. This is a fascinating panorama of humankind's longstanding conflict with unseen viral enemies, both human successes--such as control of poliomyelitis, measles, smallpox and yellow fever, and continued dangers--such as HIV and Ebola. Impeccably researched and accessibly written, Viruses, Plagues and History will fascinate all with an interest in how viral illnesses alter the course of human history.

This volume focuses on the role of sphingosine-1-phosphate (S1P) and its analogs in the induced sequestration of lymphocytes in secondary lymphoid organs or in the microenvironment of tissues involved in infection or autoimmune disease. Initial chapters define the pathways to understand S1P signaling. They cover the organization of signaling systems, the structural biology of the S1P1 receptor, and the chemical and genetic tools that are available and useful to explore this area of research and therapeutics. The later chapters highlight S1P and endothelial integrity, lymphocyte migration in the spleen, and S1P agonist in controlling immunopathologic manifestations of acute respiratory influenza virus infection (in the lung), and its accompanying cytokine storm as well as immunopathologic disease of the central nervous system, including the beginning of treatments in multiple sclerosis. One chapter reveals the possible involvement of other lipid molecules, their use for better understanding lipid signaling, and their potential in the modulation of immune responses.

This two-volume work covers the molecular and cell biology, genetics and evolution of influenza viruses, the pathogenesis of infection, resultant host innate and adaptive immune response, prevention of infection through vaccination and approaches to the therapeutic control of infection.. Experts at the forefront of these areas provide critical assessments with regard to influenza virology, immunology, cell and molecular biology, and pathogenesis. Volume I provides overviews of the latest findings on molecular determinants of viral pathogenicity, virus entry and cell tropism, pandemic risk assessment, transmission and pathogenesis in animal species, viral evolution, ecology and antigenic variation, while Volume II focuses on the role of innate and adaptive immunity in pathogenesis, development of vaccines and antivirals.

This two-volume work covers the molecular and cell biology, genetics and evolution of influenza viruses, the pathogenesis of infection, resultant host innate and adaptive immune response, prevention of infection through vaccination and approaches to the therapeutic control of infection.. Experts at the forefront of these areas provide critical assessments with regard to influenza virology, immunology, cell and molecular biology, and pathogenesis. Volume I provides overviews of the latest findings on molecular determinants of viral pathogenicity, virus entry and cell tropism, pandemic risk assessment, transmission and pathogenesis in animal species, viral evolution, ecology and antigenic variation, while Volume II focuses on the role of innate and adaptive immunity in pathogenesis, development of vaccines and antivirals.

This volume focuses on the role of sphingosine-1-phosphate (S1P) and its analogs in the induced sequestration of lymphocytes in secondary lymphoid organs or in the microenvironment of tissues involved in infection or autoimmune disease. Initial chapters define the pathways to understand S1P signaling. They cover the organization of signaling systems, the structural biology of the S1P1 receptor, and the chemical and genetic tools that are available and useful to explore this area of research and therapeutics. The later chapters highlight S1P and endothelial integrity, lymphocyte migration in the spleen, and S1P agonist in controlling immunopathologic manifestations of acute respiratory influenza virus infection (in the lung), and its accompanying cytokine storm as well as immunopathologic disease of the central nervous system, including the beginning of treatments in multiple sclerosis. One chapter reveals the possible involvement of other lipid molecules, their use for better understanding lipid signaling, and their potential in the modulation of immune responses.

This two-volume work covers the molecular and cell biology, genetics and evolution of influenza viruses, the pathogenesis of infection, resultant host innate and adaptive immune response, prevention of infection through vaccination and approaches to the therapeutic control of infection.. Experts at the forefront of these areas provide critical assessments with regard to influenza virology, immunology, cell and molecular biology, and pathogenesis. Volume I provides overviews of the latest findings on molecular determinants of viral pathogenicity, virus entry and cell tropism, pandemic risk assessment, transmission and pathogenesis in animal species, viral evolution, ecology and antigenic variation, while Volume II focuses on the role of innate and adaptive immunity in pathogenesis, development of vaccines and antivirals.

This two-volume work covers the molecular and cell biology, genetics and evolution of influenza viruses, the pathogenesis of infection, resultant host innate and adaptive immune response, prevention of infection through vaccination and approaches to the therapeutic control of infection.. Experts at the forefront of these areas provide critical assessments with regard to influenza virology, immunology, cell and molecular biology, and pathogenesis. Volume I provides overviews of the latest findings on molecular determinants of viral pathogenicity, virus entry and cell tropism, pandemic risk assessment, transmission and pathogenesis in animal species, viral evolution, ecology and antigenic variation, while Volume II focuses on the role of innate and adaptive immunity in pathogenesis, development of vaccines and antivirals.

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).

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.

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. These two volumes were timed to honor the introduction of the vaccine and to record the enormous advancements made in understanding the molecular and cell biology, pathogenesis, and control of this infectious disease. Where vaccine has been effectively delivered, endemic measles virus transmission has been eliminated. However, difficulties in vaccine delivery, lack of health care support and objection to vaccination in some communities continue to result in nearly 40 million cases and over 300,000 deaths per year from measles.

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.

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. These two volumes were timed to honor the introduction of the vaccine and to record the enormous advancements made in understanding the molecular and cell biology, pathogenesis, and control of this infectious disease. Where vaccine has been effectively delivered, endemic measles virus transmission has been eliminated. However, difficulties in vaccine delivery, lack of health care support and objection to vaccination in some communities continue to result in nearly 40 million cases and over 300,000 deaths per year from measles.