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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 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.Â
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.Â
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).
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.
Most diseases are multifactoral. Transgenic technology permits
gene(s) of interest to be expressed in a small manipulatable
laboratory animal model. By this process, murine models of human
infections can be developed and studied; effects of cytokines in
vivo, focally expressed in unique cells can be established and
manipulated, and a variety of autoimmune disorders, mimicking human
disease can be constructed. In this volume, these approaches for
study of human immunodeficiency virus, hepatitis virus, viruses
causing tumors and chronic degenerative disorders are described.
Also included are chapters of transgenic models of autoimmune
disorders like diabetes, systemic lupus and ankylosing spondylitis.
The National Institute of Mental Health (NIMH) AIDS Program is the
fourth largest acquired immune deficiency syndrome (AIDS) program
within the National Institutes of Health (NIH). Since 1983, our
program's contributions have concentrated on two major areas. The
first has been to develop effective strategies to prevent or reduce
behaviors that place individuals at risk for human immunodeficiency
virus type 1 (HIV-1) infection. The second has been to support and
foster research to enhance our understanding of the profound impact
of H IV-1 infection on the central nervous system (eNS). The brain
appears to be a prime target of the virus and may serve as a
reservoir for the virus. Post mortem examination of brain tissue
has provided evidence of eNS cell damage in 80%-90% of people who
die with AIDS. For about 10%-20% of people with AI DS, mild
neuropsychological symptoms are the first signs of the disease.
Approximately 20% of individuals infected with HIV-1 develop AIDS
dementia complex. The symptoms include apathy, difficulty
concentrat ing, irritability, depression, and personality changes.
In the later stages of the disease, people may experience
psychiatric disor ders. Death usually occurs within 6 months of the
appearance of those more severe symptoms. Up to 90% of children
infected with H IV-1 experience attention and concentration
difficulties and often experience neurodevelopmental delay or
regression over time."
Cytotoxic T lymphocytes (CTL) control several viral infections in
animals based on deletion and reconstitution experiments with CTL
clones and use of CD8 genetically deficient (knock-out) mice. In
this volume, data for the role that CTL play in human infectious
diseases is presented. As such, this represents the first volume in
which such information from several different viral and protozoan
infections is brought together.
This volume focuses on the evidence for or against molecular
mimicry as a cause of autoimmunity. Contributions from recognized
experts present their original findings, and the final chapter
reviews the overall perspective of molecular mimicry, how to use
its principles in clinical investigation and list the conceptual
traits by which autoimmune disaese can occur.
Reoviruses are one of the most important viral groups for
understanding the molecular and genetic basis for viral
pathogenesis. These two volumes cover virtually all aspects of
reovirus biology. Volume I begins with a review of reovirus
structure; further chapters deal with functions of the reovirus
structural proteins, the assembly of the genome, and reovirus
mutants. Volume II reviews general mechanisms of reovirus
persistent infection and cytopathic effects, and then discusses
reovirus-induced disease in specific organ systems including the
heart, nervous and endocrine systems, liver and biliary system, and
intestine. Together, these two volumes provide a current and
comprehensive review of the mammalian reoviruses.
The all new Concepts in Viral Pathogenesis III contains the widely
praised format of presenting up-to-date information in pithy,
easily read "mini-review" style and complements previous editions
with contributions by leading international authorities on
structure-function relationships, gene regulation, cell biology of
viral infections, transgenic mice, expression of viral genes,
retroviruses, and evolving concepts in viral diseases. Taken
together, Volume I, II and III of Concepts in Viral Pathogenesis
contain 145 unique chapters each representing the latest thinking
in important areas of virology by the foremost investigators in the
field. Clinicians, laboratory scientists, students, and others
seeking authoritative overviews of current knowledge on the
mechanism of viral diseases will welcome this valuable resource.
Leading researchers present contemporary treatment of in situ
hybridization applied to current issues in animal virus
pathogenesis. The most recent methods are given for locating viral
genes in whole animal section and for defining the number and type
of cells surrounded by viruses. The genetic programs played out in
these cells and the newer methods of hybridization at the electron
microscopic level provide valuable insight into the complexities of
virus-host interaction.
M. B. A. OLDSTONE Viruses are generally studied either because they
cause significant human, animal or plant disease or for their
utility as materials to probe a basic phenomenon in biology,
chemistry, genetics or molecular biology. Arenaviruses are
unusually interesting in that they occupy both of these categories.
Arenaviruses cause severe human diseases known primarily as the
hemor rhagic fevers occurring in South and Latin America (Bolivia:
Machupo virus and Argentina: Junin virus) and in Africa (Lassa
virus). Because such viruses produce profound disability and may
kill the persons they infect, they are a source of economic
hardship in the countries where they are prevalent. Further, they
provide new problems for health care personnel owing to the
narrowing of the world as visitors from many countries increasingly
travel to and from these endemic areas. In addition, lymphocytic
choriomeningitis virus (LCMV) can infect humans worldwide, although
the illness is most often less disabling than those elicited by
other arenaviruses. Yet LCMV is likely of greater concern to
non-arena-virologists and experimentalists using tissue culture or
animals, i. e. , workers in molecular biology, cancer research,
virology, immunobiology, etc. , because normal appearing cultured
cells or tissues and animals used for research may be persistently
infected with LCMV without manifesting clinical disease or
cytopathology and transmit that infection to laboratory workers
(reviewed OLDSTONE and PETERS 1978). For example, HINMAN et al.
M. B. A. OLDSTONE Viruses are generally studied either because they
cause significant human, animal or plant disease or for their
utility as materials to probe a basic phenomenon in biology,
chemistry, genetics or molecular biology. Arenaviruses are
unusually interesting in that they occupy both of these categories.
Arenaviruses cause severe human diseases known primarily as the
hemor rhagic fevers occurring in South and Latin America (Bolivia:
Machupo virus and Argentina: Junin virus) and in Africa (Lassa
virus). Because such viruses produce profound disability and may
kill the persons they infect, they are a source of economic
hardship in the countries where they are prevalent. Further, they
provide new problems for health care personnel owing to the
narrowing of the world as visitors from many countries increasingly
travel to and from these endemic areas. In addition, lymphocytic
choriomeningitis virus (LCMV) can infect humans worldwide, although
the illness is most often less disabling than those elicited by
other arenaviruses. Yet LCMV is likely of greater concern to
non-arena-virologists and experimentalists using tissue culture or
animals, i. e. , workers in molecular biology, cancer research,
virology, immunobiology, etc. , because normal appearing cultured
cells or tissues and animals used for research may be persistently
infected with LCMV without manifesting clinical disease or
cytopathology and transmit that infection to laboratory workers
(reviewed OWSTONE and PETERS 1978). For example, HINMAN et al.
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.
By itself measles virus infection has and still provides some of
the most interesting phenomena in biology. Following infection of
dendritic cells, measles virus causes a profound suppression of the
host s immune response that lasts a number of months after apparent
recovery from infection. Indeed, measles virus was the first virus
to be associated with immunosuppression with many of the
manifestations to be observed one hundred years later with HIV
infection. Measles is also associated with development of both
post-infectious encephalomyelitis, an autoimmune demyelinating
disease, and subacute sclerosing panencephalitis, a slowly
progressive neurodegenerative disorder. How measles virus infects
cells, spreads to various tissues and causes disease, as well as
the role of the immune response, generation of new vaccines, and
use as a vector for gene delivery are topics covered in these two
volumes. "
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).
Reoviruses are one of the most important viral groups for
understanding the molecular and genetic basis for viral
pathogenesis. These two volumes cover virtually all aspects of
reovirus biology. Volume I begins with a review of reovirus
structure; further chapters deal with functions of the reovirus
structural proteins, the assembly of the genome, and reovirus
mutants. Volume II reviews general mechanisms of reovirus
persistent infection and cytopathic effects, and then discusses
reovirus-induced disease in specific organ systems including the
heart, nervous and endocrine systems, liver and biliary system, and
intestine. Together, these two volumes provide a current and
comprehensive review of the mammalian reoviruses.
Ebola's Curse: 2013-2016 Outbreak in West Africa is about
hemorrhagic fever viruses, especially Ebola, its initial origin in
central Africa 1976, its unprecedented appearance in West Africa in
2013. The book records in sequence and detective style how the
initial outbreak of Ebola from the index case in rural Guinea
traveled to Sierra Leone, the work and fate of those working in the
Kenema Government Hospital (KGH) isolation ward in Sierra Leone.
The book provides vignettes of the three main players involved with
Ebola at KGH, Sheik Khan, Pardis Sabeti, and Robert Garry. Khan was
the head of the unit, declared a national hero by his Sierra Leone
government. He died fighting Ebola and was/is recognized in the USA
by American societies by awards created for his historic work and
death. Pardis Sabeti, a geneticist from Harvard and Broad MIT
Institute, who was honored as a "Scientist of the Year" by Time
Magazine and the Smithsonian Institute. Robert Garry, head of the
operation to fight hemorrhagic fevers and Ebola, shuttled between
Tulane University, KGH, and The White House to make aware through
the press and others the dilemma and tragedy that was unfolding,
and the need to obtain additional medical and health care support
and supplies. Sabeti and Garry currently work with Oldstone on
Ebola at KGH and thus personal communication and knowledge was/is
available to the author for the book.
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