Books on the topic 'Influenza viruses HEALTH SCIENCES'

Influenza is a highly infectious, acute illness which has affected humans and animals since ancient times. Influenza viruses form the Orthomyxoviridae family and are grouped into types A, B, and C on the basis of the antigenic nature of the internal nucleocapsid or the matrix protein. Infl uenza A viruses infect a large variety of animal species, including humans, pigs, horses, sea mammals, and birds, occasionally producing devastating pandemics in humans, such as in 1918 when it has been estimated that between 50–100 million deaths occurred worldwide.There are two important viral surface glycoproteins, the haemagglutinin (HA) and neuraminidase (NA). The HA binds to sialic acid receptors on the membrane of host cells and is the primary antigen against which a host’s antibody response is targeted. The NA cleaves the sialic acid bond attaching new viral particles to the cell membrane of host cells allowing their release. The NA is also the target of the neuraminidase inhibitor class of antiviral agents that include oseltamivir and zanamivir and newer agents such as peramivir. Both these glycoproteins are important antigens for inducing protective immunity in the host and therefore show the greatest variation.Influenza A viruses are classified into 16 antigenically distinct HA (H1–16) and 9 NA subtypes (N1–9). Although viruses of relatively few subtype combinations have been isolated from mammalian species, all subtypes, in most combinations, have been isolated from birds. Each virus possesses one HA and one NA subtype.Last century, the sudden emergence of antigenically different strains in humans, termed antigenic shift, occurred on three occasions, 1918 (H1N1), 1957 (H2N2) and 1968 (H3N2), resulting in pandemics. The frequent epidemics that occur between the pandemics are as a result of gradual antigenic change in the prevalent virus, termed antigenic drift. Epidemics throughout the world occur in the human population due to infection with influenza A viruses, such as H1N1 and H3N2 subtypes, or with influenza B virus. Phylogenetic studies have led to the suggestion that aquatic birds that show no signs of disease could be the source of many influenza A viruses in other species. The 1918 H1N1 pandemic strain is thought to have arisen as a result of spontaneous mutations within an avian H1N1 virus. However, most pandemic strains, such as the 1957 H2N2, 1968 H3N2 and 2009 pandemic H1N1, are considered to have emerged by genetic re-assortment of the segmented RNA genome of the virus, with the avian and human influenza A viruses infecting the same host.Influenza viruses do not pass readily between humans and birds but transmission between humans and other animals has been demonstrated. This has led to the suggestion that the proposed reassortment of human and avian influenza viruses takes place in an intermediate animal with subsequent infection of the human population. Pigs have been considered the leading contender for the role of intermediary because they may serve as hosts for productive infections of both avian and human viruses, and there is good evidence that they have been involved in interspecies transmission of influenza viruses; particularly the spread of H1N1 viruses to humans. Apart from public health measures related to the rapid identification of cases and isolation. The main control measures for influenza virus infections in human populations involves immunization and antiviral prophylaxis or treatment.

Pandemics, Publics, and Narrative explores how members of the general public experienced the 2009 swine flu pandemic. It examines the stories related to us by individuals about what happened to them in 2009, their reflections on news and expert advice given to them, and how they considered vaccination, social isolation, and other infection control measures. The book charts also the storytelling of public life, including the “be alert, not alarmed” messages from the beginning of the outbreak through to the “boy who cried wolf” problem that emerged later in the outbreak when the virus turned out to be less serious than first thought for most people. Key themes of the book are the significance of personal immunity for people as they reflected on how to respond to the threat of an influenza virus and the ways in which universal public health advice was interpreted quite differently by people according to their medical and biographical situation. The book provides unprecedented insight into the lives of ordinary people during 2009, some affected profoundly and others hardly affected at all. By drawing on currents in sociocultural scholarship of narrative, illness narrative, and narrative medicine, it develops a novel “narrative public health” approach that bridges health communications and narrative. The book provides therefore important new insights for health communicators and researchers across the social and health sciences.

While infections have always played an important role in the history of mankind, advances in science and technology as well as rapid globalization have resulted in an unprecedented wave of new and old infections thrust into the limelight. The recent pandemic of H1N1 influenza virus infection demonstrates the recurrent theme of emerging and reemerging pathogens that continue to impact public health and patient care areas. Drug resistance among various organisms (not limited to bacteria) has unfortunately become the expectation and, not infrequently, we have been left with few or no efficacious treatment options, an experience not witnessed in more than 7 decades. Human immunodeficiency virus infection continues to challenge our abilities to provide the desired level of care in most areas of the world. Novel syndromes of infection continue to be defined as newer forms of immunosuppression and the development of unique medical devices become standard practice in all areas of medicine and surgery. For trainees and practitioners in the field of infectious diseases today, these factors mandate intense study to establish an expertise in the field that is required to provide best practices now and beyond. This board review will be pivotal in that education. This book is designed and intended primarily for infectious diseases trainees and practitioners preparing for the infectious disease subspecialty examination of the American Board of Internal Medicine. We believe that this book will also be useful to infectious diseases practitioners as well as general internists and other clinicians who desire a comprehensive but practical overview of contemporary infectious diseases topics.

From HIV to H1N1, pandemics pose one of the greatest threats to global health in the twenty-first century. Defined as epidemics of infectious disease across large geographic areas, pandemics can disseminate globally with incredible speed as humans and goods move faster than ever before. While vaccines, drugs, quarantine, and education can reduce the severity of many outbreaks, factors such as global warming, population density, and antibiotic resistance have complicated our ability to fight disease. Respiratory infections like influenza and SARS spread quickly as a consequence of modern, mass air travel, while unsafe health practices promote the spread of viruses like HIV/AIDS and hepatitis C. In Pandemics: What Everyone Needs to Know, Nobel Prize-winning immunologist Peter C. Doherty addresses the history of pandemics and explores the ones that persist today. He considers what promotes global spread, the types of pathogens most present today and the level of threat they pose, and how to combat outbreaks and mitigate their effects. Concise and informative, Pandemics will serve as the best compact consideration of this topic, written by a major authority in the field.

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.

Genomics has transformed the biological sciences. From epidemiology and medicine to evolution and forensics, the ability to determine an organism’s complete genetic makeup has changed the way science is done and the questions that can be asked of it. Genomics: A Very Short Introduction explores the science of genomics and its rapidly expanding toolbox. Sequencing a human genome can now take only a few days and those of simple bacteria and viruses, a matter of hours. The resulting sequences can be used to better understand our biology in health and disease and to ‘personalize’ medicine. This VSI explains the implications for science and society today and in the future.