Molecular insights into human immunodeficiency virus type 1 pathogenesis
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Abstract Mice infected with lymphocytic choriomeningitis (LCM)3 virus are a useful model for understanding the pathogenesis of disease associated with both acute and chronic virus infections (1, 2). In this model, tissue injury is caused by the interaction of the host's anti-viral immune response with virus or virus-infected cells. In acute infection, injection of adult mice with LCM virus leads either to recovery or death depending on the dose of virus administered, the route of inoculation used, and the ability of the host to mount an anti-viral immune response (3, 4). In chronic infection, the time scale of the response to LCM virus is lengthened and the severity of disease is related to the location and amount of LCM virus carried, the magnitude of the anti-viral antibody response made, and the interaction between virus and antibody (5). In our initial studies on the pathogenesis of disease associated with LCM virus infection, we studied the susceptibility of different murine strains to LCM virus (5–7).
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At present, the pathogenesis of the novel coronavirus disease 2019 (COVID‑19) has not been fully elucidated. Clinical and experimental findings from studies investigating COVID‑19 have suggested that the immune‑inflammatory response has a crucial role in severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) infection. The present article aimed to systematically review the available literature on the pathogenesis of COVID‑19. Severe COVID‑19 is characterized by organ dysfunction, hypercytokinemia and lymphopenia. It is assumed that the direct cytopathological damage of host cells and the dysregulated immune response caused by SARS‑CoV‑2 may be the primary underlying mechanisms of COVID‑19. Based on the published literature, this review attempts to provide an integrated view of the immunological mechanisms and the potential pathogenesis of COVID‑19, providing an in‑depth summary of the host‑pathogen interaction and host immune responses. It is of great importance to elucidate the possible pathogenesis of COVID‑19 to determine the direction of future research.
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Investigation into the pathogenesis of foot-and-mouth disease (FMD) has focused on the study of the disease in cattle with less emphasis on pigs, small ruminants and wildlife. 'Atypical' FMD-associated syndromes such as myocarditis, reproductive losses and chronic heat intolerance have also received little attention. Yet, all of these manifestations of FMD are reflections of distinct pathogenesis events. For example, naturally occurring porcinophilic strains and unique virus–host combinations that result in high-mortality outbreaks surely have their basis in molecular-, cellular- and tissue-level interactions between host and virus (i.e. pathogenesis). The goal of this review is to emphasize how the less commonly studied FMD syndromes and host species contribute to the overall understanding of pathogenesis and how extensive in vitro studies have contributed to our understanding of disease processes in live animals.
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Pathogens are disease-causing agents and pathogenesis is the study of the disease process. In cultured cells, observed changes caused by viral infection are ascribed directly to the infection. Disease is a more complex process involves virus effects on particular cells, immune responses or a combination of both. Research in viral pathogenesis seeks to understand the underlying molecular events that cause observed damage. This requires development of model systems. Models may include adaption of a human virus to growth in animals. Alternatively, studying the pathogenesis of an animal virus in its natural host may provide insight into pathogenesis of a related human virus. Modern genetic tools are providing new avenues of model development, including genetic engineering of animals. Results from several different models can be combined to gain an understanding of the pathogenesis of a virus.
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Orthohantaviruses are zoonotic viruses that are naturally maintained by persistent infection in specific reservoir species. Although these viruses mainly circulate among rodents worldwide, spill-over infection to humans occurs. Orthohantavirus infection in humans can result in two distinct clinical outcomes: hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS). While both syndromes develop following respiratory transmission and are associated with multi-organ failure and high mortality rates, little is known about the mechanisms that result in these distinct clinical outcomes. Therefore, it is important to identify which cell types and tissues play a role in the differential development of pathogenesis in humans. Here, we review current knowledge on cell tropism and its role in pathogenesis during orthohantavirus infection in humans and reservoir rodents. Orthohantaviruses predominantly infect microvascular endothelial cells (ECs) of a variety of organs (lungs, heart, kidney, liver and spleen) in humans. However, in this review we demonstrate that other cell types (e.g. macrophages, dendritic cells and tubular epithelium) are infected as well and may play a role in the early steps in pathogenesis. A key driver for pathogenesis is increased vascular permeability, which can be direct effect of viral infection in ECs or result of an imbalanced immune response in an attempt to clear the virus. Future studies should focus on the role of identifying how infection of organ-specific endothelial cells as well as other cell types contribute to pathogenesis.
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The pathogenesis of viral myocarditis is still not completely clear all over the world now.However, the damage to the body caused by the viral myocarditis has been highlighted and its pathogenesis has become a research hot spot.With the development of immunology and molecular biology, the pathogenesis of viral myocarditis has made great breakthrough.Many scholars advocate that the course of viral myocarditis should be divided into three phases: viral replication, immune response and inflammatory dilated cardiomyopathy.This review summarizes the progress of the pathogenesis of viral myocarditis from the above three phases through reviewing previous articles, aiming to provide new evidence and references for clinical diagnosis and therapy of viral myocarditis.
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Pathogens are disease-causing agents and pathogenesis is the study of the disease process. In cultured cells, observed changes (i.e., death, altered morphology, transformation) can be ascribed directly to virus infection. However disease is a more complex process that may result from direct virus effects, immune responses to infection, or a combination of both. Modern studies of viral pathogenesis seek to understand not only the damage to an organism but the underlying molecular events that cause the observed damage. Diseases caused by human viruses are often studied in animal models. Developing such models may include adaption of a human virus to growth in animals. Or human viruses may be used to inoculate animals by unnatural routes, or at very high doses. Alternatively, studying the pathogenesis of an animal virus in its natural host may provide insight into pathogenesis of a related human virus. Development of model systems can be difficult and expensive but modern genetic methods are providing new avenues of study. Often results from several different models are combined to gain an understanding of the pathogenesis of a single virus.
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