Host pathogen interactions

Several microbial pathogens have been reported to interact with glycosaminoglycans (GAGs) on cell surfaces and in the extracellularmatrix. Herewe demonstrate thatM protein, a major surface-expressed virulence factor of the human bac-terial pathogen, Streptococcus pyogenes, mediates binding to various forms of GAGs. Hence, S. pyogenesstrains expressing a large number of different types of M proteins bound to dermatan sulfate (DS), highly sulfated fractions of heparan sulfate (HS) and heparin, whereas strains deficient in M protein surface expression failed to interact with these GAGs. ...

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Host species specificity of the polyomaviruses simian virus 40 (SV40) and mouse polyomavirus (PyV) has been shown to be determined by the host DNA polymerase a-primase complex involved in the initiation of both viral and host DNA replication. Here we demonstrate that DNA repli-cation of the related human pathogenic polyomavirus JC virus (JCV) can be supportedin vitro by DNA polymerase a-primase of either human or murine origin indicating that the mechanism of its strict species specificity differs from that of SV40 and PyV.

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Trichodermaspecies have been investigated as biological control agents for over 70 years owing to their ability to antagonize plant pathogenic fungi. Mycoparasitism, one of the main mechanisms involved in the antagonistic activity ofTrichodermastrains, depends on the secretion of complex mix-tures of hydrolytic enzymes able to degrade the host cell wall. The antifun-gal activity of an a-1,3-glucanase (EC 3.2.1.59, enzymes able to degrade a-1,3-glucans and also named mutanases) has been described in T. harzia-num and its role in mycoparasitic processes has been suggested....

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The interaction of proteinase inhibitors produced, in most cases, by host organisms and the invasive proteinases of pathogens or parasites or the dietary proteinases of predators, results in an evolutionary ‘arms race’ of rapid and ongoing change in both interacting proteins.

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Bacterial lipoproteins play crucial roles in host–pathogen interactions and pathogenesis and are important targets for the immune system. A promi-nent example is the outer surface protein A (OspA) ofBorrelia burgdorferi, which has been efficiently used as a vaccine for the prevention of Lyme dis-ease.

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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: Draft genome sequence of the Daphnia pathogen Octosporea bayeri: insights into the gene content of a large microsporidian genome and a model for host-parasite interactions...

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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: PHIDIAS: a pathogen-host interaction data integration and analysis system...

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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: " First Dominique Dormont international conference on "Host-pathogen interactions in chronic infections – viral and host determinants of HCV, HCMV, and HIV infections...

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Tuyển tập các báo cáo nghiên cứu về bệnh học thý y được đăng trên tạp chí Acta Veterinaria Scandinavica cung cấp cho các bạn kiến thức về bệnh thú yđề tài: Adaptation of mammalian host-pathogen interactions in a changing arctic environment...

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Tuyển tập các báo cáo nghiên cứu về sinh học được đăng trên tạp chí sinh học Journal of Biology đề tài: No better time to FRET: shedding light on host pathogen interactions...

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Numerous virus–target cell interactions have been described, and it is now clear that different viruses can use similar host-cell receptors for entry. The list of certain and likely host receptors for viral pathogens is long. Among the host membrane components that can serve as receptors for viruses are sialic acids, gangliosides, glycosaminoglycans, integrins and other members of the immunoglobulin superfamily, histocompatibility antigens, and regulators and receptors for complement components.

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Table 114-1 Examples of Microbial Ligand-Receptor Interactions Microorganism Type of Microbial Ligand Host Receptor Viral Pathogens Influenza virus Hemagglutinin Sialic acid Measles virus Vaccine strain Hemagglutinin CD46/moesin Wild-type strains Hemagglutinin Signaling lymphocytic activation molecule (SLAM) Human herpesvirus type 6 ? CD46 Herpes simplex virus Glycoprotein C Heparan sulfate HIV Surface glycoprotein CD4 and chemokine receptors CXCR4) (CCR5 and Epstein-Barr virus Envelope protein CD21 (=CR2) Adenovirus Fiber protein Coxsackie-adenovirus recepto...

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The microbiology laboratory must be an ally in the diagnostic endeavor. Astute laboratory personnel will suggest optimal culture and transport conditions or alternative tests to facilitate diagnosis. If informed about specific potential pathogens, an alert laboratory staff will allow sufficient time for these organisms to become evident in culture, even when the organisms are present in small numbers or are slow-growing.

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Viral Adhesins (See also Chap. 161) All viral pathogens must bind to host cells, enter them, and replicate within them. Viral coat proteins serve as the ligands for cellular entry, and more than one ligand-receptor interaction may be needed; for example, HIV uses its envelope glycoprotein (gp) 120 to enter host cells by binding to both CD4 and one of two receptors for chemokines (designated CCR5 and CXCR4). Similarly, the measles virus H glycoprotein binds to both CD46 and the membrane-organizing protein moesin on host cells.

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Host Factors in Infection For any infectious process to occur, the pathogen and the host must first encounter each other. Factors such as geography, environment, and behavior thus influence the likelihood of infection. Although the initial encounter between a susceptible host and a virulent organism frequently results in disease, some organisms can be harbored in the host for years before disease becomes clinically evident. For a complete view, individual patients must be considered in the context of the population to which they belong.

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Harrison's Internal Medicine Chapter 113. Introduction to Infectious Diseases: Host–Pathogen Interactions Host–Pathogen Interactions: Introduction Despite decades of dramatic progress in their treatment and prevention, infectious diseases remain a major cause of death and debility and are responsible for worsening the living conditions of many millions of people around the world. Infections frequently challenge the physician's diagnostic skill and must be considered in the differential diagnoses of syndromes affecting every organ system.

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The complement system (Chap. 308) consists of a group of serum proteins functioning as a cooperative, self-regulating cascade of enzymes that adhere to— and in some cases disrupt—the surface of invading organisms. Some of these surface-adherent proteins (e.g., C3b) can then act as opsonins for destruction of microbes by phagocytes. The later, "terminal" components (C7, C8, and C9) can directly kill some bacterial invaders (notably, many of the neisseriae) by forming a membrane attack complex and disrupting the integrity of the bacterial membrane, thus causing bacteriolysis.

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The Immune Response Innate Immunity As they have co-evolved with microbes, higher organisms have developed mechanisms for recognizing and responding to microorganisms. Many of these mechanisms, referred to together as innate immunity, are evolutionarily ancient, having been conserved from insects to humans. In general, innate immune mechanisms exploit molecular patterns found specifically in pathogenic microorganisms. These "pathogen signatures" are recognized by host molecules that either directly interfere with the pathogen or initiate a response that does so.

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