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54 Cards in this Set
- Front
- Back
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what is the aim of the host response to viral infection do?
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prevent entry, but failing this, eliminate the virus as quickly as possible and lessen the amount of damage done by the virus
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what does the host response to viral infection?
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destroy virus-infected cells, prevent virus replication (w/o killing cells), destroy free virus
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what mechanisms does the host response to viral infection include?
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innate (nonspecific) & acquired (specific) immunity
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what is innate (nonspecific) immunity?
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active immediately and against a wide variety of viruses
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what is acquired (specific) immunity?
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an induced response (requires several days to become active) and active only against the infecting virus
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what are the components of innate (nonspecific) defences?
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physical barriers, genetic barriers, macrophages, natural killer (NK) cells, interferon, complement, inflammation
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what are the components of acquired (specific) defences?
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antibody, cytotoxic T cells,
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what is the most powerful weapons in the 'immunological armory'?
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acquired (specific) defences
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what cells and factors occur when in immune response?
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INFα first, followed by NK cell (killing), then T cell (killing), followed by antibodies
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how do genetic barriers affect tropism and innate immunity?
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receptor proteins are genetically determined and the absense of receptor proteins render host resistant to infection
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what is an example of genetic barriers affectings tropism?
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human beings not susceptible to canine parvovirus (CPV2) due to absense of genes that codae for CPV2 receptors
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what is the primary role of macrophages in host response?
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phagocytes: engulf and destroy viruses and virus-infected cells
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where are macrophages located?
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in submucosa through out body, lymph nodes, lung, liver, spleen, blood, body cavities
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what is the task of macrophages?
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prevent entry, destroy virus infected cells, destroy free virus
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what is the primary role of interferon in host response?
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cause cells to produce antiviral proteins to prevent virus replication (without killing cells by blocking viral biosynthesis)
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where are IFNs active?
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produced in response to viral infection (ds RNA, others) and released from infected cell to diffuse to neighboring and distant cells
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what does IFN stand for?
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interferon
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what does NK stand for ?
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natural killer
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what are NK cells NOT?
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non-B, non-T lymphocytes
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what do NK cells do?
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detect and destroy virus-infected cells
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how are increases in activity of and number of NK cells induced?
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increased IFN
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how do NK cells recognize virus-infected cells?
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may detect cells with low levels of MHC class I molecules
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how does the inflammatory response occur during viral infections?
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virus induced tissue injury results in mast cell degranulation which release vasocactive amines resulting in vasodilation and increased vascular permeability which focuses macrophages, NK cells, complement, IFNs, antibody, cytotoxic T cells at sites of virus infection
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what is the result of an inflammatory response?
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vasodilation & increased vascular permeability
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what does the complement system do?
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mediate certain immune responses
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where are complement components found?
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circulate in blood in inactive forms
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how are complement components activated?
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contact with antigen-antibody complexes (classical pathway) & contact with the surface of virus or virus-infected cells (alternative pathway)
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what occurs after the activation of complement?
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form a complex that enzymatically punctures the host cell membrane resulting in cell lysis, releasing by products that cause vasodilation, increase vascular permeability, chemotaxic for neutrophils.
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how is the acquired (specific) immune response generated?
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by the interaction of macrophages, T cells, and B cells within lymph nodes, spleen, and lymphoid tissues
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what causes B cells to differentiate into antibody producing plasma cells?
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B cell differentiation via soluble and particulate (viorion) antigens, an exogenous presentation
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what caues T cells to differentiate into cytotoxic T cells?
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CD+ Tc differentiation driven by virus antigen-MHC1, an endogenous presentation that requires virus infected cells
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how do antibodies participate in the immune response to virus infection?
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destroy free virus (neutralization), destroy virus-infected cells, & antibody-dependent cell-mediated cyotoxicity (ADCC)
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what is the process of cytotoxic T cell differentiation in acquired immunity?
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virus infection results in production of viral proteins which are degraded and picked up by MHC1 molecules that are displayed at cell surface where CD8+ cells recognize the virus antigen-MHC I complex (TCR) are directed to differentiate into cytotoxic T cells by TH1 cells, which then attack other virally infected cells displaying the viral antigen-MHC I complex
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what is virus neutralization?
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antibody destruction of free virus
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how does virus neutralization occur?
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antibody binds virus and prevents attachment, penetration, uncoating, or antibody binds virus and promotes uptake by macrophages (opsonization), or complement +/- antibody prevents attachment
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how do antibodies detect virus-infected cells?
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during virus infection, virus proteins are incorporated in cell plasma membrane
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what mechanisms do antibodies use to destroy virus-infected cell?
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antibody + complement = lysis OR antibody-mediated cell cytotoxicity (ADCC) = lysis
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what does complement consist of?
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30 serum proteins; numbered C1-C9
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how is the complement activated?
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by antigen-antibody complexes on by virus-infected cell and surface of virus or virus-infected cell (w/o antibody)
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what is the function of complement?
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destroy virus infected cells (cell lysis), destroy free virus, inflammation (C3a/C5a)
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how does ADCC work?
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NK cells, macrophages, PMN recognize infected cell via Fc receptors on antibodies
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what does ADCC stand for?
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Antibody-dependent cell-mediated cytotoxicity
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what do cytotoxic T cells do?
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they are virus-specific and recognize infected cells via MHC1-virus progein complex to destroy virus-infected cells via secretion of cytotoxins
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how does recovery occur?
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if a failure to prevent entry (via physical and genetic barriers, macrophages) activates a wide array of immune responses (interferon, complement, macrophages, NK cells, inflammatory reactions, antibody, cytotoxic T cells)
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how does protection from reinfection occur?
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protective immunity derived by virus exposure/immunization: antiviral IgA on body surfaces, antiviral IgG in blood, and if antibody is not sufficient, anamnestic T & B cell responses (memory cells) are activated
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what is protective immunity?
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protection from reinfection
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what is mucosal immunity?
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immunity to reinfection at a mucosal surface is mediated by: IgA anibodies that are produced by plasma cells in submucosa, circulating antigen-specific T cells, to lesser extent IgG/IgM antibodies
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what is passive immunity?
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maternally-derived immunity
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what animals require passive immunity?
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non-primate species which are immunologically naïve at birth and are born into a world teeming with potentially lethal microorganisms
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how is passive immunity acquired?
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maternal antibodies passed to neonate at birth and during post-partum period via milk and colostrum
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how does passive immunity occur?
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IgG antibodies are absorbed from intestines to blood during first 1-2 days postpartum, and IgG & IgA in colostrum and milk provide intestinal protection
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how long does passive immunity serum IgG antibodies persist?
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6 mo (cattle, horses), 3 mo (dogs, cats, pigs), 1 mo (chickens, turkeys)
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what is the primary risk with passive immunity?
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failure of passive transfer renders neonate susceptible, provides protection for limited time only, interferes with vaccination during the neonatal period
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what can interfere with immunization of neonates?
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maternal antibodies
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