Micro Exam 6 (Final) PDF

Chapter 16: Innate immunity ​ 3 lines of defense against pathogens ○​ First: skin, mucous membranes, antimicrobial substances ○​ Second: inflammation, fever, phagocytes ○​ Third: humoral and cellular immunity ​ If a microbe gets in, BOTH the 2nd and 3rd lines of def...

Chapter 16: Innate immunity ​ 3 lines of defense against pathogens ○​ First: skin, mucous membranes, antimicrobial substances ○​ Second: inflammation, fever, phagocytes ○​ Third: humoral and cellular immunity ​ If a microbe gets in, BOTH the 2nd and 3rd lines of defence are working ○​ 2nd: fast ○​ 3rd: slow ​ The concept of immunity ○​ Immunity (resistance): ability to ward off disease ○​ Susceptibility: lack of resistance to a disease ○​ Innate immunity: defenses against any pathogen; rapid, present at birth ​ 1st and 2nd lines of defense ​ There is no memory and does not target specific microbes ○​ Adaptive immunity: immunity or resistance to a SPECIFIC pathogen ​ Slower to respond and has MEMORY ​ 3rd line of defense ○​ First line of defense: toll-like receptors bind to pathogen-associated molecular patterns ​ Binding triggers immune response and induces the release of cytokines from the host cell ​ Cytokines: immune proteins that regulate the intensity and duration of immune responses ○​ Recruit other WBCs – macrophages and dendritic cells ○​ Role in activating B and T cells ​ 1st line of defense: physical factors = barriers and secretions ○​ Skin – intact skin is great barrier ​ Dry, salty, acidic, exfoliation, normal flora ○​ Mucous membranes ​ Line the entire GI, respiratory, and GU tracts ​ Secretions ​ Mucous: viscous glycoproteins that trap microbes and prevent tracts from drying out ​ Lacrimal apparatus: secretes and drains tears; washes eye; contains IgA ​ Saliva: contains lysozyme and IgA ​ Physician factors ○​ Mucociliary escalator: transports microbes trapped in mucus away from the lungs ○​ Cerumen: prevents microbes from entering the ear ○​ Urine cleans the urethra ○​ Vaginal secretions move microorganisms out of the vaginal tract ​ Chemical factors ○​ Sebum: forms a protective film and lowers the pH of skin ○​ Lysozyme: in perspiration, tears, saliva, and urine destroys bacterial cell walls – breaks bonds between peptidoglycan ○​ Gastric juice: low pH (1.2-3.0) destroys most bacteria and toxins ○​ Vaginal secretions: pH of 3-5 inhibits microbial growth ​ Normal microbiota and immunity ○​ Probiotics: live microbial cultures that give health benefit to host ○​ Prebiotics: promote growth of beneficial bacteria ​ Innate immune system: 2nd line of defense and microbe is inside ○​ WBC action – inflammation and fever ○​ Antimicrobial substances: complement interferons, iron binding proteins, antimicrobial peptides ​ Granulocytes ○​ Leukocytes with VISIBLE granules in their cytoplasm ○​ Neutrophils or PMNs: phagocytic, work in early stages of infection ○​ Basophils: release histamine; work in allergic response and inflammation ○​ Eosinophils: slightly phagocytic, toxic against parasites and helminths ​ Will increase with allergic reactions and parasitic worm infections ​ Use peroxide to kill ​ Agranulocytes ○​ Leukocytes with granules in their cytoplasm that are NOT visible with a light microscope ○​ Monocytes: mature into macrophages in tissues where they become phagocytic ○​ Dendritic cells: found in the skin, mucous membranes, and thymus – phagocytic ○​ Lymphocytes: T cells, B cells, and NK cells, play a role in adaptive immunity ​ The lymphatic system ○​ Filters the blood plasma left behind at capillary beds and returns it ot the circulatory system ○​ Lymph vessels carry lymph and possibly microbes, to lymph nodes where lymphocytes and macrophages destroy the pathogens ​ Phagocytes: cell eating ○​ Fixed macrophages: residents in tissues and organs ​ dendritic cells on skin ​ Kupffer cells in liver ​ Microglial cells in NS ○​ free/wandering macrophages: roam tissues and gather at sites of infection and tissues have lots of macrophages ​ The mechanism of phagocytosis ○​ Chemotaxis: chemical signals that attract phagocytes  ​ Microbial products, WBC parts, cytokines ​ Protein fragments from the complement pathway ○​ Adherence: attachment of a phagocyte to microorganism ​ TLR attaching to PAMPs ​ Will release cytokines to recruit more phagocytes ○​ Ingestion ​ Opsonization: microorganism is coated with serum proteins making ingestion easier ○​ Digestion: microorganisms digested inside phagolysosome ​ Inflammation ○​ Pain, redness, immobility, edema, and heat ○​ Protection and injury repair ​ 1. Destroys injurious agent or limits its effects on the body ​ 2. If can't destroy – walls off area to protect body ​ 3. Repairs and replaces tissue damaged by the injurious agent ○​ Acute = neutrophils ○​ Chronic = monocytes and macrophages ​ Steps of inflammation ○​ 1. Vasodilation and increased permeability of the blood vessels ​ Can be caused by histamine ​ Defensive substances normally found in the blood can now move into affected tissue ​ CHEMOTAXIS: chemicals produced by damaged cells, microbes, neutrophils cause the movement of leukocytes toward site of inflammation ​ AREA IS WALLED OFF: clotting elements brought to injury site to prevent microbes/toxins from entering the bloodstream ○​ 2. Phagocyte migration and phagocytosis s ​ Neutrophils initially then macrophages ​ Microbes destroyed ○​ 3. Tissue repair ​ Can't be completed until all harmful or dead cells are removed ​ Inflammation: tissue repair ○​ Cannot be completed until all harmful substances are removed or neuralized ○​ Stroma is the supporting connective tissue that is repaired – fibrosis ○​ Parenchyma is functioning part of the repaired tissue – regeneration ​ Fever ○​ Vasoconstriction and shivering occur ○​ As infection clears thermostat is reset, vasodilation and sweating occurs (crisis) ​ The complement system  ○​ Greater than 30 serum proteins produced by the liver that assist/complement the immune system in destroying microbes ○​ Proteins are designated with uppercase C and numbered in order of discovery ​ These proteins are inactive until they split ○​ Can be recruited and work together with the adaptive immune system ○​ 3 pathways: classical, alternative, lectin pathways ​ 1. The classical pathway ○​ This method of activation of complement is initiated by the adaptive immune response ○​ Antibodies bind to antigens, activating C1 ○​ C1 splits and activates c2 and c4 ○​ C2a and c4b combine and activated c3 by splitting it into c3a and c3b ○​ C3a functions in inflammation and c3b functions in cytolysis (MAC) and opsonization ​ 2. The alternative pathway ○​ C3 present in blood combines with factors B, D, and P on microbe surface ○​ C3 splits into C3a and C3b functioning the same as in the classical pathway ○​ NO ANTIBODIES ​ 3. The lectin pathway ○​ Macrophages ingest pathogens, releasing cytokines that stimulate LECTIN production in the liver ○​ Mannose-binding lectin binds to mannose, activating C2 and C4 ○​ C2a and C4b activate C3, which functions the same as in the classical and alternative pathways ​ Outcomes of complement activation ○​ Cytolysis: activated complement proteins create a membrane attack complex – gram neg is more susceptible ○​ Opsonization: coats fell and makes it sticky and promotes phagocytosis ○​ Inflammation: activated complement proteins bind to mast cells, releasing histamine ​ Interferons: antiviral/bacterial cytokines ○​ IFN-a and IFN-b produced by cells in response to viral infections ​ Cause neighboring cells to produce antiviral proteins that inhibit viral replication ○​ IFN-y: causes neutrophils and macrophages to produce nitric oxide ​ Inhibits ATP production ​ Kills bacteria and tumor cells ​ Iron binding proteins ○​ Most pathogenic bacteria require iron for their growth, many pathogens require it to the survive and leads to competition between the host and pathogen for iron  ○​ Iron in host: ​ Transferrin: found in blood and tissue fluids ​ Lactoferrin: found in milk, saliva, and mucus ​ Ferritin: found in liver, spleen, and red bone marrow ​ Hemoglobin: located in RBCs ○​ Humans use of iron ​ In cytochromes of ETC ​ Cofactors of some enzymes ​ Part of hemoglobin ○​ Bacteria produce siderophores to compete for iron ​ Some bacteria have receptors that will bind with siderophore iron complex and endocytosis ​ Some will take iron from the siderophore ​ S. pyogenes releases hemolysin which will destroy RBC and will gather in released iron ​ Antimicrobial peptides ○​ One of the most important components of innate immunity ○​ Produced in response to surface molecules on microbes ​ Produced by sweat glands and neutrophils ○​ Have 3 mechanisms of action ​ 1. Inhibit cell wall synthesis ​ 2. Form pores in plasma membrane ​ 3. Destroy DNA and RNA ○​ Broad spectrum of activity – bacteria, viruses, fungi, and eukaryotic parasites ​ Kills bacteria ​ Activate and enhance responses of immune system ​ Microbes do not appear to develop resistance ○​ Over 600 discovered in nearly all plants and animals – made by the host Chapter 17: Adaptive immunity ​ Adaptive immunity ○​ Adaptive immunity: defenses that target a specific pathogen ○​ Primary response: first time the adaptive immune system combats a particular foreign substance – SLOW, several days or more ○​ Secondary response: second and subsequent attacks by the same particular foreign substance – FAST and stronger response due to memory cells = IMMUNITY ​ Humoral immunity ○​ B lymphocytes (b cells) ​ Coated in antibodies and will become activated when in contact with specific antigen  ​ Activated B cells produces antibodies ○​ Best against invaders outside of cells – bacteria, toxins, and extracellular viruses ​ Cellular immunity ○​ T lymphocytes: recognize antigens processed by phagocytic cells ​ Activated T cells will either destroy target cell or secrete cytokines ○​ Best at tightening intracellular infections such as viruses or some bacteria ​ Cytokines ○​ Cytokines are chemical messengers of immune cells ○​ Produced in response to a stimulus ○​ Only act on cells that have receptors ​ Interleukins: cytokines between leukocytes ​ Chemokines: induce migration of leukocytes ​ Interferons: interfere with viral infections, warn neighboring cells of a viral infection ​ Tumor necrosis factor: promotes inflammation – excessive TNF is involved in the inflammatory response responsible for autoimmune diseases ○​ Cytokines can stimulate the production of more cytokines – positive feedback loop ○​ Harmful overproduction of cytokines leads to a cytokine storm → tissue damage ​ Can be caused by superantigens ​ Antigens that provoke a strong immune response ​ Proliferation of t lymphocytes ​ Fever, N/V/D, shock, death-TSS ​ Antigens: foreign substances that cause the production of antibodies/ T cells ○​ Antibodies interact with epitopes (antigenic determinants) = specific sites on the antigens ○​ Haptens: antigens too small to provoke immune responses by themselves; attach to carrier molecules ​ Antibodies = immunoglobulins ○​ Globular proteins called immunoglobulins ○​ Valence is the number of antigen-binding sites on an antibody ​ Most human antibodies have 2 binding sites = bivalent ○​ Antibody molecules can form monomers. Dimers or pentamers ○​ Four protein chains form a y-shape ​ Two identical light chains and two identical heavy chains joined by disulfide links ○​ Variable regions are at the ends of the arms = antigen binding sites ○​ Constant region is the stem, which is identical for a particular Ig class ○​ Five classes: IgG, IgM, IgA, IgD, and IgE ​ IgG ○​ Monomer ○​ 80% of serum antibodies ○​ In the blood, lymph, and intestines ​ Can leave the blood easily in response to inflammation ○​ Only antibody that crosses the placenta → naturally acquired passive immunity ○​ Trigger complement, enhance phagocytosis, neutralize bacterial toxins and viruses, protect fetus ○​ Long lived – does not indicate an active infection ​ IgM (macro) ○​ Pentamer made of 5 monomers held with a J chain ○​ 6 % of serum antibodies ○​ Remain in blood vessels due to large size ○​ Agglutination and complement fixation ​ Cause clumping of cells and viruses and involved in ABO blood typing ○​ First response to an infection ; short lived ​ If IgM is present then the pathogen is usually present ​ IgA ○​ Monomer in serum and dimer in secretions ○​ 13% of serum antibodies but is the most common found in MUCOUS MEMBRANES ○​ Prevent microbial attachment to mucous membranes ​ IgD ○​ Monomer ○​ 0.02% of serum antibodies ○​ Structure similar to IgG ○​ In blood, lymph, and on B cells ○​ No well defined function; may eliminate B cells that produce antibodies against self ​ IgE ○​ Monomer ○​ Found on mast cells, on basophils, and in blood ○​ Allergic reactions!!! ○​ Cause the release of histamine when bound to antigen; lysis of parasitic worms ​ Life of B cells ​ 1. Produced: B are produced in the red bone marrow = immature lymphocytes ​ 2. Maturation: any self-reactive B cells are destroyed – clonal deletion ​ Numbers decreases – about a billion different B and T cells now ​ B cells mature in red bone marrow  ​ 3. Migration: B cells migrate to secondary lymphatic organs, especially the spleen and the lymph nodes ​ 4. Wait to meet antigen: some cells never meet their antigen ​ 5. Activation: encounter antigen AND confirmation ​ Activated B cell - clonal selection ​ 6. Proliferation: activated B cell produced clones of itself (plasma cells) = clonal expansion ​ 7. Plasma cells secrete Ab into circulation ​ 8. Memory cells: the best B cells are saved and maintained providing immunity ​ Activation of B cells ○​ B cells contain surface Igs with specific antigen receptors ○​ B cell internalizes and processes antigen ○​ Antigen fragments are displayed on MHC class II molecules on surface of B cell ○​ T helper cell contacts the displayed antigen fragment and releases cytokines and activate B cells = CONFIRMATION ○​ B cell undergoes proliferation (clonal expansion) ​ Activation of B cells: antigens ○​ T-dependent antigen ​ Antigen that requires a Th cell to produce antibodies ○​ T-independent antigens ​ Stimulate the B cell without the help of T cells ​ Provoke a weak immune response, usually producing IgM ​ No memory cells generated ​ Results of antibody production ○​ An antigen-antibody complex forms when antibodies bind to antigens ​ Protections the host by tagging foreign molecules or cells for destruction ​ 1. agglutination ​ 2. opsonization ​ 3. Antibody-dependent cell-mediated cytotoxicity — for cells too big to be eaten ​ 4. neutralization ​ 5. Activation of complement system ​ Life of T cells ○​ 1. Produced in red bone marrow ○​ 2. Mature: in the thymus, any self reactive T cells are destroyed = thymic selection ○​ 3. Migrate: from the thymus to spleen and lymph nodes ○​ 4. Wait to meet antigen ○​ 5. Antigen encounter and costimulation → activation  ​ Attach to antigens via T-cell receptors and requires APCs ○​ 6. Proliferation: activated T cells produce an army of effector T cells = clonal selection ○​ 7. Battle is fought = effector T cells ○​ 8. Memory cells: the effector T cells are saved and maintained providing immunity ​ Activation of T cells requires MHC II molecules ○​ MHC proteins: major histocompatibility complex genes encode glycoproteins on the cell surface ​ Class I MHC are on the membrane of nucleated animal cells - Mark cell as SELF ​ Class II MHC are only on the surface of antigen-presenting cells = B cells, dendritic cells, and activated macrophages – important in presentation of antigen to T cells ​ Antigen-presenting cells ○​ Dendritic cells = primary APCs ​ Engulf and degrade microbes - present antigens with MHC II molecules to T cells ​ Found in the skin, genital tract, lymph nodes, spleen, thymus, and blood ○​ Macrophages ​ Activated by cytokines or the ingestion of antigenic material ​ Migrate to lymph tissue, present antigen with MHC II molecule to T cells ​ Classes of T cells ○​ CD4+ = T helper cells ​ Bind to MHC class II molecules and antigen on B cells and APCs ​ Cytokine signaling with B cells; interact directly with antigens ○​ CD8+ = cytotoxic T lymphocytes ​ Bind MHC class I molecules ​ T helper cells ○​ APC or Th secrete costimulatory molecule, activating the Th cell ○​ Th cells produce cytokines and differentiate into ​ Th1 cells: produce IFN-y which activates macrophages, enhances complement, and stimulates antibody production ​ Th2 cells: activate B cells to produce IgE; activate eosinophils ​ Th 17 cells: cells produce IL-17 and contribute to inflammation ​ T regulatory cells ○​ Formally known as T suppressor cells ○​ Suppress T cells against self ○​ Protect intestinal bacteria required for digestion ○​ Protect fetus ​ T cytotoxic cells ○​ CTLs recognize and kill self-cells altered by infection ​ Self cells carry endogenous antigens on a surface presented with MHC class I molecules ​ CTLs release perforin and enzymes that induce apoptosis in the infected cell ○​ Induce apoptosis of infected self cells ​ Programmed cell death ​ Prevents the spread of infectious viruses to other cells ​ Extracellular killing by the immune system​ ○​ Natural killer (NK) cells – 2nd line of Defense ​ Are considered a lymphocyte – same lineage as B and T cells ​ Agranular leukocytes - destroy cells that don't express MHC class I self-antigens (foreign cells) ​ Kill virus-infected and tumor cells and attack parasites ​ Not always stimulated by an antigen ​ Form pores in the target cell, leading to lysis or apoptosis ​ Not as specific as CTLs, can cause collateral damage ​ Immunological memory ○​ Secondary memory response occurs after second exposure to an antigen ○​ FAST, lasts many days, greater in magnitude ​ Memory cells (produced in response to the initial exposure) are activated ​ Memory cells → plasma cells ​ STRONG FAST RESPONSE – levels of antibody are higher than in primary response ​ Reflects intensity of the humoral response ​ Types of adaptive immunity ○​ Naturally acquired active immunity ​ Resulting from infection ○​ Naturally acquired passive immunity ​ Transplacental or via colostrum or milk ○​ Artificially acquired active immunity ​ Injection of vaccination (immunization) ○​ Artificially acquired passive immunity ​ Injection of antibodies, antitoxin, antivenom ​ Antiserum: blood-derived fluids containing antibodies ​ Globulins: serum proteins ○​ Gamma globulins: serum fraction containing antibodies – all classes of antibodies found in serum ​ Serology: the study of reactions between antibodies and antigens Chapter 18: Practical Applications of Immunology ​ Variolation: initially by inhaling dried scabs, later inoculation of smallpox on the skin ​ Jenner termed vaccination by Pasteur ​ Vaccine: suspension of organisms or fractions of organisms that induce immunity ​ Principles and effects of vaccination ○​ Provokes a primary immune response ○​ Leads to the formation of antibodies and memory cells – without causing illness ○​ Produces a rapid intense secondary response = immunity ​ Herd immunity ○​ Immunity in most of the population ​ Types of vaccines and their characteristics ○​ Live attenuated vaccines ​ Weakened pathogen ​ Closely mimic actual infection ​ Activates both cellular and humoral responses ○​ Inactivated vaccines ​ Require repeated booster doses ​ Induce mostly humoral immunity ○​ Subunit vaccines use antigenic fragments to stimulate an immune response ​ Recombinant vaccines: subunit vaccines produced by genetic modification of nonpathogenic microbe ​ Polysaccharide vaccines – made from molecules in the pathogens capsule ○​ Virus-like particle vaccines: resemble intact viruses but do not contain viral genetic material ○​ Toxoids: initiated toxins ○​ Conjugated vaccines: combine antigen with a protein to boost immune response ○​ Nucleic acid vaccines: DNA vaccine: inject DNA into patient's cells produce the protein antigen ○​ mRNA vaccines: mRNA codes for an antigen from the pathogen that will trigger humoral and cell mediated immune responses ​ T-independent antigens​ ○​ Stimulate the B cell without the help of T cells ○​ Provoke a weak immune response, usually producing IgM ○​ No memory cells generated ​ Vaccination– emerging technology ○​ Nanopatch: delivers a dry formulation of a vaccine to the skin ​ Requires no refrigeration ○​ Multiple combination vaccines – less injections needed ​ Diagnostic immunology ○​ Adaptive immunity reactions are very specific  ○​ Antibodies are fantastic tools for diagnostics and for research ○​ Sensitivity of a diagnostic test: probability that a test is reactive if the specimen is a true positive ○​ Specificity: probability that a test is NOT reactive if the specimen is true negative ​ Agglutination reactions ​ Direct agglutination tests ○​ Antibodies bind directly to large antigen molecules ​ Indirect (passive) agglutination tests ○​ Antigen is too small for direct agglutination ○​ Usually use latex beads to make antigens or antibodies larger ​ Hemagglutination ○​ Agglutination of RBC surface antigens and complementary antibodies ○​ Used in blood typing ​ Antitoxin = antibodies produced in response to a toxin ​ Direct vs indirect ELISA ○​ Direct: detects antigens ○​ Indirect: detects antibodies Chapter 19: Immune system disorders ​ Hypersensitivities: antigenic response that leads to undesirable effects ○​ Occurs when sensitized by previous exposure to an antigen ​ Hygiene hypothesis: suggests that limiting childhood exposure to pathogens may lower immune tolerance and the ability to cope with harmless antigens resulting in more allergies ​ Type I (anaphylactic) reactions ○​ Occurs minutes after a person sensitized to an antigen is exposed to that antigen ○​ Antigens combine with IgE antigens ○​ IgE attaches to mast cells and basophils ​ Mast cells and basophils undergo degranulation which releases capillaries ​ Histamine: vasodilation and increased permeability of blood capillaries ​ Leukotrienes cause prolonged contraction of smooth muscles – bronchospasms ○​ Systemic anaphylaxis ​ Released mediators will cause vasodilation and serious decrease in BP ○​ Localized anaphylaxis ​ Usually associated with ingested or inhaled antigens ​ Hives, hay fever, food intolerance, asthma ​ Preventing anaphylactic reactions ○​ Antigens are inoculated beneath the epidermis to test for a rapid inflammatory reaction  ○​ Desensitization: increasing dosages if antigen beneath the skin ​ Type II (cytotoxic reactions) ○​ Activation of complement by the combination of IgG or IgM antibodies with an antigenic cell ○​ Transfusion reactions: ABO blood group system, antibodies form against certain carbohydrate antigens on RBCs ○​ Rh factor antigen found on RBC of 85% of the population ○​ Hemolytic disease of the newborn ​ Rh- mother with an Rh+ fetus causes the mother to produce anti-Rh antibodies ​ Second Rh+ fetus will receive anti-rh antibodies damaging fetal RBCs ○​ Drug induced cytotoxic reactions ​ Thrombocytopenic purpura ​ Platelets combine with drugs, forming a complex that is antigenic ​ Antibody and complement destroy platelets ​ Agranulocytosis ​ Drug molecules coat white blood cells → immune destruction of granulocytes ​ Hemolytic anemia ​ As above but with RBCs ​ Type III (immune complex reactions) ○​ Form immune complexes that lodge in the basement membranes beneath the cells → activate complement causing inflammation ○​ Glomerulonephritis ​ Inflammatory damage to the kidney glomeruli due to immune complexes as a result of infection ​ Type IV (delayed cell-mediated) reactions ○​ Cell-mediated immune responses caused by T cells – no antibodies are involved ○​ Delayed hypersensitivity: delay is in the time needed for T cells and macrophages to migrate to antigen ○​ Antigens are phagocytized and presented to receptors on t cells causing sensitization ○​ Allergic contact dermatitis ​ Haptens combine with proteins in the skin producing an immune response ​ Autoimmune diseases ○​ Immune system mistakenly responds to self antigens, causing damage to the organs and 75% affect females ○​ Autoimmunity is loss of self-tolerance → inability to discriminate self from nonself ​ Cytotoxic autoimmune reactions  ○​ MS ​ Abnormal T cells, autoantibodies, and macrophages attack myelin sheath in CNS ​ Numbness and tingling, cognitive dysfunction, depression, fatigue, muscle spasms ​ Immune complex autoimmune reactions ○​ Graves disease ​ Abnormal antibodies that mimic TSH → excessive amounts of thyroid hormone ○​ Myasthenia gravis ​ Abnormal antibodies coat acetylcholine receptors and muscles fail to receive nerve signals ○​ Lupus ​ Produce abnormal antibodies directed at cell components including DNA ○​ RA ​ Immune complexes cause chronic inflammation in joints and SEVERE damage ​ Cell mediated autoimmune reactions ○​ Type 1 diabetes ​ T cell destruction of insulin-secreting B cells in pancreas ○​ Psoriasis: considered a T helper disease ​ Reactions related to the human leukocyte antigen complex ○​ Rejection reactions ​ To prevent rejection – HLA and ABO blood groups closely matched ○​ Human leukocyte antigen: MHC class I molecules in humans ​ Reactions to transplantation ○​ Transplants to a privileged site and privileged tissue do not cause an immune response ​ Privileged site: antibodies don't normally circulate in this area of the body ​ Privileged tissue: removal of surface antigens ​ Graft = transplant of tissue ○​ Autograft: use of one's own tissue ○​ isograftL use of identical twins tissue ○​ allograftsL use of tissue from another person ○​ Xenotransplantation product: use of nonhuman tissue ​ Must overcome hyperacute rejection: response to nonhuman antigens ○​ Graft versus host disease ​ Graft material mounts an immune response against the host cells ​ Can result from transplanted bone marrow that contains immunocompetent cells  ​ Cancer cells removed by immune surveillance ​ Congenital immunodeficiencies: due to defective or missing genes ​ Acquired immunodeficiencies: developed/acquired during an individuals life D/T drugs, cancer, infections HIV/AIDS ​ Describe some of the opportunistic infections that led to the discovery of AIDS ○​ Pneumocystis pneumonia and Kaposi sarcoma ​ Describe the structure of the human immunodeficiency virus ○​ RNA nucleic acid ○​ Retrovirus ○​ Reverse transcriptase enzyme ○​ gp120 and gp41 spikes ○​ Fuse with receptor on T helper cell ​ Describe HIV in terms of an active vs latent infection ○​ Active infection: new viruses bud from the host cell ○​ Latent infection: DNA is hidden in the chromosome as a provirus ​ Explain how the high mutation rate of HIV affects the course of the disease ○​ Virus may mutate several times a day ○​ Lack proofreading capability ○​ Retroviruses in general have high mutation rate ​ Describe what occurs in each stage of an HIV infection ○​ Stage 1 – asymptomatic or lymphadenopathy ​ May find 10 million viral RNA particles/ml in first week ​ Billions of T helper cells indicted in first few weeks ○​ Stage 2 – steady decline of T cells ​ Persistent infections, fever, oral leukoplakia ○​ Stage 3 – AIDS develops ​ Opportunistic infections ​ Explain what the criteria are to be diagnosed with AIDS ​ Explain how HIV dodges the immune system ​ Discuss, in detail, how HIV is transmitted and how we can use this knowledge to prevent the spread of the disease ​ Describe some of the challenges of making and HIV vaccine ○​ No model of natural immunity to mimic ○​ Attenuated vaccine too dangerous ○​ Virus quickly enters host cell so antigens aren’t available for long