| A | B |
|---|
| testing sensitivity | The percentage of the results that will be positive when HIV is present |
| testing specificity | The percentage of the results that will be negative when HIV not present. |
| humoral immunity | exogenous, antibody-mediated; (involves humours of the body) |
| plasma cells | APC; differentiate from B cells upon stimulation by CD4+ lymphocytes |
| delayed-type hypersensitivity (T_h1) response | takes 2-3 days to develop; 1. CD8 + CD4 recognize antigen+MHC-I/II 2. MO (APC) release IL-1, stimulating CD4 proliferation |
| innate immunity | involves the inflammatory response, body temperature, lysozyme, complement, interferon and stomach acid |
| specific/adaptive immunity | specificity, diversity, memory, and self/non-self recognition; activated by innate immune response |
| anergy | lack of reaction by the body's defence mechanisms when foreign substances come into contact with the body; indicates lack of immune response |
| western blot test / immunoblot | uses gel electrophoresis to separate denatured proteins by mass. The proteins are then transferred out of the gel and onto a membrane, where they are "probed" using antibodies specific to the protein |
| ELISA assay | (Enzyme-Linked ImmunoSorbent Assay); used to detect presence of antigen or antibody |
| enhancing antibody | an antibody that enhances or promotes -- rather than inhibits disease progression |
| neutralizing antibody | form of antibody that reacts with an infectious agent and destroys or inhibits its infectivity and virulence |
| lymph node regions | 1. cortex 2. paracortex 3. medulla |
| T helper/effector cells | involved in activating and directing other immune cells; no cytotoxic or phagocytic activity; they cannot kill infected host (also known as somatic) cells or pathogens, and without other immune cells they would usually be considered useless against an infection |
| T_h1 cells | produce IFN-γ and TNF-β; maximises the killing efficacy of the macrophages and in the proliferation of cytotoxic CD8+ T cells, and it has been suggested that their primary role during an immune response is to activate and/or proliferate the cellular immune system |
| T_h2 cells | produce IL-4, 5, 13; express a variety of cytokines, many of which stimulate B-cells into proliferation, to induce B-cell antibody class switching, and to increase antibody production. Th2 cells are therefore considered necessary for the full maturation of the humoral immune system |
| Antibody-Dependent Cellular Cytotoxicity (ADCC) | 1. Recognition of the infected cell by Fc receptors on the surface of the effector (NK) cell. 2. Effector cell's Fc receptors recognize the Fc (constant) portion of antibodies bound to the surface of a pathogen-infected cell |
| Three Mechanisms of Cell-Mediated Immunity | 1. Natural Killer Cells (NK Cells) 2. Cytotoxic T-Lymphocytes (CTL) 3. Antibody-Dependent Cellular Cytotoxicity (ADCC) |
| syncytium | a large region of cytoplasm that contains many nuclei; may form by not undergoing cytokinesis (post-S-phase) or viral fusion proteins (ie GP-41) cause cellular fusion with neighboring cells |
| Steps In Activation of naïve helper T cells | INCOMPLETE |
| TNF | (tumor necrosis factor); causes the necrosis of some tumors, but may stimulate the growth of others; stimulates MO phagocytosis; promotes inflammatory response |
| interleukin | cytokines expressed by leukocytes (as well as other cells) for intercellular communication |
| IL-2 | secreted by T cells, stimulates growth and differentiation of T cell response |
| IL-10 | inhibits Th1 cytokine production |
| IL-4 | involved in proliferation of B cells, and the development of T cells and mast cells. Important role in allergic responses. |
| IFN-γ / type II interferon | cytokine; secreted by T-lymphocytes and NK cells; activates APCs and promotes Th1 differentiation |
| CAF | INCOMPLETE (cellular antiviral factor) |
| DC-SIGN | transmembrane protein on dendritic cells; 1. Binds HIV 2. Transports to lymph nodes 3. Infects T-cells |
| Steps of HIV Entry into Target Cells | 1. Binding (of virus to receptors) 2. Binding (of GP120, co-receptor to cell) 3. Fusion (viral envelope & plasma membrane) 4. Reverse transcription (viral RNA to DNA) 5. Entry into nucleus 6. Integration (into host DNA) |
| CD4+ T-lymphocytes / Helper T cells | release cytokines; main HIV target (one of); orchestrates immune system |
| CD8+ T-lymphocytes / Cytotoxic T-cells | destroys cancer cells & virally-infected cells |
| GAG | [Group-specific AntiGen] gene coding for structural proteins |
| POL | gene coding for viral enzymes (reverse transcriptase, integrase, protease) |
| ENV | [ENVelope] coding for GP-120, GP-41 |
| GP-120 | [GlycoProtein 120] binde to CD4 receptor on host cell; can fall off and circulate in the blood (a. induces apoptosis, b. induces syncytia, c. interferes with T-cell formation) |
| GP-41 | [GlycoProtein 41] (upon GP-120 binding) conformational change - fusion with host cell; can fall off of virion and into blood, inhibiting proliferation of T-cells |
| TAT | [TransActivator of Transcription] causes apoptosis of surrounding cells; inhibits CD4+ lymphocyte proliferation and susceptibility to HIV; affects brain tissue, causes KS lesions |
| APOBEC3G | [APOlipoprotein B Enzyme, Catalytic polypeptide-like 3G] human protein interfering with HIV replication |
| REV | [REgulator of Virion] allows export of HIV mRNA to be exported from nucleus to cytoplasm; acts like scorpion toxin on brain tissue; necessary for TAT expression |
| VIF | [Viral Infectivity Factor] inhibits APOBEC3G from entering virion during budding and killing it |
| VPR | [Viral Protein R] regulates nuclear import of HIV; induces apoptosis (CD4+); activates HIV in low concentrations; affects thymus gland (atrophy) |
| VPU | [Viral Protein U] involved in viral budding; decreases cell-mediated reponse |
| cytokine/lymphokine/interleukin/chemokine | proteinaceous signalling compound for inter-cell cummunication of immune system |
| CCR5 (gene & receptor) | [Chemokine (C-C motif) Receptor 5] on T-cells/MO/dendritic cells/microglia; one of major co-receptors used by HIV; used by M-tropic, wild (NSI) strains |
| CXCR4/fusin | [Chemokine (C-X-C motif) Receptor 4] T-tropic; usually on late mutant (SI) strains |
| LTR | INCOMPLETE |
| TAR | INCOMPLETE |
| B cells | "Born" in bone marrow; differentiate into plasma & memory B-cells; produce antibodies against soluble antigens |
| HIV receptors | 1. CD4; 2. Galactosyl ceramide (brain & bowel); 3. Fc (MO); Complement (MO) |
| Major fusion co-receptors | 1. CCR5/CKR5 (on MO) - primary infection; 2. CXCR4 (on T-cells) - later, progressive infection |
| TAR | [TAt Responsive element] prevents RNA polymerase from falling off (increasing transcription efficiency) |
| NEF | [NEgative regulatory Factor] downmodulates expression of MHC-I/II, CD4+/CD8+ T-cells; causes apoptosis in uninfected cells; inhibits apoptosis in infected cells; promotes chemokine release in MO; acts like scorpion toxin on brain tissue |
| NFkB | [Nuclear Factor Kappa B] transcription factor involved in conversion from latent to lytic state |
| 3 HIV Regulatory Proteins | 1. TAT (TransActivator of Transcription); 2. REV (REgulator of Virion); 3. NEF (NEgative regulatory Factor) |
| 3 HIV Structural/Enzymatic Proteins | 1. GAG (Group-specific AntiGen); 2. ENV (ENVelope); 3. POL |
| 3 Parts of HIV Reverse Transcriptase Complex | 1. RNA polymerase (copies RNS to single-stranded DNA); 2. Ribonuclease (destroys RNA copy after DNA copy is made); 3. DNA Polymerase (copies DNA to double-stranded DNA) |
| Fc | INCOMPLETE |
| complement | group of circulating serum proteins; among other things, triggers the membrane attack complex (MAC) to lyse target cell |
| lysozyme | enzyme in mucous sectretions that can degrade bacterial cell walls |
| interferons | group of proteins produced by virally-infected cells; binds to uninfected cells, making them resistant to viral infection |
| SLPI | [Secretory Leukocyte Protease Inhibitor] binds leukocytes, blocking HIV infection; contained in saliva, breastmilk, genital secretions |
| 4 Main Types of Phagocytic Cells | A. Blood: 1. Monocytes, 2. Neutrophils; B. Tissue: 1. Macrophages, 2. Dendritic cells |
| 4 Cardinal Signs of Inflammation | 1. Rubor (redness); 2. Tumor (swelling); 3. Calore (heat); 4. Dolore (pain) {5. Functio laesa (loss of function)} |
| diapedesis | emigration of phagocytes between capillary endothelial cells into the tissue during inflammation |
| erythrocytes | red blood cells; undergo aptosis after 120 days |
| FDC | [Follicular Dendritic Cells] filter antibody-bound antigens from circulating lymph; may be infected by free viral particles, then subsequently infect CD4+ cells in circulation |
| autofusion | GP-120 + CD4 on same cell causes membrane to fold, become misshapen - induces cellular lysis |
| superantigens | antigens capable of interacions with a large number of T-cells (including MHC-II + T-cell receptor on APCs) |
| FAS ligand | INCOMPLETE |
