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159 Cards in this Set
- Front
- Back
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What are 4 cytopathic effects?
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Rounding and detachment of cells
(shutdown/disruption of cytoskeleton proteins) Formation of giant cells (syncytia, faulty membrane integrity and mediated fusion) Production of inclusion bodies (dense bodies of viral and host protein where viral protein is made) Cell death (membrane lysis) |
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What are 5 characteristics of acute productive viral infections?
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Progeny viruses produced
Cytopathic effects Lots of virions produced Gross alteration of cellular functions (borrowing of host cell functions) Cell death |
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How does Poliovirus disrupt ribosomal cap recognition during host translation?
How does it bypass that impaired recognition? |
Poliovirus cleaves eIF4G.
Polio has IRES site that allows ribosome to directly bind and translate. |
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What is cap snatching?
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Viral RNA takes cap away from host RNA and uses it to be recognized by eIFG4.
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How do viruses encourage transcription of their own genes AND discourage transcription of their host cell genes?
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Produce a viral protein that will recruit host TF to drive viral gene expression
Viral protein modifies host TF so that the host TF prefers viral promoters |
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What are 4 characteristics of persistent infections?
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Viral genome persists in cells
Low number of virions may be shed Low virus output does not kill the host cell NO CPE, taking over of cellular transcription machinery, etc. |
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What causes viral reactivation in a latent or chronic infection?
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Other infections
Nerve trauma Physiological and Physical changes Immunosuppression |
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How does a virus survive as the immune system?
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Viral modulation of its own gene expression
No protein = no antibody or CTL responses Infection of Immune privileged sites CNS Altering cytokine expression of infected host cell Prevent a proper innate immune response from developing |
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What are the 2 possible outcomes for a nonproductive infection?
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No progeny virions are produced
Viral genome is “lost” or undetectable Aborted infection OR Viral genome persists in the host cell Latent infection (cytomegalovirus) Tumors (papillomavirus) No progeny viruses are made EVER AGAIN (in a healthy human) |
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What are the causes of nonproductive viral infections?
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Host cell lacks the appropriate receptor
example: CCR5 (-) people are resistant to HIV infection Viral genome cannot replicate in host cell Viral genome cannot be expressed Example: May still be able to make some viral proteins and replicate genome, but not assemble virions |
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What viruses are oncogenic?
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DNA viruses & retroviruses
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What are four characteristics of a cell that has unregulated cell growth due to a virus?
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Immortalized
Able to grow in soft agar No contact inhibition Tumor production when injected into animals |
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What are 3 ways viruses deregulate cell growth?
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Viral oncoproteins alter cell cycle regulators
Viral oncoproteins are homologs to cell cycle proteins and directly activate the cell cycle Viral products are homologs to host cell signal transducers to stimulate growth |
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What is E2F? What is RB? How do you inactive RB?
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Transcription factor, important for making cells go into S phase. Not constitutively active.
RB binds to E2F to prevent it from being a transcription factor. Phosphorylation |
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What is p53?
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p53 detects genetic mistakes and makes cells either to correct mistakes or die.
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What disease/proteins affects E2F, RB, and P53?
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HPV.
E6- blocks P53 E7- knocks RB off E3F |
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What viral homologs to host cell signal transducers stimulate cell growth?
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EGFR, HER1, erbB1
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How do viral proteins act as cell cycle proteins to stimulate oncogenic growth?
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They act as cyclins and cyclin kinases
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Why is congenital deficiency in only T cells rare?
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If there is a deficiency in helper T cells, it tends to impact B cells leading to SCID.
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Where does bacteria enter the body?
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skin and gastrointestinal and respiratory tracts
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Where are antigens in the blood captured?
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captured by antigen-presenting cells in the spleen
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What carries antigen to secondary lymph tissue?
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dendritic cells
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What in the lymph nodes captures free antigen?
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macrophages
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Why do lymph nodes swell?
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lymphocyte accumulation
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What is decline (homeostasis)?
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When T-cells die off after the infection has been dealt with, leaving only memory cells
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What uis the immunological synapse?
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Space between Tcell and APc where integrins cluster around MHC/TCR connection
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What makes integrins on T cells hold onto APC tightly?
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Chemokines switch integrins from low affintiy to high affinity
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What makes up TCR complex? Why is CD3 there?
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CD3 and TCR
CD3 has ITAM motifs that active T cells (in other cells it drives phagocytosis). |
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What molecule helps with costimulation?
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B7
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What are the 3 pathways that activate NFAT, AP-1, and NF-kB?
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Calcineurin (calcium dependent)- IP3 releases intracellular calcium from stores. Activates NFAT.
MAP kinases- they activate AP-1. IKK- activates NF-kB. |
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How fast does it take for NK-kb, NFAT, and AP-1 to react?
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minutes
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What is bidirectional signaling?
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Upon activation, T cells produce cytokines and CD40L that stimulate APCs. In response to CD40L-CD40 stimulation, APCs produce more B7 (CD80/CD86) and cytokines that then further stimulate the T cell.
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What does B7 activate?
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CD28
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How do T cells can “license” additional APCs?
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The TCR and CD40L on activate T cells can engage MHC-peptide and CD40 on another APC (that has been exposed to the antigen but is not fully stimulated). This serves to stimulate the expression of B7 molecules and the secretion of cytokines from this second APC. Thus, activated T cells can recruit additional APCs to participate in the immune response. These APCs can then stimulate additional T cells.
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What T cell product promotes cell cycle progression and clonal proliferation?
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IL-2
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What are the targets of immunosuppressant drugs?
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T cell activation pathways
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Why do T cells become anergic? What type of tolerance is this?
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No costimulation
Peripheral |
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How does CTLA-4 shut down T cell activation?
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1. competitively prevents CD28 binding to B7
2. Following binding to B7, CTLA-4 actively shuts down TCR-dependent signaling pathways. |
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What makes FasL? What makes Fas? What does their interaction do?
What disease is associated with a defect in Fas expression? |
CTL
effector T cells cause apoptosis of target cell Autoimmune Lymphoproliferative Syndrome |
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What are the 4 types of effector T cells?
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Th1- intracellular
Th2- helminths Th170- extracellular aTreg- counter regulation |
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What determines the type of effector T cell made?
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dendritic cell stimulus and local cytokines
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How makes IFN-γ?
What does IFN-γ do? |
Th1 cells
stimulates macrophages for killing/phaogcytosis |
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Beside IFN-γ, what are other function so Th1 cells?
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stimulate B lymphocytes to produce IgG antibodies that opsonize microbes for phagocytosis
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What is the IL-12-IFN-γ axis?
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A feedback loop between macrophages and T cells that helops with killing of intracellular infection.
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What often causes Immunodeficiencies of IL-12-IFN-γ Axis? What is fatal?
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faulty IFN-gamma receptor
BCG vaccine |
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What are the Effector functions of TH2 cells?
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secrete IL-4 and IL-5. IL-4 acts on B cells to stimulate production of antibodies that bind to mast cells, such as IgE. IL-5 activates eosinophils, a response that is important for defense against helminth (worm) infections. The TH2 response is associated with asthma and allergic inflammatory reactions
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What is the Effector functions of TH17 cells? What is the downside?
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secrete IL-17 which acts on epithelial cells, fibroblasts and other stromal cells to stimulate production of hematopoietic factors and chemokines that increase the production and migration of neutrophils to the site of infection. This response is important for defense against extracellular bacteria and fungi.
The TH17 response is associated with a number of chronic inflammatory conditions including rheumatoid arthritis, inflammatory bowel disease, and psoriasis of the skin. |
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What are the 2 types of leprosy? Why is one type so bad?
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lepromatous (worse because no T cell response)
tuberculoid |
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What are the 3 ways to activate CTL?
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1. strong interaction of T cell with costimulatory signal from APC
2.CD4+ effector T cells produce cytokines that increase CTL proliferation from CD8+ cells 3. CD4+ enhance aPCmability to stimulate differentiation. |
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What are the stages of CTL (and NK) mediated killing of cells?
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1. attachment
2. cytoplasmic rearrangement 3. CTL granule exocytosis 3. disassociation 4. recycling |
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What helps T cells make porins in target cells?
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Perforin
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What induces apoptosis in the targets of CTL?
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Granzyme B
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How do CTL find their way to infected tissue? How do CTL achieve physical entry into tissue?
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chemokines
selectin and integrin |
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What 2 properties enable immune components to access the site of infection?
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vascular leakage and vasodilation
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What is SCID?
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Caused by an absence of functional T cells which has a combined effect on B cell function.
Often fatal in young infants who are ill by age three months and fail to thrive. Persistent thrush (candida), extensive diaper rash, intractable diarrhea, or petussis-like cough due to interstitial pneumonia cause by P. jirovecki. Persistent infections with candida, P. jirovecki and a variety of viruses. Death from viral infection may occur very rapidly. BCG vaccination usually fatal. Diagnosis by observation of lymphopenia (lack of T cells) Lymphocytes fail to respond to nonspecific mitogens. Levels of immunoglobulins are low or undetectable. Spleen, lymph nodes, and tonsils are absent. No thymic shadow on chest X-ray. Medical emergency that requires bone marrow transplantation. Weekly gamma globulin therapy enables patients to survive. Can be caused by one of several genetic defects. |
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What causes SCID?
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IL-2 receptor gamma chain deficiency (X-linked SCID). Gamma chain is also a component of IL-7 receptor required for T cell development, thus lack of T cells.
Adenosine Deaminase (ADA) deficiency results in accumulation of nucleotide metabolites toxic to developing T and B lymphocytes. Thus complete absence of B or T lymphocytes. |
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How long does the primary immune response take? What immunoglobulin is most common?
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5-10 days
IgM |
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What are the 4 possible outcomes for a B cell after clonal expansion?
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1. plasma cell --> antibody secretion
2. isotype switching 3. affinity maturation 4. memory B cell |
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Are more B cells in circulation or lymph nodes?
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MAJORITY IN LYMPH NODES
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What are the 3 things that can happen to free antigen in a lymph node?
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1) Phagocytosized and presented by macrophage
2) Trapped in native form in the follicle. 3) Bound by a BCR of a B cell. This is the first step of B cell activation. |
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What does cross-linking of BCRs by antigen do?
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Activate B cells
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Both B and T cell recognition is most likely linked to the same (antigen or epitope)?
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antigen
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Proliferation of what creates the germinal center?
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Centroblasts
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Where does B cell proliferation occur? Where does B cell selection occur?
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Dark side
Light Side |
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B cells compete for antigen held by what?
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follicular DCs
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How does a B cell receive survival and differentiation signals to become a plasma cell?
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Centrocytes compete for antigen bound to follicular dendritic cells. Those that take up antigen present it in the context of MHC class II.
If a centrocyte presents antigen it can then engage T cells |
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Where do B cells receive survival signals? What signals do T cells send?
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Mantle zone
IL-4 & CD40 |
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What helps B cells to switch isotypes?
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Effector helper T cells
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What isotype arises from help from Th1? Th2? APRIL, BAFF, TGF-B?
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IgG
IgE IgA |
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Where do plasma cells go?
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Some stay in lymph, so go to bone marrow (no reason)
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What is X-linked Hyper IgM Syndrome?
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Elevated IgM but no IgA and very low IgG
Susceptible to pyogenic infection Uncontrollable proliferation of IgM producing plasma cells Treated with monthly administration of immune globulin T cells are defective in CD40L, therefore no activation of germinal center B cells and no class switching Also a defect in macrophage activation which also requires interaction between CD40 and CD40L Therefore also susceptible to opportunistic pathogens such as Pneumoncystis jerevorki Macrophages also fail to produce cytokines that promote hematopoiesis and therefore white blood cell counts do not rise during infection. |
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What is a conjugate vaccine?
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The vaccine antigen has a carbohydrate portion has a protein component from another virus to help elicit a MHC response.
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What region determines the effector function of the antibody?
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Fc region
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What region do B cells have that plasma cells lack?
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transmembrane region
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What is the role of Glycosylation on antibodies?
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Glycosylation effects effector function,
polysaccharide required for binding of IgG to FcR |
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What does sialic acid do for FC receptor affinity?
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Terminal sialic acid:lowers affinity for Fc receptors
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Which immunoglobulin is a dimer?
Which is a pentamer? |
IgA
IgM |
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What are the 3 Antibody-Mediated Defenses to Extracellular Bacteria and what antibodies are associated with each?
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Opsonization- IgG1, IgG3
Neutralization-IgG IgA IgM Complement- IgM IgG |
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What are the 4 activities of complement?
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lysis
opsonization activation of inflammation clearance of immune complexes |
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What type of antibodies does C1 bind to? C1q?
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IgM
two or more IgG molecules |
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What are the 4 steps of Antibody Dependent Cell-Mediated Cytotoxicity (ADCC) mediated by NK cells?
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1. antibodies bind antigens
2. Fc receptors on NK recognize antibody 3. Crosslinking of Fc receptors signal NK to kill 4. Target cell dies |
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How antigens cause granule contest release from mast cells?
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Multivalent antigens cross link IgE
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What antibody is involved in antibody-dependent cellular cytotoxicity?
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IgG
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What antibody is found most in serum? In secretions?
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IgG
IgA |
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Where do most pathogens enter the body?
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Mucosal sites: Lungs
GI tract GU tract |
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How do IgA get from lamina propria to lumen?
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1. complex with poly-Ig receptor
2. get endocytosed into mucosal epithelial cell 2. cleave complex/exit into lumen |
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If neutrophils cannot engulf bacteria, how do they eventually engulf it?
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Antibody binds to it and activates complement. Fc and complement receptors mediate phagocytosis.
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Can an old antibody combat a new serotype of S. pneumoniae?
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No
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What type of antibody goes across placenta an is in breast milk? (Hint: serum)
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IgG
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When are babies susceptible to infections?
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when passive maternal transfer IgM wears off and new antibodies aren't fully made
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What causes X-linked Agammaglobinemia?
What are symptoms? |
Defect is Bruton’s tyrosine kinase (btk) required for early B cell development, thus number of B cells is low
Other causes of agammaglobinaemia include defects in expression of surrogate heavy or light chains also required for B cell development. Virtually no immunoglobulins Tonsils small, lymph nodes not palpable Recurrent pyogenic infections: otitis media, sinusitis, conjuctivitis, pneumonia. Eventual anatomical destruction, particularly the lungs. No problems with viruses or intracellular bacteria. |
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What is treatment?
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All forms of agammaglobinaemia treated with immune globulin pooled from human serum.
(Passive Immunization-life saving). |
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What is the name for congenital immune deficiencies?
Acquired? |
Primary
Secondary |
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What type of immune deficiency is the least common?
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T
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What type of infection occurs with a B cell deficiency? T cell? Complement?
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extracellular
intracellular, viral, fungi gonorrhea, meningitis |
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What are the 1st and 2nd cause of secondary immune deficiency?
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1. malnutrition
2. AIDS |
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In immunoglobulin electrophoresis, what is the M-spike?
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lymophoma, only IgM is made, can't isotype switch
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In radial immunodiffusion, what is distance correlated with?
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antigen concentration
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In agglutination, a large solid dot in the patient RBC + anti B means?
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positive for antibody B
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What tye of antibodies are in the serum of type O patients? Type A? Type B? Type AB?
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Anti-AB
Anti-B Anti-A None |
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What is the hemolyitc complement test?
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Patient's plasma and sheep RBC are mixed to test patient's complement ability.
Lysis= working complement |
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What is Complement Fixation Test?
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Test for antibody.
Mix antibody, antigen, sheep RBC, and complement. If no lysis, antibody present to fix complement. |
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Is ELISA radioactive?
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No.
Enzyme amplification of signal |
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What's the difference between sandwich and indirect elisa?
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sandwich- antigen between two antibodies
indirect- antigen + antibody + secondary antibody |
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What are Polyclonal Mitogens for?
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assessing T cell function
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What is a skin test used for?
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Testing delayed hypersensitivity
T cell only See if memory T-cells proliferate in response to antigen. |
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What are the respective innate immune receptor for viral DNA and RNA? What do they activate?
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TLR3
Cytoplasmic NRL Proinflammatory cytokines and Type I IFNs |
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What are Plasmacytoid DCs a source of? What can they act as?
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IFN Type I
APCs |
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How do IFN fight viral infections by inhibiting viral protein synthesis?
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RNase L breaks down mRNA
PKR phosphorylates eIF-2 (shuts down translation) |
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What 3 actions are part of the interferon response to viral infections?
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1. induce resistance to viral replication
2. increase expressions for ligands on NK cells 3. activate NK cells |
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What is the downside of IFNs?
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TOXIC
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What is Imiquimod (Aldara)?
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IFN that fights basal cell carcinoma
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Which of the following do NK cells have: TCR or CD3?
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Neither
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What is the ligand for killer inhibitor receptors on NK cells?
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MHC
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What is expressed in place of MHC when the cell is infected by a virus? What do they do?
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MHC class I-related chain (MIC)
act as ligands for activating NK cells receptors |
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Which normally wins, negative or positive signal for NK, if both are present?
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Negative MHC
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How are antibodies against viral coat generated?
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antigen is presented to T cell which induces B cell to make antibodies
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What is part of the innate antiviral response? What is part of the adaptive antiviral response?
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IFN and NK
CTL |
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What do NK cells use to cause apoptosis? CTLs?
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Granzyme A
Granzyme B |
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What causes most of the liver damage with hepatitis?
What is the treatment? |
CTLs
Low dose interferon-α (with Ribavarin) used to treat Hepatitis B and C. |
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What disease is caused by Epstein-Barr Virus?
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mononucleosis
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Why is epidermis a bad host cell for a virus?
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dead skin
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How do viruses get past the epidermis?
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punctures
insect bites skin abrasions |
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What are the host defenses of the mucous membrane of the respiratory tract?
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mucus production by goblet (prevents attachment)
protease production- destroys virions ciliated epithelial cells- sweeps virus low temp- inhibits virus replication |
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What are the 3 defense of mucus?
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physical barrier,
virus receptors competition- sialic acid containing proteins in mucus bind to influenza sIgA in mucus bings to viruses t prevent virus-host interactions |
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How does viruses defend against the immune system?
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viruses are small
some viruses are better at low temp |
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What 2 things of the GI tract discourage viruses?
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Gastric secretions have low pH
Bile salts of intestine act as disruptive detergent |
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What are viral defenses against GI tract?
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viruses use host proeases to cleave and activate own proteins
capside of naked viruses are resistant to proteases or low pH |
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What do viruses inhibit to prevent production of IFN?
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IRF-3 and IRF-7
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How does flu, herpes, pox, and hep C interfere with IFN signaling?
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Prevents activation of protein kinase PKR
Bind directly to PKR to prevent PKR activation Non-functional homolog of PKR Non-functional eIF-2 homolog |
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How do herpes viruses fight against NK?
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express UL16
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What does infected cells express to be killed by NK cells?
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NKG2D
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What does UL16 do?
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bind to ULBP and stop NKG2D and NK cell activation
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How do viruses evade mechanisms of antibodies?
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glycoslating surface proeins
antigenic variation |
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How do viruses evade antibody-dependent cell-mediated cytotoxicity (ADCC)?
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antigenic variation
Decrease in viral surface proteins -Virus-mediated -Capping -Latent infection where no viral proteins are produced |
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What does herpes bind to in order to inhibit MHC I expression?
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TAP 1 & 2
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What does adenovirus bind to in order to inhibit MHC I expression?
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MHC I
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How does adenovirus prevent apoptosis?
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preventing Fas expression
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How does poxvirus prevent apoptosis?
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preventing DISC formation ( made of Fas, FADD, procaspase-8)
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What are the 4 ways viruses evade CTLs?
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Block MHC production (herpes)
Down-regulate viral proteins that would associate with MHC class I (herpes) Infect cells that don’t have MHC (neurons) (rabies viruses) Kill T cells immune system cells (HIV) |
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What unique substance does fungi plasma membrane>
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ergostero
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What does rigid cel walls of fungi lack? What does it have
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lacks peptidoglycan
Glucans, mannans, etc. Chitin – almost always present |
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What are the 3 eukarotic general characteristics of fungi?
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Nuclear membrane
Eukaryotic type ribosomes Organelles Mitochondria – energy generation Golgi apparatus – secretory processes |
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What are mycelia?
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Mycelia are masses of multicellular filaments called hyphae
Hyphae may be nonseptate or septate |
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What are the 3 types of fungal infections?
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1. Superficial or cutaneous infections
2. Mucocutaneous infections – do not become systemic 3. Systemic – usually in immuno- compromised patients |
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Name the famous opportunist fungi?
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Candida albicans
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Name stuff about Histoplasma capsulatum?
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1. Dimorphic fungus
2. Normally found in soil contaminated with bird droppings 3. Spores or hyphal fragments inhaled 4. Mild, flu-like symptoms in healthy people 5. Serious lung or systemic disease in immunocompromised patients |
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What are the candida virulence factors?
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adhesins: fibrillar proteins and mannoproteins
biofilms |
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What is thigmotropism?
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Contact sensing by C. albicans
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What is thigmotropism?
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Contact sensing by C. albicans
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What does toxic extracellular proteins do for candida virulence factors?
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degrade host tissue, allow for epithelium penetration
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What does molecular mimicry do for yeasts?
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Yeasts coat themselves with host molecules
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Are candida resistant to pmn oxidative burst?
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yes
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Do candida use genetic rearrangements to avoid host defense?
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yes
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What are the histoplasma virulence factors?
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1. Macrophages stimulate conversion to
yeast form 2. Siderophores 3. Survive and grow in macrophages (and monocytes) 4. Some factor prevents triggering of 5. Adhesin stimulates phagocytic uptake 6. May buffer phagocytic vesicle phagocyte oxidative burst 7. Invade and live in other types of cells Endothelial cells Respiratory epithelial cells Enhances spread and persistence in host 8. Stimulate granuloma formation Microbe enters lung Normal macrophages attracted – can’t kill More phagocytes and T cell attracted Host lays down fibrin layer |
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What are fungal toxins?
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Ergot
Low molecular weight compound Lipid soluble Active ingredient in LSD – hallucinogenic Aflatoxin Cause of liver cancer and cirrhosis Found in grains and nuts |
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What are agents that affect ergosterol synthesis?
|
1. Polyenes – fungicidal
Bind ergosterol; form channels through membrane 2. Azoles – fungistatic Block ergosterol synthesis; weaken cell membrane 3. Allylamines and thiocarbamates – fungistatic Inhibit early ergosterol step Poorly absorbed; topical use 4. Morpholines – fungistatic Inhibit late ergosterol step Topical for nail infections |
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What are agents that inhibit nucleic acid synthesis?
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1. Flucytosine
Metabolite incorporated into RNA Different metabolite inhibits thymidylate synthase Used in combination with polyenes 2. Griseofulvin Binds microtubules; blocks mitosis Deposited in keratinized tissues |
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What are narrow spectrum antifungal agents?
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1. Echinocandin B
Inhibits cell wall biosynthesis Effective against Candida 2. Agents effective against Pneumocystis jiroveci Sulfonamides and trimethoprim Pentamidine |
