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30 Cards in this Set
- Front
- Back
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What are H and N in H1N1? |
Hemagglutinin (H) and Neuraminidase (N) |
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'Hemagglutinin (H) and Neuraminidase (N)' Which of these mediates entry of the virus into cells of the respiratoryepithelia and which promotes viral release? |
Hemagglutinin (H) mediates entry and Neuraminidase (N) promotes release |
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To which receptors on human respiratory epithelia does H1N1 bind? |
To those that have the α-2,6 sialic acid linkage to galactose |
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Seasonal flu epidemics occur when point mutations accumulate in H and N.These point mutations lead to a process by which neutralising antibodies areunable to block entry of the virus into cells of the respiratory epithelia.What is this process known as? |
Antigenic drift |
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Flu pandemics occur following genome re-assortment of avian and humaninfluenza viruses. In which mammalian host does genome re-assortmentoccur? |
Pig |
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What feature of the respiratory epithelium of this mammal enables genome reassortmentof human and avian strains to occur? |
Avian viruses prefer the α-2,3 sialic acid linkage to galactose. Pigs expressboth α-2,3 and α-2,6 sialic acid linkages to galactose on respiratory epitheliathereby enabling binding and entry of both human and avian strains of the virus |
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Name the 3 major components of innate immunity to viruses? |
Complement, Type 1 interferons, Natural Killer (NK) cells |
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Major adaptive immunity to viruses is mediated via which cellular [1 mark] andhumoral [1 mark] components of immunity? |
CD8 (cytotoxic T cells/CTLs) and antibody |
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What are A, B and C |
A = MHC Class I B = CD8 T cell C = T cell receptor |
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Which cellular compartments of the cell does MHC class II monitor for foreign antigen? |
Compartments of the endosomal and lysosomal pathways |
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Give an example of an effector function of complement, and name a keycomponent of complement that is directly involved in this effector function |
Inflammation – C3a C5a Opsonisation C3b Lysis (MAC) – C5-C9 |
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How does the membrane attack complex cause bacterial killing? |
By forming pores in the bacterial cell wall |
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What types of bacterial disease are associated with C9 deficiency? |
Meningitis and sepsis caused by Neisseria |
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Give an example of a vaccine that induces antitoxin antibodies. |
Diphtheria, tetanus, anthrax, pertussis |
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What is the traditional method for detoxifying the toxin before formulation into avaccine? |
Formaldehyde treatment |
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How does this detoxification method work, at a molecular level? |
It causes the formation of inter- and intra-molecular cross-links between aminogroups in lysine and glutamine residues |
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Give 2 of the problems associated with formaldehyde treatment |
Reversion, batch-to-batch variability, balance between loss of toxicity and lossof immunogenicity, production difficulties associated with the need to grow thepathogens and purify the toxin |
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Explain briefly how biotechnology is helping to provide improved toxoid vaccines. |
Genetic toxoids are created, where the protein produced is non-toxic because of the substitution of a functionally critical amino acid |
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Give an example of a bacterial polysaccharide that is targeted by a protective immune response. |
LPS O-antigens |
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At the cellular immunology level, what is the main problem associated with theinduction of long-lasting immune responses to polysaccharides? How can this problem be solved? |
Lack of T-cell involvement By linking to a protein, to create a glyco-conjugate |
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Tolerance is the process whereby self-reactive lymphocytes are removedor inactivated to avoid auto-immune disease. What are the 2 processes of cell killing and inactivation called? |
apoptosis and anergy |
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What are the 2 possible outcomes for an immature B-cell that experiencesstrong binding to a multivalent self-antigen? |
apoptosis and receptor editing |
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What is the fate of B-cells binding abundant soluble self-antigens in theperiphery? |
Anergy |
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Name 2 of the cell types responsible for negative selection of T-cells in thethymus |
Dendritic cell or (medullary) epithelial cell or macrophage |
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What are the 2 possible fates of a CD4+ T cell that interacts strongly with selfpeptide/MHCin the thymus? |
Clonal deletion/apoptosis or becoming a TREG cell |
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Human RAG-1 Deficiency is caused by an autosomal recessive mutation whichdestroys the Recombinase Activating Genes. This deficiency results in whichdisease? |
T and B cell severe combined immunodeficiency (SCID) |
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To what processes do the 12/23 and the WRC rules apply? |
The 12/23 rule applies to VDJ recombination activity whereby a 12 bp RSScan only recombine with a 23bp RSS through RAG1/2 protein recombinase. |
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12/23 and the WRC Describe briefly their two different functions |
The cytosine in the WRC consensus is the preferential hotspot for AID cytosinedeaminase activity during SHM/CSR. |
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what does AID stand for |
Activation Induced Deaminase |
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Describe briefly the mechanism(s) through which AID contributes toantibody diversity. |
Somatic hypermutation (SHM) increases the affinity maturation of antibodies.Class switch recombination (CSR) increases effector function of antibodies |
