8.0 Multiple Choice Questions (MCQs) I Flashcards
Viruses that cause zoonotic infections:<div>A. have non-humans as natural hosts</div><div>B. cause diseases with high mortality/morbidity</div><div>C. include influenza virus</div><div>D. may be transmitted by insects</div><div>E. include measles virus</div>
<div>Viruses that cause zoonotic infections:<div>A. have non-humans as natural hosts (TRUE)</div><div>B. cause diseases with high mortality/morbidity (TRUE)</div><div>C. include influenza virus (TRUE)</div><div>D. may be transmitted by insects (TRUE)</div><div>E. include measles virus (FALSE)</div></div>
The group of reversiviruses includes<div>A. human immunodeficiency virus</div><div>B. variola virus</div><div>C. hepatitis C virus</div><div>D. Rous sarcoma virus</div><div>E. hepatitis B virus</div>
<div>The group of reversiviruses includes<div>A. human immunodeficiency virus (TRUE)</div><div>B. variola virus (FALSE)</div><div>C. hepatitis C virus (FALSE)</div><div>D. Rous sarcoma virus (TRUE)</div><div>E. hepatitis B virus (TRUE)</div></div>
<div><br></br></div>
<div>Reversiviruses replicate their genome via a reverse transcriptase step - and shares this property with retroviruses.</div>
<div><br></br></div>
<div>B - F; variola virus is a poxvirus e.g. smallpox</div>
<div>C - F; a flavivirus</div>
These viruses commonly enter their host via the alimentary canal<div>A. Rotavirus</div><div>B. Blue tongue virus</div><div>C. Hepatitis B virus</div><div>D. Rhinovirus</div><div>E. Poliovirus</div>
<div>These viruses commonly enter their host via the alimentary canal<div>A. Rotavirus (TRUE)</div><div>B. Blue tongue virus (FALSE)</div><div>C. Hepatitis B virus (FALSE)</div><div>D. Rhinovirus (FALSE)</div><div>E. Poliovirus (TRUE)</div></div>
<div><br></br></div>
<div>B - F; transmitted by blood biting insects</div>
<div>C - F; transmitted via blood e.g. iatrogenic</div>
<div>D - F; transmitted via the respiratory tract e.g. common cold</div>
<div>Viruses that commonly enter via the alimentary canal include poliovirus, hepatitis A virus, rotavirus, enteric adenoviruses</div>
Interferon beta<div>A. Is induced following activation of Toll-like receptors</div><div>B. Induces expression of interferon stimulated genes (ISGs) via NFkB</div><div>C. Signals through type 1 IFN receptors</div><div>D. Directly binds viruses and blocks entry</div><div>E. Up-regulates class I MHC</div>
<div>Interferon beta<div>A. Is induced following activation of Toll-like receptors (TRUE)</div><div>B. Induces expression of interferon stimulated genes (ISGs) via NFkB (FALSE)</div><div>C. Signals through type 1 IFN receptors (TRUE)</div><div>D. Directly binds viruses and blocks entry (TRUE)</div><div>E. Up-regulates class I MHC (FALSE)</div></div>
<div><br></br></div>
<div><br></br></div>
<div>B - F; NFkB leads to the production of IFN alpha/beta which then goes on to stimulate ISGs through JAK-STAT pathway and ISGF-3</div>
<div>D - F; they induce downstream pathways that leads to increased likelihood of recognition by the immune system (MHC-class I indirectly upregulated) and they inhibit viral protein synthesis via production of OAS, Mx, PKR</div>
Yellow Fever Virus<div>A. Is a zoonotic infection</div><div>B. Is commonly transmitted congenitally</div><div>C. Causes respiratory infection</div><div>D. Is a non-enveloped RNA virus</div><div>E. Causes haemorragic fever</div>
<div>Yellow Fever Virus<div>A. Is a zoonotic infection (TRUE)</div><div>B. Is commonly transmitted congenitally (FALSE)</div><div>C. Causes respiratory infection (FALSE)</div><div>D. Is a non-enveloped RNA virus (FALSE)</div><div>E. Causes haemorragic fever (TRUE)</div></div>
<div><br></br></div>
<div>B - F; it is transmitted by the female aedes aegypti mosquito</div>
<div>C - F; causes haemorrhagic fever<br></br>D - F; is a flavivirus which are enveloped viruses; they are positive strand ssRNA viruses</div>
Influenza Virus<div>A. Is an RNA virus</div><div>B. Encodes an ion channel protein that promotes un-coating of the virus</div><div>C. Causes disease with high seasonality in temperate climates</div><div>D. Requires a high pH environment to activate membrane fusion</div><div>E. Pandemics are associated with HA drift</div>
<div>Influenza Virus<div>A. Is an RNA virus (TRUE)</div><div>B. Encodes an ion channel protein that promotes un-coating of the virus (TRUE)</div><div>C. Causes disease with high seasonality in temperate climates (TRUE)</div><div>D. Requires a high pH environment to activate membrane fusion (FALSE)</div><div>E. Pandemics are associated with HA drift (FALSE)</div></div>
<br></br><div>D - F; it requires a low pH. Low pH leads to a conformational change in the HA2 subunit that allows the fusion peptide (N terminal part) to integrate into the endosomal membrane. This destabilises the membrane and promotes fusion between the viral envelope and the endosomal membrane.</div><div>E - F; pandemics are associated with HA shift; shifts results in production of new strains due to reassortment of RNA segments between two virions of different strains within a cell infected by them both at the same time</div>
Pattern-recognition receptors (PRRs)<div>A. Are important for viral entry</div><div>B. Mediated phagocytosis of free virus particles</div><div>C. PRRs activate the JAK-STAT signalling pathway within the infected cell</div><div>D. Detect viral DNA in the cytoplasm</div><div>E. Activate the IRF3 TF within the infected cell</div>
<div>Pattern-recognition receptors (PRRs)<div>A. Are important for viral entry (FALSE)</div><div>B. Mediated phagocytosis of free virus particles (TRUE)</div><div>C. PRRs activate the JAK-STAT signalling pathway within the infected cell (FALSE)</div><div>D. Detect viral DNA in the cytoplasm (TRUE)</div><div>E. Activate the IRF3 TF within the infected cell (TRUE)</div></div>
<div><br></br></div>
A - F; PRRs are important host cell viral recognition proteins that detect PAMPS such as nucleic acids in the cytoplasm, and they activate the innate immune system.<div>C - F; the JAK-STAT pathway is activated in neighbouring cells, that helps to protect them from viral infection</div>
Human immunodeficiency virus (HIV)<div>A. Binds to macrophages using the CCR5 cytokine receptor</div><div>B. Is a zoonotic infection</div><div>C. Converts its positive sense RNA genome into DNA via reverse transcription</div><div>D. Is controlled by CD8+ cytotoxic T lymphocytes in patients termed ‘slow progressors’</div><div>E. Requires ribosomal frame-shifting to express env</div>
<div>Human immunodeficiency virus (HIV)<div>A. Binds to macrophages using the CCR5 cytokine receptor (TRUE)</div><div>B. Is a zoonotic infection (TRUE)</div><div>C. Converts its positive sense RNA genome into DNA via reverse transcription (TRUE)</div><div>D. Is controlled by CD8+ cytotoxic T lymphocytes in patients termed 'slow progressors' (TRUE)</div><div>E. Requires ribosomal frame-shifting to express env (FALSE)</div></div>
<div><br></br></div>
<div>E - F; expression of env protein requires splicing, expression of gag vs. gag-pol requires frame-shifting</div>
In viral infection:<div>A. Herpes virus establish persistent (latent) infections</div><div>B. Hepatitis B establishes persistent (chronic) infection in about 90% of normal adults</div><div>C. Measles virus always causes an acute infection</div><div>D. Varicella zoster virus establishes latency in sensory ganglia</div><div>E. Influenza viruses always cause acute infection</div>
<div>In viral infection:<div>A. Herpes virus establish persistent (latent) infections (TRUE)</div><div>B. Hepatitis B establishes persistent (chronic) infection in about 90% of normal adults (FALSE)</div><div>C. Measles virus always causes an acute infection (FALSE)</div><div>D. Varicella zoster virus establishes latency in sensory ganglia (TRUE)</div><div>E. Influenza viruses always cause acute infection (TRUE)</div></div>
<div><br></br></div>
A - they establish latent infection in sensory nerves<div>B - it establishes chronic infection in about 90% of neonates but the rates are much lower in adults [~10%]</div><div>C - if people are vaccinated they won’t necessarily get the acute infection + measles virus mutants can persist in the CNS and cause a chronic demyelinating disease (SSPE) with a frequency of about 1/million infections</div><div>D - hence classic dermatomal pattern of reactivation</div><div>E - T</div>
The following statements are true:<div>A. Cryptococcus neoformans causes a slowly progressive meningo-encephalitis</div><div>B. Invasive infections with Aspergillus fumigatus has high fatality</div><div>C. Candida albicans is a common commensal organism of human mucous membranes</div><div>D. Structural barriers play a minor role in innate protections from fungal infection</div><div>E. Protein synthesis in fungi can be blocked by nystatin</div>
<div>The following statements are true:<div>A. Cryptococcus neoformans causes a slowly progressive meningo-encephalitis (TRUE)</div><div>B. Invasive infections with Aspergillus fumigatus has high fatality (TRUE)</div><div>C. Candida albicans is a common commensal organism of human mucous membranes (TRUE)</div><div>D. Structural barriers play a minor role in innate protections from fungal infection (FALSE)</div><div>E. Protein synthesis in fungi can be blocked by nystatin (FALSE)</div></div>
<div><br></br></div>
A; T - abundant in bird droppings and possesses a thick polysaccharide capsule that is an important virulence determinant. Infection is acquired by inhalation. The organism has a strong tendency to spread from the lungs through the circulation to the CNS. In people who are HIV positive, or immunosuppressed it can cause a slowly worsening meningo-encephalitis, with progessively worsening headache, fever, confusion, hydrocephalus (insufficient reabsorption of CSF), and then coma. 20% fatality; survivors often have persistent neurological disability including blindness. Can treat with amphotericin plus flucytosine, followed by long-term high-dose fluconazole.<div>B; T - an environmental mould that occurs worldwide and produces abundant air-borne spores which are inhaled by people every day (hospital re-building work, mouldy hay, compost heaps), causes airway colonisation, aspergilloma and invasive infection of lung or paranasal sinuses and spreads along blood vessels leading to dissemintated infection. Invasive infection has a very high fatatlity. Treatment is with amphotericin or voriconazole, and surgery if possible.<br></br>C; T - moist epithelial surfaces, usually restrained by host defences and bacterial competition<br></br>D; F - the intact epithelium of the skin or moist mucosal surfaces of the mouth, intestine, genital tract are key structural barriers to prevent fungal entry. Damage to it can lead to fungal invasion, through the epithelium, into the connective tissue and blood vessels followed by dissemiantion to other parts of the body.<br></br>E; F - nystatin blocks ergosterol function in fungal membranes.</div>
Regarding fungal infection:<div>A. Ringworm is a superficial fungal infection</div><div>B. The candidate albicans toxin candidalysin targets endothelial cells</div><div>C. Cryptococcus neoformans is abundant in bird-droppings</div><div>D. Aspergillus fumigatus is a filamentous saprophyte</div><div>E. Filamentous fungi are common components of the normal human flora</div>
<div>Regarding fungal infection:<div>A. Ringworm is a superficial fungal infection (TRUE)</div><div>B. The candidate albicans toxin candidalysin targets endothelial cells (FALSE)</div><div>C. Cryptococcus neoformans is abundant in bird-droppings (TRUE)</div><div>D. Aspergillus fumigatus is a filamentous saprophyte (TRUE)</div><div>E. Filamentous fungi are common components of the normal human flora (FALSE)</div></div>
Regarding Fungi<div>A. Most are saprophytes</div><div>B. Many are parasites of humans and animals</div><div>C. They can be eukaryotes or prokaryotes</div><div>D. They have a cell wall containing both chitin and glucans</div><div>E. Many, but not all, are dimorphic</div>
<div>Regarding Fungi<div>A. Most are saprophytes (TRUE)</div><div>B. Many are parasites of humans and animals (FALSE)</div><div>C. They can be eukaryotes or prokaryotes (FALSE)</div><div>D. They have a cell wall containing both chitin and glucans (TRUE)</div><div>E. Many, but not all, are dimorphic (TRUE)</div></div>
In fungi<div>A. DNA is organised in chromosomes within a membrane-bound nucleus</div><div>B. Hyphae are branching cylinders that grow by cell division</div><div>C. At 37 degrees the spores of dimorphic fungi germinate into yeasts</div><div>D. The azole toxin drug Fluonazole inhibits the synthesis of fungal microtubules</div><div>E. The anti-fungal drug Caspofungin inhibits the synthesis of glucan, a component of the cell wall</div>
<div>In fungi<div>A. DNA is organised in chromosomes within a membrane-bound nucleus (TRUE)</div><div>B. Hyphae are branching cylinders that grow by cell division (TRUE)</div><div>C. At 37 degrees the spores of dimorphic fungi germinate into yeasts (TRUE)</div><div>D. The azole toxin drug Fluonazole inhibits the synthesis of fungal microtubules (FALSE)</div><div>E. The anti-fungal drug Caspofungin inhibits the synthesis of glucan, a component of the cell wall (TRUE)</div></div>
<div><br></br></div>
<br></br>D - F; fluconazole is an azole class but it inhibits synthesis of ergosterol which is part of the cell membrane. Ergotamine is a toxin produced by fungi.<br></br>
In haematopoiesis<div>A. NK cells derive from the common lymphoid precursor</div><div>B. Platelets are derived from erythroblasts</div><div>C. Macrophages and dendritic cells are both derived from monocytes</div><div>D. Plasma cells give rise to B cells</div><div>E. The common myeloid progenitor gives rise to both granulocytes and monocytes</div>
<div>In haematopoiesis<div>A. NK cells derive from the common lymphoid precursor (TRUE)</div><div>B. Platelets are derived from erythroblasts (FALSE)</div><div>C. Macrophages and dendritic cells are both derived from monocytes (TRUE)</div><div>D. Plasma cells give rise to B cells (FALSE)</div><div>E. The common myeloid progenitor gives rise to both granulocytes and monocytes (TRUE)</div></div>
The cell surface molecule<div>A. LFA-1 is a marker for T cells</div><div>B. CD8 binds to MHC class II molecules</div><div>C. ICAM-1 binds to LFA1</div><div>D. CD4 is expressed on helper T cells</div><div>E. CD3 is expressed on the majority of NK cells</div>
<div>The cell surface molecule<div>A. LFA-1 is a marker for T cells (FALSE)</div><div>B. CD8 binds to MHC class II molecules (FALSE)</div><div>C. ICAM-1 binds to LFA1 (TRUE)</div><div>D. CD4 is expressed on helper T cells (TRUE)</div><div>E. CD3 is expressed on the majority of NK cells (FALSE)</div></div>
<div><br></br></div>
A - F; LFA-1 is a marker for neutrophils. They are integrin family adhesion molecules that bind to Ig superfamily molecules, ICAMs. They mediate tight binding. Initially the interactions are weak but signalling through chemokine receptors causes a conformationl changes in LFA-1 that reuslts in a high affinity binding state.<div>B - F; CD8 binds to MHC class I molecules.</div><div>E - F; FCgammaRIII is involved; it recognises antigen/antibody complexes. Ligation of this receptor leads to release of cytoplasmic granules containing lytic enzymes. This leads to ADCC.</div>
Pattern recognition receptors include:<div>A. TLR5 which binds flagellin</div><div>B. TLR3 which in conjunction with CD14 recognises LPS</div><div>C. NOD2 which recognises muramyl dipeptide</div><div>D. TLR9 which binds methylated CpG-rich DNA</div><div>E. NLRP3 (also known as NALP3) which recognises cholesterol crystals</div>
<div>Pattern recognition receptors include:<div>A. TLR5 which binds flagellin (TRUE)</div><div>B. TLR3 which in conjunction with CD14 recognises LPS (FALSE)</div><div>C. NOD2 which recognises muramyl dipeptide (TRUE)</div><div>D. TLR9 which binds methylated CpG-rich DNA (FALSE)</div><div>E. NLRP3 (also known as NALP3) which recognises cholesterol crystals (TRUE)</div></div>
<br></br>B - F; TLR3 recognises double-stranded viral RNA and it forms a homodimer. LPS is recognised by TLR4 homodimer.<br></br>D - F; TLR9 recognises unmethylated CpG-rich DNA because methylated is eukaryotic.
In the acute inflammatory response:<div>A. Histamine comes from stored sources</div><div>B. Leukotrienes are actively synthesised</div><div>C. C3a, C3b, C5a are derived from precursors present in plasma</div><div>D. Mast cells release endogenous pyrogens to activate the acute phase response</div><div>E. Histamine is released from mast cells by substance P released from nerve fibres</div>
“<div>In the acute inflammatory response:<div>A. Histamine comes from stored sources (TRUE)</div><div>B. Leukotrienes are actively synthesised (TRUE)</div><div>C. C3a, C3b, C5a are derived from precursors present in plasma (TRUE)</div><div>D. Mast cells release endogenous pyrogens to activate the acute phase response (FALSE)</div><div>E. Histamine is released from mast cells by substance P released from nerve fibres (TRUE)</div></div><div><br></br></div><br></br>D - F; macrophages release endogenous pyrogens [e.g. molecules/cytokines that induce fever]. These include IL-1beta, TNF-alpha and IL-6.”
In the complement system:<div>A. The classical pathway is always first to act</div><div>B. The alternative pathway is the main pathway responsible for generating C3b</div><div>C. Factor H speeds up activation of the alternative pathway</div><div>D. DAF disrupts the C3 convertase C3bBb</div><div>E. MCP makes C3b susceptible to cleavage by factor I</div>
“<div>In the complement system:<div>A. The classical pathway is always first to act (FALSE)</div><div>B. The alternative pathway is the main pathway responsible for generating C3b (TRUE)</div><div>C. Factor H speeds up activation of the alternative pathway (FALSE)</div><div>D. DAF disrupts the C3 convertase C3bBb (TRUE)</div><div>E. MCP makes C3b susceptible to cleavage by factor I (TRUE)</div></div><div><br></br></div>A - F; the first to act is the alternative pathway, then the lectin pathway and then finally the classical pathway<div>C - F; factor H antagonises the alternative pathway. It is the main control factor responsible for regulating complement activation in solution. It is a soluble cofactor for factor I that attaches to sialic acid on host membranes. It causes dissociation of C3bBb (the alternative pathway C3 convertase) and makes C3b susceptible to cleavage by factor I.</div>”
The following statements regarding cytokines are true:<div>A. IL-12 activates NK cells.</div><div>B. IL-4 inhibits the generation of Th1 cells</div><div>C. IL-8/CXCL8 is referred to as an endogenous pyrogen</div><div>D. Neutrophils follow a concentration gradient of IL-8/CXCL8</div><div>E. IL-6 activates the acute phase response</div>
“<div>The following statements regarding cytokines are true:<div>A. IL-12 activates NK cells. (TRUE)</div><div>B. IL-4 inhibits the generation of Th1 cells (TRUE)</div><div>C. IL-8/CXCL8 is referred to as an endogenous pyrogen (FALSE)</div><div>D. Neutrophils follow a concentration gradient of IL-8/CXCL8 (TRUE)</div><div>E. IL-6 activates the acute phase response (TRUE)</div></div><div><br></br></div><br></br>C - F; CXCL8 activates and recruits NK cells, as well as neutrophils. It is a chemokine e.g. controlled in cell movement.”
In the complement system:<div>A. The membrane attack complex is initiated by cleavage of factor C5.</div><div>B. C3b and C5b increase inflammation and enhance vascular permeability.</div><div>C. Mannose-binding lectin interacts with MASP-1 and MASP-2.</div><div>D. The alternative pathway C3 convertase is C4bC2a.</div><div>E. C-reactive protein on bacterial surfaces recruits complement component C2.</div>
“<div>In the complement system:<div>A. The membrane attack complex is initiated by cleavage of factor C5. (TRUE)</div><div>B. C3b and C5b increase inflammation and enhance vascular permeability. (FALSE)</div><div>C. Mannose-binding lectin interacts with MASP-1 and MASP-2. (TRUE)</div><div>D. The alternative pathway C3 convertase is C4bC2a. (FALSE)</div><div>E. C-reactive protein on bacterial surfaces recruits complement component C2. (FALSE)</div></div><div><br></br></div><div>B - F; C3a and C5a are anaphylatoxins which stimulate inflammation; not the b parts<br></br>D - F; the classical C3 convertase is the C3bC2a. The alternative pathway C3 convertase is C3bBb<br></br>E - F; CRP on bacterial surfaces recruits complement component leads to activation of the classical pathway. Cq1 can bind to CRP, and this leads to activation of C1r and C1s subunits. C1s is able to cleave C4 to expose a reactive thioester group which can covalently attach C4b to the pathogen surface. Activated C1 then associates with and cleaves C2 depositing the C2a fragment on C4b forming C4bC2a, the classical C3 convertase. This can cleave C3 and deposit C3b on the microbial surface, and then membrane associated C3b generated can utilise the alternative pathway amplification loop by binding to factor B to generate C3bBb. The classical convertase C3bC2a can also associate with C3b to generate C4bC2aC3b, a classical pathway C5 convertase.</div>”
Immunological tolerance:<div>A. Can involve regulatory T cells which have the signature transcription factor GATA3.</div><div>B. In pregnancy involves IDO which catabolises tryptophan.</div><div>C. Depends on the transcription factor IPEX being expressed in the thymus</div><div>D. Requires that all B cells with receptors that recognise self undergo apoptosis or anergy</div><div>E. Can be induced if T-cells receive signalling through MHC 1 in the absence of costimulation</div>
“<div>Immunological tolerance:<div>A. Can involve regulatory T cells which have the signature transcription factor GATA3. (FALSE)</div><div>B. In pregnancy involves IDO which catabolises tryptophan. (TRUE)</div><div>C. Depends on the transcription factor IPEX being expressed in the thymus (FALSE)</div><div>D. Requires that all B cells with receptors that recognise self undergo apoptosis or anergy (FALSE)</div><div>E. Can be induced if T-cells receive signalling through MHC 1 in the absence of costimulation (TRUE)</div></div><div><br></br></div>A - F; T regs are positive for FOXP2. GATA3 transcription factor is the signature Th2 TF.<br></br>C - F; Depends on the TF AIRE in the thymus. IPEX is an X-linked disease that only occurs in boys in which there is a lack of Tregs due to mutations in FOXP3; they die by two years unless treated due to lymphoproliferation and autoimmunity because of a lack of self-tolerance<br></br>D - F; because they require T cell activation if the T cell is tolerised then the B cell is not a worry”
Regarding autoimmunity:<div>A. C1, C2 or C4 complement deficiency predisposes to SLE</div><div>B. Type 1 diabetes is more prevalent in individuals with an aspartate residue in position 57 in DQB1</div><div>C. EAE (experimental autoimmune encephalomyelitis) is predominantly due to TH2 T cells</div><div>D. Myasthenia gravis involves antibodies to TSH recepetor</div><div>E. TFH (T-follicular helper) cells principally activate macrophages</div>
“<div>Regarding autoimmunity:<div>A. C1, C2 or C4 complement deficiency predisposes to SLE (TRUE)</div><div>B. Type 1 diabetes is more prevalent in individuals with an aspartate residue in position 57 in DQB1 (FALSE)</div><div>C. EAE (experimental autoimmune encephalomyelitis) is predominantly due to TH2 T cells (FALSE)</div><div>D. Myasthenia gravis involves antibodies to TSH recepetor (FALSE)</div><div>E. TFH (T-follicular helper) cells principally activate macrophages (FALSE)</div></div><div><br></br></div><br></br>B - F; less prevalent with the charged aspartate<br></br>C - F; predominantly due to CD4+ T helper cells, but not specific to Th2 cells<br></br>D - F; Grave’s disease<br></br>E - F; they principally activate B cells; they are responsible for antibody development, isotope switching and affinity maturation”
In transplantation:<div>A. Direct recognition of allogeneic transplants requires donor derived dendritic cells.</div><div>B. Indirect recognition occurs only when MHC molecules are mismatched</div><div>C. HLA matching is more important for haemopoietic stem cells transplants than for liver transplants</div><div>D. HLA typing is not necessary in the autologous situation</div><div>E. A GvH response is never advantageous</div>
<div>In transplantation:<div>A. Direct recognition of allogeneic transplants requires donor derived dendritic cells. (TRUE)</div><div>B. Indirect recognition occurs only when MHC molecules are mismatched (FALSE)</div><div>C. HLA matching is more important for haemopoietic stem cells transplants than for liver transplants (TRUE)</div><div>D. HLA typing is not necessary in the autologous situation (TRUE)</div><div>E. A GvH response is never advantageous (FALSE)</div></div>
The endogenous pathway of antigen presentation involves:<div>A. Mostly peptides derived from extracellular pathogens</div><div>B. Presentation of antigen on MHC class I molecules<br></br></div><div>C. Presentation of antigen to cytotoxic T cells</div><div>D. Presentation of antigen to TH1 cells</div><div>E. Presentation of antigen to B cells</div>
“<div>The endogenous pathway of antigen presentation involves:<div>A. Mostly peptides derived from extracellular pathogens (FALSE)</div><div>B. Presentation of antigen on MHC class I molecules (TRUE)<br></br></div><div>C. Presentation of antigen to cytotoxic T cells (TRUE)</div><div>D. Presentation of antigen to TH1 cells (FALSE)</div><div>E. Presentation of antigen to B cells (FALSE)</div></div><div><br></br></div>A - F; presents intracellular antigens, on MHC I molecules for CD8 cells. Proteins within the cytosole are continually being degraded into peptides by the proteasome. These peptides are moved from the cytosol into the ER via TAP [transporter associated with antigen processing]. Suitable peptides are then loaded onto partially folded MHC class I molecules in a process that is assisted by chaperone proteins known as the peptide loading complex [PLC]. Fully loaded MHC peptide complexes are released from the chaperones, pass through the golgi, and then follow the secretory pathway to the cell surface. See diagram.<br></br>D - F; Th1 cells are CD4 cells and so interact with MHC class II<br></br>E - F; B cells do not bind to antigen presented on MHC molecules. B cells binds antigen via its specific surface BCR/Ig and internalises it. The endocytosed antigen is then processed and presented on the surface MHC class II peptide complex. This peptide is then recognised by T helper cells which interacts with the MHC II molecules with its TCR. Also requires co-stimulatory moelcules to provide signal 2. This promote B cell proliferation, B cell survival signals and promotes Ig class switching. This interaction also leads to activation of the T cell.”
C - F; B cells are non-phagocytic. They have BCRs that can interact with a wide variety of molecules in their native conformation. Antigen bound to the BCR is endocytosed and processed to be presented on MHC II molecules for presentation to B cells.
E - F; the proteasome generates the majority of peptides presented by MHC class I molecules. Peptides presented on MHC II molecules are taken up into the cell by endocytosis and are then degraded into peptides by proteases. "
B - F; they are expressed on professional antigen presenting cells e.g. macrophages, B cells and dendritic cells. Class II molecules can be induced to be expressedon other cells in the presence of IFNgamma.
D - F; B cells undergo somatic hypermutation in their production of antibodies. Point mutations are introduced into heavy and light chain variable regions. This involves deamination of cytosine to uracil by the enzyme activation induced cytidine deaminase (AID). Antibodies with increased affinity are selected by affinity maturation. The mutation rate is abut 1/1000 BP per cell division.
E - F; they are present on dendritic cells NOT follicular dendritic cells. These two types of cell are from different lineages and are not related either structurally or functionally. "
B - F; a particular mHC molecule will be specific for anchor residues, and for particular lengths of peptide but it will not be specific for the residues in between these anchor residues meaning that it can present a wide array of peptide fragments.
"
C - F; they are highly conserved across different classes of organisms. This means that we don't need as many different PRRs to detect them.
D - F; PRRs can recognise double stranded RNA. Double stranded RNA might however act as a PAMP e.g. from RNA viruses e.g. TLR3.
D - F; infectivity is not destroyed by irradiation that would destroy nucleic acids
"
C. require a high pH environment to fuse with cellular membranes
D. encode 3 viral envelope proteins
E. cause seasonal epidemics due to the process of antigenic drift
C. require a high pH environment to fuse with cellular membranes (FALSE)
D. encode 3 viral envelope proteins (TRUE)
E. cause seasonal epidemics due to the process of antigenic drift (TRUE)
B - F; encode an RNA-dependent RNA polymerase made up of PB1, PB2 and PA polypeptides
C - F; they require a low pH
"
"
C. Herpes simplex virus
D. Human cytomegalovirus
E. Hepatitis C virus
C. Herpes simplex virus (TRUE)
D. Human cytomegalovirus (TRUE)
E. Hepatitis C virus (TRUE)
B. Influenza
C. Meningitis
D. Botulism
E. Typhoid
B. EPEC produces a cholera-like enterotoxin LT (labile toxin)
C. EHEC produce yellow colonies on McConkey agar
D. ETEC produces a shiga-like toxin (SLT) that accentuates inflammation
E. E. Coli 0157 is an ETEC found in beefburgers
- EHEC produces shiga like toxin that is a glycosidase that depurinates 28S rRNA thereby blocking protein synthesis
- E. Coli 0157 is an EHEC found in beef
E - F; these are downstream of the PRRs --> however, pxo virus does target this parthway
E - F; BCG