Explore key concepts of viral immunology in 'Block 9 Micro viral immunology'. This quiz assesses understanding of antiviral defense mechanisms, including IFN-a activity, CD8+ T lymphocyte cytotoxicity, and innate host defenses. It's designed for learners aiming to deepen their knowledge in viral immunology.
RNA
Capsid
Lipid bilayer
Envelope glycoprotein
RNA polymerase
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Cell-mediated (CD8+) cytotoxicity and IFN-a secretion
Alternate activation of the complement pathway and IgM secretion
Cell-mediated (CD8+) cytotoxicity and IL-4 secretion
Classical activation of the complement pathway and IL-17 secretion
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IFN-y and IL-12
IL-4 and IFN-y
IL-4 and IL-12
IL-10 and IFN-y
IL-4 and TNF-a
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Erk1/Erk2 MAPK
NF-kB
SAPK/JNK
Jak/STAT
PI3K/Akt
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Because MHC-I restricted antigen presentation is the first step in the production of neutralizing antibodies
Because MHC-I restricted antigen presentation is the first step in the activation of both T helper 1 and T helper 2 responses
Because MHC-I restricted antigen presentation is the main pathway through which virus-infected cells are killed
Because MHC-I restricted antigen presentation is the main pathway of antibody-dependent cell-mediated cytotoxicity (ADCC)
Because MHC-I restricted antigen presentation is required for B-cell clonal expansion
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RNA
Capsid
Lipid bilayer
Envelope glycoprotein
RNA polymerase
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Virus neutralization
Activation of classical complement cascade
Extracellular degradation of virions
Pkr protein synthesis
Inhibition Jak/STAT signalling
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IFN-a increases inactive RNA-activated protein kinase (Pkr) expression which, upon activation by double-stranded RNA, inactivates the translation activator eIF2 thereby terminating mRNA translation and promoting apoptosis and autophagy.
IFN-a decreases immunoproteasome expression, thereby leading to decreased protein degradation, decreased levels of major histocompatibility complex class I (MHC-I) cell surface expression, and increased natural killer cell cytotoxicity.
IFN-a increases the expressions of both 2’,5’-oligo(A) synthetase and RNase L, after which double-stranded RNA activates 2’,5’-oligo(A) synthetase to hydrolyze 2’,5’-adenylic acid thereby activating RNase L which degrades double-stranded RNA and sends the cell into apoptosis.
IFN-a increases inducible nitric oxide synthase (iNOS) and nicotinamide adenine dinucleotide phosphate-oxidase (NADPH-oxidase) expressions, thereby decreasing the levels of free radicals in the cell and promoting apoptosis and autophagy.
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Natural killer cells (NK cells)
Macrophages
CD4+ T helper 2 lymphocytes
B-lymphocytes
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Virus neutralization
Apoptosis
IFN-a secretion
Alternative activation of the complement pathway
Autophagy
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IFN-a decreases mRNA transcription consequent to Pkr up-regulation in virally-infected cells.
IFN-a decreases mRNA transcription consequent to eIF2- dephosphorylation in virally-infected cells.
IFN-a decreases mRNA transcription consequent to RNase L down-regulation in virally-infected cells.
IFN-a decreases mRNA translation consequent to Pkr up-regulation in virally-infected cells.
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IFN-a
TNF-a
IL-1
IL-6
IFN-y
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Interferon receptor
Toll-like receptor
Jak receptor
Tumor necrosis alpha receptor
T cell receptor
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Interferon receptor
RIG-1
Jak receptor
Tumor necrosis alpha receptor
T cell receptor
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