BIOL 221 LEC 28 MCQ

Which of the following is a method for viruses to evade the host immune defenses?

A. They use the host's cytoskeleton to spread intercellularly.
B. They inhibit their binding to cell surface receptors.
C. They produce an antiphagocytic lipid capsule.
D. They prevent recruitment of the MAC by the complement cascade.
E. They produce their own "cancer kill" signal for NK cells
Click the card to flip 👆
1 / 35
Terms in this set (35)
Which of the following is a method for viruses to evade the host immune defenses?

A. They use the host's cytoskeleton to spread intercellularly.
B. They inhibit their binding to cell surface receptors.
C. They produce an antiphagocytic lipid capsule.
D. They prevent recruitment of the MAC by the complement cascade.
E. They produce their own "cancer kill" signal for NK cells
Which of the following is true of endotoxin, but not of an exotoxin?

A. Endotoxin is a cytoplasmic protein.
B. Endotoxin has much higher toxocity.
C. Endotoxin stimulates interleukin release, which results in fever.
D. Endotoxin can be the target for a vaccine.
E. Diseases caused by endotoxin can rarely be treated with antibiotics
Most of the really dangerous pathogenic fungi can do which of the following?

A. Get inhaled as mold spores and transition to yeast in the host's body
B. Produce spores within the host's body
C. Escape the immune system by living inside red blood cells
D. Produce endotoxin
E. Grow as yeast in an environmental reservoir outside the host
How does your body respond to the presence of a superantigen toxin?

A. By secreting lots of cytokines and mounting a massive inflammatory response
B. By producing many more antibodies than normal, causing hypersensitivity reactions
C. By recruiting the complement cascade to kill host cells as well as bacteria
D. By engulfing the toxin and disseminating it via the blood to the tissues
E. By destroying connective tissue, resulting in necrosis.
Which of the following is usually true of an exotoxin, but not true of endotoxin?

A. There is a serum binding protein that binds to it.
B. It is an integral part of the cell envelope
C. It is easily detected by the Limulus amoebocyte assay
D. It usually causes a fever
E. The genes encoding it can be passed among cells on a pathogenicity island
How does a phospholipase toxin kill cells?

A. By preventing phospholipid synthesis
B. By removing the head groups, thus destroying the amphipathic nature of the phospholipid
C. By adding ADP + ribose to stop protein synthesis
D. By preventing uptake via membrane fusion
E. By digesting fatty acids, causing the lipids to not pack together as well
How does a super antigen toxin function?

A. It is a very strong antigen that provokes a massive antibody response.
B. It crosslinks the TCR of TH cells to MHC2 that is not presenting an antigen.
C. It crosslinks TH cells to B cells, thereby producing lots of antibodies.
D. It dissolves the material that holds cells together in tissues.
E. It adds ADP-ribose to a protein, thereby inactivating it and killing cells
How is LPS toxic to humans?

A. It agglutinates a type of red blood cell, causing DIC.
B. It activates B cells even without antigen binding, causing massive antibody release.
C. It binds to cells in the hypothalamus, damaging them and causing fever.
D. It increases cAMP concentration, causing edema and cell death
E. It binds strongly to macrophages, causing a response that can lead to a hypovolemia
What is the function of the A part of an AB toxin? A. It binds to surface receptors on the host cell B. It hydrolyzes the head group of phospholipids C. It facilitates bacterial spread through a tissue and into the bloodstream D. It activates large numbers of TH cells E. It enters the cytoplasm and kills the host cell, often by altering cell metabolismE. It enters the cytoplasm and kills the host cell, often by altering cell metabolismFor which bacterial toxins have we found a pharmaceutical use to make anesthetics more readily able to penetrate through skin and other tissues? A. ADP-ribosylating A-B toxins B. hemolysins C. hyaluronidases D. endotoxins E. superantigen toxinsC. hyaluronidasesOne reason why a vaccine against malaria has proven difficult to design is that the malaria parasite. . . A. has no surface proteins B. has a virus-like protective coating that prevents antibody binding C. covers itself with host antigens D. lives in red blood cells, where it can avoid both cellular and humoral immunity E. can swim through a tissue, avoiding humoral immunityD. lives in red blood cells, where it can avoid both cellular and humoral immunityHow does production of phospholipase enhance bacterial survival inside macrophages? A. It binds the Fc end of IgG, thereby disguising the bacterium as a "self" cell. B. It oxidizes macrophage proteins and kills the macrophage. C. It prevents C3b from binding to the bacterial surface and activating complement. D. It digests the antibody that most commonly attacks bacteria inside macrophages. E. It disrupts the phagosome membrane, allowing the bacterium to escapeE. It disrupts the phagosome membrane, allowing the bacterium to escapeDiphtheria toxin is an AB toxin. What does this mean? A. It can be detected by the limulus amoebocyte assay. B. There can be no vaccine made against it. C. There is a receptor for it on a host cell membrane. D. Diphtheria is mainly an intracellular pathogen. E. It binds to and alters the structure of antibodiesC. There is a receptor for it on a host cell membrane.How do bacteria with Type III secretion systems (T3SS) typically enter host cells? A. The T3SS pokes a hole in the host cell membrane through which the bacteria enter. B. The T3SS kills the host cell, making it easier for the bacteria to enter. C. The T3SS enhances binding to macrophages, which engulf the bacteria. D. Effectors secreted through the T3SS cause the host cell to enfold the bacteria in membrane ruffles. E. They don't. T3SS are for secreting exotoxins, not for entering host cells.Effectors secreted through the T3SS cause the host cell to enfold the bacteria in membrane rufflesWhat is this diagram depicting? A. The typical activation of a TH cell by a macrophage B. The function of a super antigen toxin C. The function of an AB toxin D. The attachment of a bacterium to a T cell E. The activity of Staphylococcal protein AB. The function of a super antigen toxinWhy do some viruses produce an analog of MHC1? A. To stop NK cells from killing cells infected by the virus B. So the viruses can bind to the MHC1 and be internalized more readily C. To be able to present viral proteins more easily on the surface of the host cell D. It is a viral toxin that initiates an autoimmune reaction in the host E. To reduce the efficiency of interferon binding to neighboring cellsA. To stop NK cells from killing cells infected by the virusWhich of the following statements is accurate when comparing Anthrax toxin to LPS? A. LPS is more likely to be inactivated by heat or formalin. B. LPS is probably more toxic per microgram than Anthrax toxin. C. The genes for Anthrax toxin are more likely to be located on a plasmid. D. LPS contains more protein components than Anthrax toxin. E. Anthrax toxin is more likely to remain attached to the bacterial cell membrane.C. The genes for Anthrax toxin are more likely to be located on a plasmid.The bacterium that causes necrotizing fasciitis produces a hyaluronidase toxin. This toxin gives anadvantage to the bacterium because it allows the bacterium to . . . A. spread more rapidly between the cells in a tissue B. avoid the humoral immune response C. induce a huge cytokine response in the host D. be internalized more quickly by host macrophages E. break out of the phagolysosomeA. spread more rapidly between the cells in a tissueSome viruses like Papillomavirus encode an inhibitor of the eukaryotic protein p53. Why? A. so that they can coat themselves with a "self" protein B. so that they can prevent infected cells from undergoing apoptosis C. to cancel the "kill" signal that NK cells recognize D. to allow them to invade deep tissues beyond the skin E. so that they can escape from the phagosome before it fuses with the lysosomeB. so that they can prevent infected cells from undergoing apoptosisDuring some viral infections, infected cells fuse to form___________because_____________. A. giant cells ; these cells are easier for the immune system to recognize B. granulomas ; infected macrophages continue to secrete cytokines C. granulomas ; these "activated" cells have a more potent oxidative burst D. syncytia ; it allows the virus to avoid serum antibodies E. syncytia ; these fused cells cannot produce interferonD. syncytia ; it allows the virus to avoid serum antibodiesWhy can't we produce a successful vaccine against endotoxin? A. Our immune response against it is too weak. B. It can't be inactivated because it isn't a protein. C. It resembles human host proteins too closely. D. It enters host cells so quickly that antibodies never encounter it. E. It is found on a plasmid, and can spread too rapidly through a bacterial population.B. It can't be inactivated because it isn't a protein.For which type of bacterial toxin is there a medical use - to make anesthetics more readily able to penetrate through skin and other tissues? A. cAMP-producing A-B toxins B. phospholipases C. IgA proteases D. hyaluronidases E. superantigen toxinsD. hyaluronidasesThe malaria parasite has a particularly effective method of avoiding both humoral and cellular hostimmune defenses. Which of the following is correct about this parasite? A. It lives in red blood cells B. It produces keratinase C. It grows within and travels between host epithelial cells D. It coats itself with host proteins so that it resembles "self" E. It causes host cells to fuse into syncytiaA. It lives in red blood cellsWhat would be the most effective way to protect a patient against bacterial endotoxin? A. Vaccinate the patient with an endotoxoid vaccine. B. Test to see if intravenous fluids given to the patient coagulate Limulus blood cells. C. Autoclave all intravenous fluids that might be given to the patient. D. Use a Western Blot to screen any intravenous fluids given to the patient. E. Passively immunize the patient against bacterial endotoxinB. Test to see if intravenous fluids given to the patient coagulate Limulus blood cells.All of the following are characteristic of bacterial A-B toxins EXCEPT . . . A. The A part can cause increased production of cAMP B. Multiple B parts can bind to multiple receptors C. The B part can be used to produce a toxoid vaccine D. An "attenuated" bacterium might have a mutation in the A part E. They hydrolyze the A part of phospholipids away from the B partE. They hydrolyze the A part of phospholipids away from the B partWhy is there not yet a vaccine directed against bacterial endotoxin? A. There is no market for one, so no one has tried hard enough to produce it. B. There are too many different varieties of endotoxin. C. Endotoxin is also a self-antigen in humans. D. Endotoxin does not produce a strong enough immune response E. Endotoxin cannont be inactivated to produce a toxoidE. Endotoxin cannont be inactivated to produce a toxoidHow does a bacterial A-B toxin work? A. It digests the host's cell membrane phospholipids. B. The B part blocks protein synthesis; the A part activates cAMP production. C. The B part binds to receptors; the A part enters the host cell. D. The A part activates the B part, which then binds to host cells and kills them. E. The B part protects the A part from attack by the host's immune system.C. The B part binds to receptors; the A part enters the host cell.How could you tell if a particular pathogen produced a superantigen toxin when it infected a patient? A. Look for complete clearing when the pathogen is grown on a Blood Agar plate. B. Look for tissue damage in a patient. Only superantigen toxins can do that. C. Look for the release of cytokines from TH cells that do not recognize the pathogen. D. Look for a larger than normal antibody titer against the pathogen. E. Look for symptoms of DIC. Any pathogen that causes DIC probably produces a superantigen toxinC. Look for the release of cytokines from TH cells that do not recognize the pathogen.Viruses use all of the following strategies to avoid the immune system EXCEPT . . . A. production of an IgA protease B. production of an interferon repressor C. formation of syncytia D. inhibition of the tumor suppressor p53 E. reversing the MHC-I antigen presentation pathwayA. production of an IgA proteaseCan the structure shown at the right be toxic? If so, how? If not, why not? A. Yes, the part labeled 'A' can combine with antibodies to create a hypersensitivity reaction B. Yes, the part labeled 'B' can bind to a protein that induces a strong cytokine response from macrophages C. Yes, the whole structure can bridge the interaction between naiveTH cells and APCs D. No, the structure as shown lacks the toxic portion, and can onlybind to receptors. E. No, the structure is not bacterial and has nothing to do with a toxin.B. Yes, the part labeled 'B' can bind to a protein that induces a strong cytokine responseWhich of the following statements about AB toxins is accurate? A. The B-part of the toxin can inhibit the function of B cells. B. The A-part of the toxin can hydrolyze phospholipid head groups. C. The B-part of the toxin can be used as a vaccine antigen. D. They have a medical use to allow anesthetics to penetrate tissue better. E. They are only produced by Gram positive bacteriaC. The B-part of the toxin can be used as a vaccine antigenA naked virus, HPV, produces a protein called E6. Recalling what infection HPV causes,how does the E6 protein contribute to the infection? A. It prevents the action of the p53 tumor suppressor gene in the host. B. It blocks the MHC-I antigen presentation pathway in the host. C. It allows the virus to form syncytia between infected host cells. D. It prevents activation of TH cells by acting like an analog of MHC-II.E. It stimulates the action of NK cells, which cause the HPV skin lesionsA. It prevents the action of the p53 tumor suppressor gene in the host.The malaria parasite spends most of the human part of its life cycle in red blood cells(RBCs). What does this imply about the body's response to the presence of this parasite? A. Antibodies can't bind to the parasite, but TC cells can still kill infected RBCs. B. Infected RBCs can only be killed by NK cells. C. The parasite can be neutralized by antibodies once the antibodies bind to RBCs. D. The parasite is exposed to neither humoral nor cellular immune responses. E. The parasite's surface proteins resemble those of the host.D. The parasite is exposed to neither humoral nor cellular immune responses