Deck 13: Failures of the Bodys Defenses

Question 1

Which of the following pairs is mismatched?

A)X-linked agammaglobulinemia: gamma globulin injections
B)X-linked hyper IgM syndrome: GM-CSF injections
C)X-linked hyper IgM syndrome: gamma globulin injections
D)hereditary angioedema: C1INH infusions
E)None of the above is mismatched.

Answer 1

E

Question 2

Superantigens bind to all of the following molecules except _____.

A)CD4
B)MHC class II α chain
C)CD28
D)T-cell receptor V_β chain.

Answer 2

A

Question 3

primary immune response against influenza virus produces antibodies that bind to _____.

A)hemagglutinin and neuraminidase
B)variable surface glycoproteins
C)EBNA-1
D)protein toxins
E)gp41 and gp120.

Answer 3

A

Question 4

Paroxysmal nocturnal hemoglobinuria is caused by _____.

A)a profound deficiency of neutrophils
B)leukocytosis
C)immune-complex deposition in tissues
D)defects in recruitment of phagocytes to infected tissues
E)complement-mediated lysis of erythrocytes.

Question 5

Individuals with an antibody deficiency are more susceptible to infections by all of the following except _____.

A)Streptococcus pneumoniae
B)Haemophilus influenzae
C)Streptococcus pyogenes
D)Mycobacterium tuberculosis
E)Staphylococcus aureus.

Question 6

Herpesviruses include all of the following except _____.

A)varicella-zoster
B)Epstein-Barr virus
C)herpes simplex virus
D)cytomegalovirus
E)All of the above are herpesviruses.

Question 7

Epstein-Barr virus-infected cells are poor targets for CD8 T-cell killing because _____.

A)the virus inhibits MHC class I expression
B)the virus escapes from the phagosome into the cytosol
C)infected cells do not express any viral proteins during latency
D)the proteasome cannot generate viral peptides for presentation by MHC class I molecules.

Question 8

Which of the following statements regarding herpes simplex virus is false?

A)Because sensory neurons express low levels of MHC class I molecules,they provide appropriate sites for viral dormancy.
B)Reactivation of herpesviruses follows stressful incidents.
C)Cold sores develop as a consequence of CD8 T-cell killing.
D)In one's lifetime,periodic episodes of reactivation are common.
E)Herpes simplex virus infects B lymphocytes.

Question 9

Shingles is associated with infection by _____.

A)Epstein-Barr virus
B)Staphylococcus aureus
C)herpes zoster
D)Candida albicans
E)Listeria monocytogenes.

Question 10

Dominant mutant forms of IFNγR1 exhibit all of the following in heterozygotes except _____.

A)they are recycled by endocytosis more quickly than the normal receptor
B)the cytoplasmic tail is truncated
C)they are able to form stable dimers with the normal form
D)they cause less severe immunodeficiency than do the homozygous recessive forms
E)they are unable to transduce signals when bound to the normal form.

Question 11

_____ is a strategy used by herpesviruses where replication and the generation of virus-derived peptides are avoided in order to hide from the immune response.

A)latency
B)antigenic shift
C)antigenic drift
D)seroconversion
E)gene conversion.

Question 12

Genes encoding _____ rearrange in trypanosomes permitting replication and survival of the pathogen until the host produces an antibody response against the altered gene product.

A)pilin
B)flagellin
C)variable surface glycoproteins (VSGs)
D)hemagglutinin.

Question 13

Which of the following is not associated with the reactivation of herpesviruses?

A)hormonal fluctuations
B)antibody deficiency
C)bacterial infection
D)immunosuppression
E)ultraviolet radiation.

Question 14

Staphylococcal superantigen-like protein 7 (SSLP7)produced by Staphylococcus aureus,binds to _____ and thereby prevents the killing of the bacterium by the host's immune system during infection.(Select all that apply.)

A)NK-cell activating receptors
B)C5 complement protein
C)CD8 co-receptor
D)T-cell receptor V_β chain
E)Fc region of IgA.

Question 15

_____ results when a gene affecting the immune system mutates,thereby compromising the body's defense against infection.

A)gene conversion
B)epidemics
C)primary immunodeficiency disease
D)secondary immunodeficiency disease
E)seroconversion.

Question 16

of the following are associated with the ability of influenza virus to escape from immunity except _____.

A)age
B)error-prone replication of its DNA genome
C)co-infection with avian and human influenza viruses
D)recombinant strains
E)the phenomenon of 'original antigenic sin.'

Question 17

Deficiencies in complement components C5-C9 and properdin (factor P)are associated with _____.

A)immune-complex disease
B)susceptibility to Neisseria
C)secondary immunodeficiency diseases
D)hereditary angioedema
E)leukocyte adhesion deficiency.

Question 18

of the following use gene conversion to avoid immune detection except _____.

A)Salmonella typhimurium
B)Trypanosoma brucei
C)Treponema pallidum
D)Neisseria gonorrhoeae.

Question 19

_____ cause(s)mild and limited disease,whereas _____ cause(s)more severe disease and higher mortality.

A)Antigenic drift; antigenic shift
B)Antigenic shift; antigenic drift
C)Epidemics; pandemics
D)Pandemics; epidemics.

Question 20

All of the following are associated with hereditary angioedema except _____.

A)possible death by suffocation
B)overproduction of vasoactive C2a fragment and peptide bradykinin
C)hyporesponsiveness of classical complement pathway
D)subepithelial edema
E)C1 inhibitor deficiency.

Question 21

An epidemic affects _____,whereas a pandemic affects _____.

A)susceptible individuals; immune individuals
B)immune individuals; susceptible individuals
C)global populations; local populations
D)local populations; global populations.

Question 22

Epstein-Barr virus infects and establishes latency in _____,gaining entry by binding to _____.

A)B cells; CR2
B)T cells; CD4
C)T cells; CD8
D)neurons; MHC class I
E)B cells; EBNA-1.

Question 23

Listeria monocytogenes replicates in _____ of macrophages after _____.

A)the phagosome; inhibition of fusion of the phagosome with the lysosome
B)the cytosol; escaping from the phagosome
C)a specialized membrane-bound vesicle; infection of the cell
D)extracellular spaces; coating itself with human proteins
E)nucleus; fusion with the nuclear membrane.

Question 24

Which of the following statements regarding C1 inhibitor (C1INH)is false? (Select all that apply.)

A)C1INH belongs to a family of serine and cysteine protease inhibitors called the serpins.
B)C1INH inhibits C1r but not C1s,so partial serine protease activation is achieved in the classical complement pathway.
C)C1INH is cleaved by C1.
D)When bound to C1 as a pseudosubstrate,it activates the protease activity of C1.
E)Heterozygous individuals who have a single-gene defect in C1INH cannot make sufficient quantities of the gene product and must receive recombinant C1INH by infusion.

Question 25

Which of the following is not a virus that can cause a persistent infection in the host by establishing latency?

A)influenza virus
B)herpes simplex virus
C)varicella-zoster
D)Epstein-Barr virus
E)human immunodeficiency virus.

Question 26

Protective antibodies generated in response to influenza virus bind to _____ of the viral envelope.

A)hemagglutinin and neuraminidase
B)polysaccharides
C)variable surface glycoproteins
D)superantigens
E)gp41 and gp120.

Question 27

Which of the following statements regarding inherited immunodeficiency diseases is correct?

A)Affected individuals are less susceptible to infection.
B)Mortality rates are reduced by the administration of antibiotics to affected individuals.
C)Most deficiency syndromes are caused by dominant gene defects.
D)Women are more likely than men to inherit X-linked immunodeficiencies.
E)Extracellular bacterial infections are common in deficiency syndromes with T-cell defects.

Question 28

Severe combined immune deficiency (SCID)describes a condition in which neither _____ nor _____ are functional.

A)classical; alternative pathways of complement
B)T-cell-dependent antibody responses; cell-mediated immune responses
C)innate; acquired immune responses
D)MHC class I; MHC class II molecules.

Question 29

The mode of evolution responsible for the production of recombinant influenza viruses composed of a genome derived from two different influenza variants is called _____.

A)gene conversion
B)antigenic shift
C)latency
D)immune evasion
E)antigenic drift.

Question 30

Which of the following contribute to new epidemics and the long-term survival of the influenza virus in the human population? (Select all that apply.)

A)New viral strains possess epitopes not recognized by antibodies made in the previous epidemic.
B)The first influenza strain provoking a primary immune response constrains the types of antibodies made during a subsequent encounter with a different strain.
C)The virus loses the capacity to express hemagglutinin,thereby rendering neutralizing antibodies useless.
D)The virus uses gene rearrangement to achieve antigenic variation,which creates new epitopes.
E)The RNA genome of the influenza virus is subject to point mutations during viral replication.

Question 31

Trypanosomes escape from adaptive immunity by altering the type of _____ expressed on the parasite surface.

A)neuraminidase
B)hemagglutinin
C)variable surface glycoprotein (VSG)
D)superantigen
E)capsular polysaccharide.

Question 32

Patients who lack _____ are very susceptible to infections with intracellular bacteria,including the ubiquitous nontuberculous strains of mycobacteria.(Select all that apply.)

A)CD40 ligand
B)the IL-12 receptor
C)the IFN-γ receptor
D)properdin (factor P)
E)CD18.

Question 33

Mutations affecting all of the following except _____ interfere directly with the rearrangement of immunoglobulin and T-cell receptor genes.

A)Artemis
B)purine nucleoside phosphorylase (PNP)
C)DNA-dependent protein kinase (DNA-PK)
D)RAG-1
E)RAG-2.

Question 34

Which of the following explains why Streptococcus pneumoniae can infect an individual recurrently?

A)Previous infection with S.pneumoniae wears down the immune system over time.
B)S.pneumoniae is never completely eradicated during an infection and can reactivate if the host is immunocompromised.
C)Immune responses against S.pneumoniae are serotype-specific and protect only against strains that possess the same capsular polysaccharide antigens.
D)Anti-capsular antibodies are cleared from the host quickly after an active infection.
E)The capsular polysaccharide antigens of S.pneumoniae do not induce immunological memory.

Question 35

Which of the following is not used by the herpes simplex virus to subvert host immune responses?

A)a virus-encoded Fc receptor
B)a virus-encoded complement receptor
C)inhibition of MHC class I expression
D)inhibition of peptide transport by transporter associated with antigen processing (TAP)
E)inhibition of ICAM-1 expression.

Question 36

Which of the following is not a characteristic of staphylococcal enterotoxins?

A)They bind to MHC class I molecules and T-cell receptors.
B)They cause T cells to divide and differentiate into effector T cells.
C)They stimulate between 2% and 20% of the total T-cell population.
D)They cause excessive synthesis and release of cytokines.
E)They induce suppression of the immune response by causing T cells to undergo apoptosis.

Question 37

Wiskott-Aldrich syndrome involves an impairment of _____.

A)lymphocytes and platelets
B)classical complement and blood-clotting pathways
C)the expression of MHC class I and class II molecules
D)T-cell and B-cell development
E)cytokine and cytokine receptor production.

Question 38

Women who are heterozygous for a defective Bruton's tyrosine kinase (Btk)gene _____.

A)are more susceptible to infections caused by extracellular pyogenic bacteria
B)have a 50% chance of having a son with X-linked hyper IgM syndrome
C)mount normal B-cell immune responses despite having lowered levels of serum IgG
D)exhibit X-linked agammaglobulinemia
E)have non-random X inactivation in their B cells.

Question 39

A genetic defect in _____ results in the accumulation of toxic levels of nucleotide metabolites and loss of T-cell function.

A)NADPH oxidase
B)glucose-6-phosphate dehydrogenase
C)myeloperoxidase
D)SH2D1A
E)adenosine deaminase (ADA).

Question 40

What type of immune deficiency would you see in a child lacking the common γ chain of the receptor for cytokines IL-2,IL-4,and IL-7,among others? Explain your answer.
B.Why would you see the same type of immunodeficiency in a child lacking Jak3 kinase function?
C.What treatment might be possible to remedy this immunodeficiency?

Question 41

Explain why a staphylococcal infection might produce a medical emergency.

Question 42

Name three immunodeficiency diseases caused by defects in phagocytes.
B.Which immunodeficiency disease is caused by a defect in the phagocyte NADPH oxidase system,and what is the cellular effect of this defect?
C.What are the main clinical effects of defects in phagocyte function?

Question 43

Bare lymphocyte syndrome leading to a lack of HLA class II molecule expression is due to a defect in _____.

A)transcriptional regulators of HLA class II loci
B)the sequence of the conserved X box of the HLA class II promoter
C)a TAP peptide transporter
D)RAG-1 or RAG-2
E)thymic development.

Question 44

Chronic granulomatous disease (CGD),a condition resulting in chronic bacterial and fungal infections,is caused by one or more defects in _____,compromising the ability of macrophages to _____.

A)CD18; produce cell adhesion molecules
B)NADPH oxidase; produce superoxide radical (O₂^-)
C)CD40 ligand; produce GM-CSF
D)C5-C9; defend against Neisseria
E)C3; opsonize capsulated bacteria.

Question 45

Which statement regarding retrovirus proviruses is false?

A)Proviruses form immediately after the RNA genome assembles with viral proteins and infectious virions are produced.
B)Proviruses consist of double-stranded DNA.
C)Proviruses are flanked by repetitive sequences called long terminal repeats (LTRs).
D)The host cell must provide the transcriptional and translational machinery in order for RNA and protein products to be made from proviruses.
E)A cDNA intermediate is required in order to produce a provirus.

Question 46

Herpes simplex virus favors neurons for latency because of the low level of _____,which reduces the likelihood of killing by CD8 T cells.

A)LFA-3
B)Toll-like receptors (TLRs)
C)transporter associated with antigen processing (TAP)
D)MHC class I
E)MHC class II.

Question 47

Individuals with an immunodeficiency affecting B-cell function are more susceptible to infections caused by which of the following pathogens?

A)Toxoplasma gondii
B)respiratory syncytial virus
C)Haemophilus influenzae
D)Listeria monocytogenes
E)Mycobacterium tuberculosis.

Question 48

Which of the following deficiency syndromes affects T-cell but not B-cell function?

A)X-linked agammaglobulinemia
B)X-linked hyper IgM syndrome
C)X-linked lymphoproliferative syndrome
D)X-linked SCID
E)X-linked Wiskott-Aldrich syndrome.

Question 49

Deficiencies in antibody production can be due to a variety of underlying genetic defects.Name two immunodeficiency diseases,other than the severe combined immunodeficiencies,in which a defect in antibody production is the cause of the disease,and for which the underlying genetic defect is known.For each disease,say (i)how antibody production is affected,and (ii)what the underlying defect is and why it has this effect.
B.What is the main clinical manifestation of immunodeficiency diseases in which antibody production is defective but cell-mediated immune responses are intact?

Question 50

_____ results in defective phagocytic processes causing chronic bacterial infections.(Select all that apply.)

A)Chédiak-Higashi syndrome
B)Wiskott-Aldrich syndrome
C)myeloperoxidase deficiency
D)X-linked agammaglobulinemia (XLA)
E)chronic granulomatous disease (CGD).

Question 51

Christiana Carter had no obvious problems until she was 18 months old,when she stopped gaining weight,her appetite became poor,and she had recurrent episodes of diarrhea.At 24 months,Christiana developed a cough with pulmonary infiltrates unresponsive to treatment with the antibiotics clarithromycin and trimethoprim/sulfamethoxazole.Within 3 months,she developed lymphadenopathy,hepatosplenomegaly,and fevers.A computed tomography scan revealed enlarged mesenteric and para-aortic lymph nodes.A biopsy of an enlarged axillary lymph node revealed acid-fast bacilli,and cultures from the lymph node and blood grew Mycobacterium fortuitum.HIV was ruled out after negative tests by ELISA and PCR.Serologic testing for tetanus antitoxoid antibody showed a normal post-vaccination level.Christiana's peripheral blood mononuclear cells (PBMCs)were cultured with interferon-γ plus lipopolysaccharide with no significant increase in TNF-α production.A variety of broad-spectrum and anti-mycobacterial antibiotics were administered,lowering the fever,and over the course of the next 2 months Christiana began to gain weight but continued to show signs of persistent infection.Which of the following is the most likely explanation for these clinical findings?
a.leukocyte adhesion deficiency
b.chronic granulomatous disease
c.interferon-γ receptor deficiency
d.X-linked agammaglobulinemia
e.severe combined immune deficiency.

Question 52

Explain why women who show no disease symptoms themselves can pass on some heritable diseases to their sons,whereas their daughters seem to be unaffected.Would a disease with this pattern of inheritance be caused by a recessive or a dominant allele?

Question 53

_____ participates in the T-cell cytoskeletal reorganization required for T-cell cytokine production and cell-mediated interactions.

A)adenosine deaminase (ADA)
B)purine nucleotide phosphorylase (PNP)
C)Wiskott-Aldrich syndrome protein (WASP)
D)myeloperoxidase
E)Bruton's tyrosine kinase (Btk).

Question 54

Why does it benefit the African trypanosome (T.brucei)to maintain more than 1000 genes encoding surface glycoproteins,when only one of these glycoproteins is expressed on the surface of the parasite at any given time?

Question 55

Which antigens are most important in the immune response to the influenza virus?
B.Explain the difference between antigenic drift and antigenic shift in the influenza virus.
C.Which is most likely to lead to a major worldwide pandemic?
D.What is the role of the phenomenon of 'original antigenic sin' in immunity to this virus?

Question 56

Explain why HIV-infected individuals develop resistance more quickly to protease inhibitors than to inhibitors of reverse transcriptase.

Question 57

What would you predict might happen to the course of the HIV infection in a person who developed toxic shock syndrome while in the latent phase of HIV? Explain your answer.
ANSWERS

Question 58

Reverse transcriptase is a _____ encoded by _____.

A)DNA-dependent DNA polymerase; HIV
B)DNA-dependent DNA polymerase; influenza virus
C)RNA-dependent DNA polymerase; HIV
D)RNA-dependent DNA polymerase; influenza virus
E)RNA-dependent RNA polymerase; HIV.

Question 59

The pol gene of HIV produces all of the following except _____.

A)integrase
B)protease
C)matrix protein
D)reverse transcriptase.

Question 60

Explain the mechanism by which human immunodeficiency virus (HIV)enters a host cell.
B.Explain the cellular tropism of HIV,discussing the difference between macrophage-tropic and lymphocyte-tropic HIV.
C.Some people seem to be resistant to HIV infection because a primary infection cannot be established in macrophages.What is the reason for this?

Question 61

For infectious HIV virions to be made,the infected cell must _____.(Select all that apply.)

A)be CD4-positive
B)express low levels of CCR5
C)express functional NFκB
D)be latent
E)be polyreactive.

Question 62

Preferred viral targets for HIV therapy include (select all that apply):

A)reverse transcriptase
B)matrix protein
C)gp120
D)CD4
E)protease.

Question 63

In reference to column B in Question 13-70,which of the protein products are present in the virion? (Select all that apply.)

Question 64

What does the term seroconversion mean in relation to an HIV infection?
B.What relationship does seroconversion have to the time course of an HIV infection?

Question 65

A patient is diagnosed with AIDS when CD4 T-cell counts _____.

A)rise markedly after T-cell activation
B)fall below the CD8 T-cell count
C)fall below 1000 cells/ $\mu$ l
D)fall below 500 cells/ $\mu$ l
E)fall below 200 cells/ $\mu$ l.

Question 66

Which property of HIV renders the virus difficult to eradicate by the body's immune defenses and also limits the efficacy of drug therapies?

Question 67

During infection with HIV,a person is said to undergo seroconversion when _____.

A)HIV variants convert from macrophage-tropic to lymphocyte-tropic late in infection
B)anti-HIV antibodies are detectable in their blood serum
C)cellular transcription favors the production of HIV-encoded RNA
D)HIV is transferred from an infected person to an uninfected recipient
E)the initial phase of infection is followed by clinical latency.

Question 68

Which of the following statements about human immunodeficiency virus (HIV)are correct? (Select all that apply.)

A)HIV has a DNA genome.
B)HIV must synthesize reverse transcriptase immediately after infecting a cell.
C)HIV infects cells expressing CD4.
D)HIV requires the CXCR4 co-receptor for internalization by T cells.
E) is a transcription factor that facilitates the transcription of proviral RNA.

Question 69

Explain the difference between (A)elite controllers and (B)elite neutralizers.

Question 70

Which of the following is required for fusion of the human immunodeficiency viral envelope with the host cell membrane and subsequent internalization?

A)reverse transcriptase
B)gp120
C)gp41
D)integrase
E)protease.