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CHAPTER 11
Failures of the Body’s Defenses
Questions
11–1
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.
11–2
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.
11–3
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.
11–4
An epidemic affects _____, whereas a pandemic affects _____.
a. susceptible individuals; immune individuals
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b. immune individuals; susceptible individuals
c. global populations; local populations
d. local populations; global populations.
11–5
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.
11–6
_____ 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.
11–7
Which of the following viruses can cause a persistent infection in the host by establishing
latency? (Select all that apply.)
a. influenza virus
b. herpes simplex virus
c. varicella-zoster
d. Epstein–Barr virus
e. human immunodeficiency virus.
11–8
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.
11–9
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.
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11–10
Which of the following are used by the herpes simplex virus to subvert host immune responses?
(Select all that apply.)
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.
11–11
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.
11–12
Which of the following are characteristic of staphylococcal enterotoxins? (Select all that apply.)
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.
11–13
Using the Table below, match the deficiency disease in column 1 with its specific abnormality in
column 2.
Column 1
Column 2
a. Hereditary angioneurotic edema
1. Thymic aplasia
b. DiGeorge’s syndrome
2. Defective transporter associated
with antigen processing (TAP)
c. X-linked hyper IgM syndrome
3. Defective RAG1 or RAG2
d. Severe combined immunodeficiency
4. Defective C1 inhibitor
e. Bare lymphocyte syndrome (MHC class I)
5. Defective CD40 ligand
f. X-linked agammaglobulinemia
6. Defective Btk tyrosine kinase
g. Leukocyte adhesion deficiency
7. Defective CD18
h. Chronic granulomatous disease
8. Defective NADPH oxidase
11–14
Which of the following statements regarding inherited immunodeficiency diseases is correct?
a. Affected individuals are less susceptible to infection.
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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.
11–15
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.
11–16
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.
11–17
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.
11–18
_____ 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).
11–19
_____ 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)
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d. myeloperoxidase
e. Bruton’s tyrosine kinase (Btk).
11–20
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.
11–21
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).
11–22
Explain why a staphylococcal infection might produce a medical emergency.
11–23
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.
11–24
Explain why it is necessary to match at least some of the HLA allotypes between donor and
recipient in a bone marrow transplant given to remedy SCID.
11–25
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.
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11–26
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. NFB is a transcription factor that facilitates transcription of proviral RNA.
11–27
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.
11–28
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/l.
d. fall below 500 cells/l.
e. fall below 200 cells/l.
11–29
Which of the following is the most likely explanation for an individual who lacks CCR5 as a
result of a homozygous defect in the CCR5 gene becoming infected with HIV?
a. The mutated CCR5 genes reverted to the normal form, rendering macrophages
susceptible to macrophage-tropic HIV variants.
b. The macrophage-tropic HIV variant entered host cells using CD4 alone.
c. The viral nucleic acid alone was taken up by cells, as in cell transformation by bacterial
DNA.
d. The individual had received a transplant of HIV-infected cells expressing normal CCR5.
e. The primary infection involved a lymphocyte-tropic strain of HIV that used CXCR4 as
its co-receptor.
11–30
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.
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11–31
The high degree of mutation in HIV, the accumulation of variant viruses, and the development of
resistance to drug regimes are attributed to
a. antigenic shift
b. gene conversion
c. absence of proofreading capability of reverse transcriptase
d. antigenic variation of variable surface glycoproteins (VSGs)
e. mutation of HIV RNA genome by host-cell RNA polymerase.
11–32
Preferred viral targets for HIV therapy include (select all that apply):
a. reverse transcriptase
b. matrix protein
c. gp120
d. CD4
e. protease.
11–33
Explain why HIV-infected individuals develop resistance more quickly to protease inhibitors
than to inhibitors of reverse transcriptase.
11–34
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.
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Answers
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