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Summer Immuno Lecture 13

1.

A child has severe recurrent viral and fungal infections because thymic development failed. Which diagnosis best fits?

A. Wiskott-Aldrich syndrome

B. Hyper-IgM syndrome

C. DiGeorge syndrome

D. Canale-Smith syndrome

C. DiGeorge syndrome

2.

In DiGeorge syndrome, absent thymic tissue most directly impairs development of which organ?

A. Thymus

B. Spleen

C. Bone marrow

D. Lymph node

A. Thymus

3.

A patient with DiGeorge syndrome has profound cellular immune dysfunction. Which cell type is primarily affected?

A. B cells

B. Neutrophils

C. Macrophages

D. T cells

D. T cells

4.

The life-threatening infections in DiGeorge syndrome are mainly due to loss of which immune function?

A. Antibody secretion

B. T-cell function

C. Complement activation

D. Neutrophil migration

B. T-cell function

5.

Which sequence correctly lists the major phases of HIV infection?

A. Acute, latent, recovered

B. Acute, chronic, profound immunosuppression

C. Chronic, acute, latent

D. Prodrome, remission, recovery

B. Acute, chronic, profound immunosuppression

6.

After HIV enters a target cell, which enzyme copies viral RNA into DNA?

A. DNA polymerase

B. RNA primase

C. Reverse transcriptase

D. RAG recombinase

C. Reverse transcriptase

7.

Reverse transcriptase converts HIV genetic material into which product?

A. cDNA

B. mRNA

C. rRNA

D. tRNA

A. cDNA

8.

After reverse transcription, which event allows HIV DNA to persist inside the host genome?

A. Capsid degradation

B. Ribosomal binding

C. Antibody neutralization

D. Insertion into host DNA

D. Insertion into host DNA

9.

Once HIV DNA is inserted into host DNA and remains inactive, which effector cells fail to detect it?

A. B cells

B. NK cells

C. CTLs

D. Neutrophils

C. CTLs

10.

A patient is born with nonfunctional CD40L. Which co-stimulatory pathway is directly defective?

A. CD28-B7

B. CD40-CD40L

C. Fas-FasL

D. IgE-Fc receptor

B. CD40-CD40L

11.

Loss of functional CD40 or CD40L most directly prevents which immune response?

A. T-dependent antibody response

B. NK-cell cytotoxicity

C. Neutrophil oxidative burst

D. Complement membrane attack

A. T-dependent antibody response

12.

A patient with defective CD40 signaling has impaired germinal-center function. Which two processes are compromised?

Class switching and hypermutation

13.

Without functional CD40/CD40L signaling, antibody production is biased toward which class?

IgM

14.

Which immunodeficiency syndrome eliminates both major adaptive lymphocyte arms?

SCID

15.

Severe combined immunodeficiency involves dysfunction of which lymphocyte groups?

B and T cells

16.

A patient with a congenital C3 defect has lymph nodes lacking which structure?

____ ____

Germinal centers

17.

A C3-deficient patient lacks germinal centers. Which antibody class would B cells mainly produce?

A. IgM

18.

Initial HIV transmission commonly begins after viral penetration through which barrier?

A. Respiratory epithelium

B. Keratinized skin

C. Gastric mucosa

D. Rectal or vaginal mucosa

D. Rectal or vaginal mucosa

19.

After crossing mucosal surfaces, HIV initially infects which target cell population?

A. B cells

B. Neutrophils

C. T cells

D. Eosinophils

C. T cells

20.

Once inside T cells, HIV replicates by taking over which resource?

A. Complement proteins

B. Host machinery

C. Granule enzymes

D. Antibody genes

B. Host machinery

21.

During acute HIV infection, viral replication across the body does what?

A. Stops immediately

B. Remains localized

C. Clears completely

D. Multiplies systemically

D. Multiplies systemically

22.

During acute HIV infection, viral levels typically peak at approximately what time?

A. 3-4 weeks

B. 2-3 days

C. 6-8 months

D. 1-2 years

A. 3-4 weeks

23.

During the chronic phase of HIV infection, what happens to viral levels?

A. Disappear completely

B. Peak immediately

C. Decline but persist

D. Remain undetectable

C. Decline but persist

24.

As HIV progresses toward profound immunosuppression, what ultimately explains susceptibility to fatal infections?

Loss of ____ cells

Loss of T cells

25.

HIV-1 stores its genetic information in which nucleic acid form?

RNA

26.

Why can killer T cells fail to detect HIV-infected cells during latency?

A. HIV destroys antibodies

B. HIV blocks all cytokines

C. HIV exits immediately

D. HIV remains hidden intracellularly

D. HIV remains hidden intracellularly

27.

A newly infected patient asks whether HIV is detected immediately. Which feature explains delayed immune recognition?

A. Acute sterilization

B. Latent cellular buildup

C. Permanent antibody absence

D. Immediate viral clearance

B. Latent cellular buildup

28.

During the latent period of HIV, infected cells mainly serve as what?

A. Complement reservoirs

B. Reactivatable viral reservoir

C. Neutrophil traps

D. IgE-producing cells

B. Reactivatable viral reservoir

29.

Each HIV replication cycle introduces mutations. What is the immune consequence?

A. Easier T-cell recognition

B. Faster complement fixation

C. Reduced viral diversity

D. Harder immune recognition

D. Harder immune recognition

30.

High mutation rates help HIV maintain which advantage?

A. Immune escape

B. Antibody deletion

C. Eosinophil recruitment

D. Mast-cell activation

A. Immune escape

31.

Which set contains the major HIV-1 target cells?

A. B cells, eosinophils, neutrophils

B. NK cells, basophils, mast cells

C. Helper T cells, macrophages, dendritic cells

D. Platelets, fibroblasts, keratinocytes

C. Helper T cells, macrophages, dendritic cells

32.

HIV infection of macrophages and dendritic cells is especially harmful because these cells normally perform which role?

A. Kill helminths directly

B. Produce thyroid hormone

C. Form epithelial barriers

D. Activate killer T cells

D. Activate killer T cells

33.

One reason AIDS is deadly is that HIV can persist in which state?

A. Latent phase

B. Spore phase

C. Germinal phase

D. Vegetative phase

A. Latent phase

34.

HIV spreads efficiently because it hijacks which system?

A. Endocrine system

B. Immune system

C. Skeletal system

D. Digestive system

B. Immune system

35.

Untreated HIV-1 infection commonly leads to death within approximately how long?

A. 6 months

B. 2 years

C. 50 years

D. 10 years

D. 10 years

36.

People with AIDS are treated with which medication class?

A. Antihistamines

B. Antiretrovirals

C. Glucocorticoids

D. Antifungals

B. Antiretrovirals

37.

Some patients naturally control HIV-1 without typical progression. What are they called?

A. Elite controllers

B. Latent carriers

C. Viral amplifiers

D. Seronegative hosts

A. Elite controllers

38.

In elite controllers, pattern-recognition receptor signaling increases secretion of which two antiviral cytokines?

IFN-alpha and IFN-beta

39.

IFN-alpha and IFN-beta help elite controllers mainly by blocking which viral process?

A. Viral entry

B. Antibody production

C. Antigen presentation

D. Viral replication

D. Viral replication

40.

Some elite controllers have stronger MHC I molecules. Which immune response improves?

A. Faster B-cell switching

B. Stronger IgE binding

C. Faster killer T activation

D. Increased eosinophil survival

C. Faster killer T activation

41.

Better MHC I presentation in HIV elite controllers most directly activates which cell type?

Killer T cells

42.

Which feature best explains why HIV is difficult to eliminate after initial infection?

A. Fixed surface antigens

B. No cellular reservoir

C. Immediate immune clearance

D. Latent reactivatable reservoir

D. Latent reactivatable reservoir

43.

A virus infects APCs needed for cytotoxic T-cell activation. Which HIV target cell group explains this? A. Eosinophils and basophils B. Macrophages and dendritic cells C. Plasma cells and B cells D. Keratinocytes and fibroblasts

B. Macrophages and dendritic cells

44.

A patient’s HIV mutates repeatedly as it replicates. Which outcome best follows?

A. Antigenic variation

B. Thymic regeneration

C. IgE blockade

D. Fas correction

A. Antigenic variation

45.

Which combined features make AIDS especially deadly?

A. Low mutation, rapid clearance

B. IgE binding, mast activation

C. Latency, mutation, APC infection

D. Spore formation, toxin release

C. Latency, mutation, APC infection

46.

Immune weakness can result from mutation of how many genes?

One gene

47.

Compared with genetic immunodeficiencies, which category affects millions of people?

_______ immunodeficiencies

Acquired immunodeficiencies

48.

Genetic immunodeficiencies are best described as which pattern?

A. Rare disorders

B. Universal disorders

C. Acquired disorders

D. Infectious disorders

A. Rare disorders

49.

Which virus is most intensely studied as the cause of AIDS?

HIV-1

50.

The abbreviation HIV-1 refers to which virus?

A. Human T-cell virus one

B. Human immunodeficiency virus one

C. Herpes immunodeficiency virus one

D. Host integration virus one

B. Human immunodeficiency virus one

51.

During acute HIV infection, the dramatic rise in total circulating virus is called what?

Viral _____

Viral load

52.

After acute HIV peaks, viral load decreases mainly because which cells begin working?

A. Virus-specific CTLs

B. Memory B cells

C. Follicular dendritic cells

D. Tissue mast cells

A. Virus-specific CTLs

53.

Many viral infections fully clear after the acute phase. What is this clearance called?

_____

Sterilization

54.

Unlike many viruses, full HIV-1 infection enters which long-term phase after acute infection?

A. Chronic phase

B. Germinal phase

C. Vegetative phase

D. Allergic phase

A. Chronic phase

55.

During chronic HIV infection, which immune populations initially remain high?

_____ and _____ cells

CTLs and Th cells

56.

During chronic HIV infection, Th-cell numbers slowly decrease because HIV does what?

_____ them

Kills them

57.

In chronic HIV, CTLs eventually decline because they lose help from which cells?

_____ cells

Th cells

58.

Late in untreated HIV, CTL decline causes which virologic change?

Viral ____ rises

Viral load rises

59.

Profound immunosuppression in AIDS most directly predisposes to which fatal complication?

A. Seasonal allergy

B. Autoimmune arthritis

C. Opportunistic infection

D. Contact dermatitis

C. Opportunistic infection

60.

HIV can initiate latent infection within approximately what time after exposure?

A. 24 hours

B. 3-4 weeks

C. 6 months

D. 5-10 days

D. 5-10 days

61.

Latent HIV reservoirs may form before full activation of which system?

A. Innate immune system

B. Adaptive immune system

C. Complement system

D. Coagulation system

B. Adaptive immune system

62.

Why does HIV latency form especially early relative to adaptive immunity?

A. Antibodies appear immediately

B. CTLs mature prenatally

C. Adaptation takes about one week

D. Neutrophils suppress latency

C. Adaptation takes about one week

63.

HIV reverse transcriptase is especially dangerous because it is highly what?

____-prone

Error-prone

64.

The error-prone nature of HIV reverse transcriptase produces which viral consequence?

High _____ rate

D. High mutation rate

65.

HIV escape mutants can arise after approximately how long?

A. 3-4 weeks

B. 10 days

C. 2 years

D. 10 years

B. 10 days

66.

Once HIV escape mutants arise, original CTLs usually fail to do what?

A. Produce antibody

B. Enter lymph nodes

C. Recognize them

D. Bind complement

C. Recognize them

67.

Which molecule functions as HIV-1’s docking protein? _____

CD4

68.

By infecting macrophages and dendritic cells, HIV damages cells needed for which process?

A. IgE crosslinking

B. CTL activation

C. Keratinocyte growth

D. Fas signaling

B. CTL activation

69.

HIV-infected immune cells can carry virus from tissues to which site?

A. Bone marrow

B. Thymic cortex

C. Splenic red pulp

D. Lymph nodes

D. Lymph nodes

70.

Within lymph nodes, HIV can undergo which change?

Faster ________

Faster proliferation

71.

In lymph nodes, HIV may be coated by antibodies or which other system?

A. Coagulation

B. Kallikrein

C. Complement

D. Fibrinolysis

C. Complement

72.

Opsonized HIV in lymph nodes can become trapped on which stromal immune cell?

A. Macrophages

B. Follicular dendritic cells

C. Mast cells

D. Neutrophils

B. Follicular dendritic cells

73.

ART improves survival but does not do what?

A. Eliminate HIV

B. Block replication

C. Target viral enzymes

D. Slow progression

A. Eliminate HIV

74.

ART works mainly by targeting components of which process?

A. Antibody class switching

B. Complement activation

C. Viral replication cycle

D. T-cell thymic selection

C. Viral replication cycle

75.

The main clinical benefit of ART is best described how?

A. Sterilizes latent reservoirs

B. Lengthens patient survival

C. Restores thymus completely

D. Prevents all cancers

B. Lengthens patient survival

76.

Patients on ART have increased risk of cancer and which neurologic complication?

_____ disorders

Cognitive disorders

77.

_____-term ART-treated HIV patients have increased risk affecting kidneys, liver, bone, and the heart.

long

78.

Average lifespan on ART is approximately how much shorter than uninfected individuals?

A. 5 years

B. 10 years

C. 15 years

D. 20 years

D. 20 years

79.

Approximately what fraction of HIV-infected individuals are elite controllers?

A. 3%

B. 0.3%

C. 10%

D. 30%

B. 0.3%

80.

Some elite controllers can control HIV infection for as long as what duration?

A. 30 years

B. 10 days

C. 3-4 weeks

D. 5-10 days

A. 30 years

81.

In some elite controllers, CTLs are described as unusually what?

A. Suppressed

B. Vicious

C. Latent

D. Opsonized

B. Vicious