WorksheetsLearning Outcomes
Total questions: 88
Worksheet time: 44mins
Which mechanism best explains influenza antigenic drift and its effect on immunity?
Point mutations accumulate in HA or NA
Genome reassortment between different strains
Gene conversion among surface glycoproteins
Latent infection with periodic reactivation
Trypanosomes evade host antibodies primarily through which process?
Secretion of SSLP7 to block opsonization
Latency in sensory neurons like HSV-1
Antigenic variation via VSG gene conversion
Integrating RNA genome into host DNA
Herpesvirus latency is characterized by which feature in HSV-1 infection?
Viral genome persists in neurons with minimal gene expression
Continuous lytic replication in epithelial cells
Integration of viral RNA into host chromosomes
Formation of immune complexes in circulation
Which statement best describes bacterial immune subversion strategies?
Modifying vesicle trafficking to resist killing
Surviving within host phagolysosomes
Undergoing antigenic shift via genome reassortment
Escaping into cytosol to avoid vesicles
Staphylococcus aureus uses superantigens to achieve which outcome?
Massive, non-specific T cell activation and immune dysregulation
Targeted killing of infected macrophages by CTLs
Enhanced phagocytosis through opsonin binding
Blocking reverse transcriptase during replication
Which pairing correctly distinguishes primary from secondary immunodeficiencies?
Primary: autoantibodies; Secondary: inborn enzyme deficiencies
Primary: environmental exposures; Secondary: chromosomal deletions
Primary: acquired infections; Secondary: inherited mutations
Primary: congenital genetic defects; Secondary: acquired conditions
Match the HIV component to its role in cell entry and replication.
gp41 mediates membrane fusion
p64 capsid binds integrase during entry
gp120 binds CD4 and co-receptors
Reverse transcriptase copies RNA to DNA
Which sequence correctly outlines the three phases of HIV infection?
Latency in neurons, lytic reactivation, immune resolution
Primary immunodeficiency, secondary immunodeficiency, recovery
AIDS stage, acute seroconversion, convalescent phase
Acute viremia, clinical latency, AIDS-defining immunodeficiency
Why does antiretroviral therapy control HIV but does not cure it?
HIV lacks genetic variation to escape therapy
Drugs cannot inhibit reverse transcriptase at all
Antibodies immediately eliminate all infected cells
Latent reservoirs persist despite suppressed replication
Which features of HIV challenge vaccine development yet motivate broadly neutralizing antibodies?
Obligate latency in sensory neurons
Rapid antigenic variation of Env
High envelope glycan shielding
Conserved receptor-binding sites on gp120
Which statement best distinguishes innate from adaptive immunity in early infection control?
Adaptive acts quickly to limit infection
Adaptive does not clear infection at all
Innate acts quickly to limit infection
Innate responds slowly to clear infection
A pathogen that becomes more competitive under host immune pressure is most likely to show which outcome?
Greater success at causing disease
Immediate eradication by innate cells
Reduced transmission between hosts
Permanent inability to infect humans
Select the mechanisms that directly enable pathogens to escape or subvert host immunity.
Enhanced nutrient acquisition only
Hiding through latency in host cells
Gene conversion creating new variants
Genetic variation in surface antigens
Which description best captures the primary role of the immune system in host defense?
Protect and defend against pathogens
Limit competition among microbes
Promote pathogen evolution and spread
Neutralize only adaptive responses
A virus remains dormant within neurons for years and periodically reactivates. Which immune evasion strategy is illustrated?
Genetic variation of antigens
Gene conversion of loci
Hiding through latency
Subversion of complement
Gene conversion benefits pathogens primarily by
Increasing host cell apoptosis rate
Generating antigenic diversity rapidly
Eliminating adaptive memory entirely
Blocking innate cytokine secretion
Which pair correctly matches immunity arm with typical timing and outcome?
Adaptive: quick, limits infection
Adaptive: absent, clears infection
Innate: slow, clears infection
Innate: quick, limits infection
Subversion as an immune evasion mechanism most likely involves
Eliminating pathogens’ own antigens
Exclusive reliance on genetic drift
Only passive dormancy without change
Manipulating host immune signaling
Which feature of influenza replication most directly leads to antigenic drift?
RNA-dependent RNA polymerase errors
Segmented genome reassortment events
Host cell reverse transcriptase editing
DNA polymerase proofreading fidelity
Hemagglutinin and neuraminidase are best described as which type of viral components?
Envelope glycoprotein spikes
Matrix-associated ion channels
RNA polymerase subunits
Capsid-forming structural proteins
Which statement explains why previously-made antibodies may fail after antigenic drift?
Neuraminidase removes all antibodies
Antibodies degrade rapidly in serum
Epitopes on H or N are altered
Memory B cells stop proliferating
Antigenic drift typically results in which epidemiologic pattern?
Global pandemics with very high mortality
Eradication due to cross-immunity
Relatively mild, limited outbreaks
Localized zoonoses without human cases
During infection, small mutations in hemagglutinin most likely affect which viral process?
Binding to host cell receptors
Genome packaging into nucleocapsid
Synthesis of polymerase subunits
Assembly of the M2 ion channel
Which pair correctly matches influenza proteins with roles shown in the diagram?
Hemagglutinin: host-cell binding
Neuraminidase: virion release
Matrix M1: RNA replication
Transcriptase complex: RNA synthesis
Nucleoprotein NP: encapsidates ssRNA
In the illustrated sequence, why does virus V* infect person P despite prior exposure to virus V?
Virus V* carries more genomic segments
Mutated hemagglutinin evades neutralizing antibodies
Neuraminidase destroys mucosal barriers
Person P lacks T cell memory entirely
Which mechanism distinguishes antigenic drift from antigenic shift?
Horizontal gene transfer in bacteria
Reassortment between different viruses
RNA editing by host ADAR enzymes
Point mutations within H or N
Which statement about influenza RNA-dependent RNA polymerase is accurate?
Replicates DNA as a template
High proofreading reduces mutations
Lacks proofreading, causing errors
Integrates into host genome stably
Which outcomes are plausible after minor antigenic changes in H or N?
Partial protection in some individuals
Complete loss of all immunity globally
Immediate emergence of a pandemic
Subgroups with differing immunity levels
Which component does neuraminidase primarily facilitate during viral life cycle?
Packaging of RNA segments
Release of progeny virions
Fusion of envelope to endosome
Attachment to sialic acid receptors
Which statement best summarizes antigenic drift in influenza?
Acquisition of host genes increases virulence
Silent mutations with no phenotypic effect
Incremental mutations alter antigenic epitopes
Large genomic rearrangements create new subtypes
Which statement best describes antigenic shift in influenza A?
Minor glycoprotein tweaks within one lineage
Host immune memory boosting after vaccination
Rare reassortment creating a recombinant strain
Gradual point mutations over many seasons
Antigenic shift most commonly involves which influenza type?
Influenza A strains infecting multiple species
Influenza B strains restricted to humans
Influenza C strains causing mild colds
Universal influenza strains across all species
What necessary event enables antigenic shift to occur?
Environmental temperature abruptly drops
Two different influenza A strains coinfect one host
Host receives a mismatched seasonal vaccine
Single virus persists in a chronic carrier
Why can antigenic shift lead to pandemics in humans?
Population immunity recognizes conserved neuraminidase
Pre-existing antibodies neutralize the variant quickly
Transmission is limited to nonhuman host reservoirs
Most people lack antibodies to the new hemagglutinin
Select all outcomes that can result from antigenic shift.
Formation of recombinant influenza viruses
Immediate sterilizing immunity in exposed hosts
Global pandemics among humans
Epidemics in specific animal species
Which scenario illustrates antigenic shift in the diagram?
Avian cell resisting human strain entry
Human cell infected by a single human strain
Pig coinfected with human and avian strains
Human antibodies blocking a familiar hemagglutinin
In the middle panel, what molecular change is highlighted?
Loss of viral RNA segments during budding
Neutralization of virus by cross-reactive antibodies
Recombination producing a new hemagglutinin variant
Integration of influenza genome into host DNA
In the right panel, why are humans vulnerable to the new virus?
Innate barriers prevent initial colonization
T cells rapidly clear the recombinant strain
Antibodies overly bind conserved nucleoprotein
Antibodies fail to recognize the new hemagglutinin
Which mechanism allows trypanosomes to change their variable surface glycoprotein (VSG) and escape host antibodies?
Antigenic shift via reassortment
Phase variation through promoter flipping
Gene conversion replacing expressed VSG
Somatic hypermutation in parasite B cells
Trypanosoma brucei primarily causes which human disease?
Chagas disease in South America
African sleeping sickness in Africa
Malaria in tropical regions
Leishmaniasis in Middle East
What best describes the trypanosome surface during infection?
Single dominant VSG covering the parasite
Multiple glycoproteins expressed simultaneously
Lipid-only membrane without proteins
Alternating VSG and flagellin layers
Which statement accurately explains the cycle leading to chronic infection in trypanosomiasis?
Parasites stop replicating to avoid immunity
Host T cells destroy every parasite rapidly
Minority VSG clones expand after clearance
Antibodies eliminate all variants permanently
Select all outcomes directly linked to repeated VSG switching by gene conversion.
Resolution without inflammation
Waves of parasitemia over weeks
Reduced parasite replication rates
Formation of immune complexes
Where are many inactive VSG genes located relative to expression capacity?
Only one expression site is available
Multiple expression sites across genome
All VSGs expressed constitutively
No dedicated expression site exists
During an antibody response to a dominant VSG, what happens next in the parasite population?
Upregulates the same VSG indefinitely
Downregulates all surface proteins
Switches to a novel VSG via gene conversion
Integrates host immunoglobulin genes
Which pathophysiologic consequence is associated with chronic trypanosome infection?
Viral reactivation in B cells
Autoimmune hemolytic anemia predominance
Eosinophil-mediated anaphylaxis episodes
Immune complex deposition causing inflammation
Which pair correctly matches component and role in trypanosome immune evasion?
Vector insect—kills parasites in bloodstream
VSG genes—encode variable surface coat
Flagellum—secretes neutralizing antibodies
Mitochondrion—performs somatic recombination
Which statement best describes the typical course of herpesvirus infection in humans?
Initial lytic phase followed by latency
Immediate latency without cell death
Alternating latency and chronic viremia
Persistent replication without latency
HHV-1 primarily infects which cell type during the lytic phase on the face?
Neurons of trigeminal ganglion
Mucosal epithelial cells
Monocytes in blood
B cells in lymph nodes
Where does HHV-1 establish latency after primary infection of facial skin?
Macrophages of oral mucosa
Neurons in trigeminal ganglion
Epithelial cells of the lips
Dermal fibroblasts of the cheek
Which sequence of events is most accurate for HHV-1 pathogenesis on the face?
Simultaneous lysis and latency in neurons
Neuronal lysis then epithelial latency
Epithelial lysis then neuronal latency
Latency in neurons then epithelial lysis
Which herpesvirus is associated with chickenpox and shingles?
HHV-4 Epstein–Barr virus
HHV-8 Kaposi’s sarcoma virus
HHV-5 Cytomegalovirus
HHV-3 Varicella-zoster virus
Which is a common route of spread for HHV-1?
Transfusion and tissue transplant
Respiratory droplet alone
Close oral and sexual contact
Contact with breast milk
Which pair correctly matches virus and typical latency cell type?
EBV — B cells
HHV-8 — B cells
CMV — monocytes
Roseolovirus — epithelial cells
HHV-1 — neurons
During reactivation of HHV-1, which process allows recurrence at the same facial site?
Virus travels along sensory axons
Latent genome replicates in neurons
Virions bud from epithelial Golgi
Macrophages release latent virions
Which clinical outcome is typical of HHV-1 lytic infection of facial epithelium?
Blisters due to epithelial cell death
Pustules with systemic viremia
Necrotizing fasciitis on cheeks
Diffuse rash without blisters
Which statement about the herpesvirus family is accurate?
Comprises exactly six human viruses
Causes severe disease in all infections
Comprises eight viruses infecting different cells
Infects only neuronal tissues
Which strategy allows Mycobacterium tuberculosis to avoid immune killing inside macrophages?
Persisting in extracellular biofilm near macrophages
Remaining inside vesicular system of macrophages
Rapidly escaping to bloodstream for dissemination
Forming spores that resist lysosomal enzymes
Listeria monocytogenes evades phagocytic destruction primarily by doing what?
Triggering apoptosis of macrophages immediately
Blocking MHC I presentation on infected cells
Escaping the phagosome and replicating in cytoplasm
Inhibiting complement activation at the surface
Toxoplasma gondii survives intracellularly by creating which structure?
A capsule that neutralizes antibodies
A flagellated vacuole that enhances motility
A biofilm that coats host organelles
An impenetrable vesicle that avoids fusion
Treponema pallidum reduces immune detection by:
Secreting proteases that cleave IgA
Producing cytolysins that kill neutrophils
Remaining dormant in bone marrow niches
Coating itself in human proteins
Which organisms are specifically noted for secreting superantigens?
Staphylococcus species
Streptococcus species
Mycobacterium tuberculosis
Listeria monocytogenes
Treponema pallidum
Superantigens characteristically cause:
Targeted activation of a single T cell clone
Broad activation of several T cell clones
Selective depletion of neutrophils only
Suppression of cytokine secretion globally
Approximately what fraction of CD4 T cell clones can be activated by superantigens?
Exactly 50% of clones
About 2–20% of clones
Nearly 100% of clones
Less than 1% of clones
Excessive production of which cytokines is linked to superantigen exposure?
IL-2
IFN-γ
TNF-α
IL-10
TGF-β
Combined, Staphylococcus and Streptococcus produce how many different superantigens?
Fewer than five distinct toxins
Exactly one universal superantigen
About ten distinct toxins
More than thirty distinct superantigens
Which pairing best describes a superantigen binding interaction that can lead to full activation of CD4 T cells?
Binding CD28 while blocking B7:CD28
Binding MHC class II peptide groove directly
Docking only to co-receptor CD4
Cross-linking MHC class II and TCR Vβ
Engaging TCR α chain exclusively
Staphylococcus aureus toxic shock syndrome toxin 1 (TSST-1) preferentially binds which TCR component?
TCR β chains from Vβ2 gene
TCR α chains from Vα7 gene
CD28 cytoplasmic tail region
Co-receptor CD4 D1 domain
CD3ζ chains near ITAM motifs
Enterotoxin B (SEB) from Staphylococcus aureus engages TCR β chains encoded by which set of Vβ genes?
Vβ1.1, 3.2, 6.4, 15.1
Vβ2 exclusively
Dβ1 locus primarily
Jβ2 segments mainly
Vα3.1 and Vα8.2 only
Which statement best explains how superantigens substitute for normal antigen recognition?
They require B7:CD28 costimulation blockade
They form stable peptide-MHC complexes
They bind outside peptide groove to Vβ
They mimic peptide-MHC anchoring residues
They recruit CD4 to stabilize MHC class I
Which combination of receptors can be bridged by certain superantigens to drive CD4 T-cell activation?
B7 and CD28
TCR and CD28
MHC class II and TCR
CD4 and MHC class I
FcαRI and IgA
Which feature distinguishes superantigen binding from conventional peptide antigen recognition?
Exclusive binding to TCR Cβ region
Interaction with TCR Vβ framework
Requirement for processed peptides
Restriction by MHC class I molecules
Dependence on TAP transporters
SSLP7 secreted by Staphylococcus aureus binds which host molecules to protect bacteria from phagocytosis?
MHC class II β chain
Complement component C5
CD28 co-stimulatory receptor
FcαRI receptor
IgA Fc region
How does SSLP7 interfere with IgA-mediated phagocytosis?
By degrading IgA heavy chains
By blocking IgA binding to FcαRI
By neutralizing B7:CD28 signaling
By opsonizing bacteria with C3b
By internalizing FcαRI on macrophages
Which scenario depicts the outcome when SSLP7 is present during an IgA response to Staphylococcus aureus?
Macrophages ingest opsonized bacteria efficiently
IgA bridges bacteria to FcαRI for killing
Bacteria evade killing and persist
CD4 T cells undergo anergy induction
Complement MAC forms on bacterial surface
Which statements about superantigen targeting of human TCRs are correct?
All superantigens bind Vα chains exclusively
TSST-1 targets TCR Vβ2 chains
Different superantigens prefer different Vβ families
SEB engages multiple Vβ genes
Superantigen binding is peptide-groove restricted
Which statement best defines an immunodeficiency?
Overproduction of antibodies during infection
Temporary fever triggered by vaccine exposure
Compromised immune function due to component failure
Enhanced immune activation against harmless antigens
Primary immunodeficiencies most commonly arise from which cause?
Long-term exposure to environmental pollutants
Acute infections that deplete lymphocytes
Nutritional deficiencies in early childhood
Inherited genetic mutations affecting immune components
Secondary immunodeficiencies are typically associated with which factor?
Physiologic aging without external exposures
Spontaneous correction of deleterious alleles
Environmental influences that impair immune function
Chromosomal translocations in immune cells
Which scenario exemplifies a secondary immunodeficiency?
A newborn with a mutation in RAG1
An adult on chemotherapy with recurrent infections
A child with X‑linked agammaglobulinemia
A family with autosomal recessive complement defect
Chemotherapy can lead to immunodeficiency primarily by which mechanism?
Selective expansion of memory B cells
Cytotoxic suppression of hematopoietic and immune cells
Activation of complement cascade against pathogens
Induction of thymic hyperplasia and T cell surplus
Which infection is specifically noted as causing secondary immunodeficiency?
Influenza A virus during winter season
Human immunodeficiency virus (HIV) infection
Epstein–Barr virus during mononucleosis
Varicella‑zoster virus after vaccination
In the disease group table, which group focuses on predominantly antibody deficiencies?
Group 2: combined immunodeficiencies with syndromic features
Group 3: predominantly antibody deficiencies
Group 6: defects in intrinsic and innate immunity
Group 8: complement deficiencies
Which disease group lists congenital defects of phagocyte number, function, or both?
Group 1 on cellular and humoral immunity
Group 5 in the classification table
Group 4 with immune dysregulation
Group 7 with autoinflammatory disorders
Which groups in the table explicitly involve complement or innate immunity pathways?
Group 6: defects in intrinsic and innate immunity
Group 1: cellular and humoral immunity
Group 3: predominantly antibody deficiencies
Group 8: complement deficiencies
Which statement correctly contrasts primary versus secondary immunodeficiencies?
Primary affect only antibodies; secondary affect only T cells
Primary are transient; secondary are always lifelong
Primary are genetic in origin; secondary result from environmental factors
Primary arise from environmental toxins; secondary from Mendelian mutations
A patient with autosomal dominant allele causing immune dysregulation most likely maps to which disease group in the table?
Group 7: autoinflammatory disorders
Group 2: combined immunodeficiencies
Group 1: cellular and humoral immunity
Group 4: diseases of immune dysregulation
Which option lists environmental causes of secondary immunodeficiency highlighted in the material?
Inherited X‑linked gene defects
Immunosuppressive drug therapy
Chemotherapy exposure
HIV infection
