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PABI 6100 Immunobiology- Exam > Immunity to Infectious Diseases-2 > Flashcards

Immunity to Infectious Diseases-2 Flashcards

1
Q

What are viruses composed of?

A
  • small segments of nucleic acid with a protein/ lipoprotein coat
  • enter host cells through specific cell-surface receptors
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2
Q

What is a feature of viral genome replication?

A
  • virus enters cell > diverts machinery to replicate itself
  • for some viruses, genome replication is error-prone > mutations
    > mutants with survival/ immune evasion strategies can arise
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3
Q

What are the innate immune effectors that eliminate many viruses?

A
  • complement activation
  • antimicrobial peptides
  • recognition of viral PAMPs (dsRNA) by PRRs > PRR signaling > type I interferons (IFN-α/ IFN-β)/ inflammasome assembly/ NK cell activation
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4
Q

What is the antiviral response induced by interferons?

A
  • IFN-α/ IFN-β bind to and dimerize IFNAR
  • this recruits and activates JAK1/ TYK2
  • JAK1/ TYK2 bind and phosphorylate STAT1/ STAT2
  • STAT1/ STAT2 dimerize/ enter nucleus/ stimulate antiviral proteins
    > PKR/ 2’,5-oligo-A-synthetase/ Mx proteins/ IFIT proteins
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5
Q

What are the 4 antiviral IFN-stimulated genes?
> important for inhibiting viral replication

A
  • PKR > binds viral dsRNA/ inhibits activity of elf2α > inhibits translation
  • 2’5’-oligo-A-synthetase > activates RNase L > degrades viral/ cellular mRNA
  • Mx proteins > form ring-like structures > inhibit virus replication
  • IFIT proteins >bind to viral RNA/ elF3 > inhibits translation
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6
Q

What role do antibodies have in viral infections?

A
  • many viruses are neutralized by antibodies
  • antibodies specific for viral surface antigens > block spread/ secondary infection
  • surface IgA/ circulating IgG are most protective > primary response
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7
Q

What are neutralizing antibodies?

A
  • antibodies that bind to key viral structures in a way that interferes with their ability to attach to host cells (prevent attachment)
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8
Q

What antibodies are produced during a primary response when virions are recognized in extracellular spaces?

A
  • surface/ mucosal IgA
  • circulating IgG
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9
Q

What are 4 mechanisms of viral neutralization by antibodies after viral attachment to host cells?

A
  • bind to epitopes that mediate fusion of viral envelope/ plasma membrane > block viral penetration
  • complement-mediated lysis of enveloped virus
  • agglutination of viral particles/ opsonization > Fc/ C3b receptor-mediated phagocytosis of virions
  • some antibodies bound to infected target cells can trigger ADCC by NK cells
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10
Q

What is the #1 mechanism for eliminating viral infections?

A
  • cell-mediated immunity is required once viral genome is integrated into host chromosomal DNA
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11
Q

What are the mechanisms of antiviral cell-mediated immunity?

A
  • both CD8+ Tc/ CD4+ TH1 cells required
  • TH1 cells produce IL-2/ IFN-γ/ TNF-α
    > IFN-γ induces antiviral state in nearby cells/ activates NK cells
    > IL-2 activates CTL precursors/ NK cells
  • TH1 cells license pAPCs for cross-presentation > activate naive CD8+ T cells
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12
Q

What is the timing of virus-specific CTL activity?

A
  • arises within 3-4 days of viral infection
  • peaks by 7-10 days
  • virions usually eliminated in those first 7-10 days
  • virus-specific memory CD8+ T cells > future antiviral protection
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13
Q

What is required for the activation of naive Tc cells by exogenous antigens?

A
  • DC licensing by TH cells
    > DCs internalize/ process/ present antigen to CD4+ TH cells via MHC II (exogenous pathway)
    > activates cells through CD40/ CD40L engagement
  • DC cross-presentation
    > activated TH cells serve as bridge to activate CD8+ CTLs
    > provide IL-2/ license DCs to cross-present internalized antigen via MHC I
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14
Q

What 4 strategies do viruses employ to evade host immune defences?

A
  • evade action of IFNα/ IFNβ
  • inhibit antigen presentation by infected host cells
  • change surface antigens
  • cause immunosuppression
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15
Q

How does EBV evade the immune system?

A
  • produces protein homologous to IL-10 > immunosuppression
  • protein suppresses cytokine production by TH1 cells > inhibits antiviral inflammatory response
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16
Q

What are 2 examples of viruses that inhibit antigen presentation by infected host cells? (to evade host defence mechanisms)

A
  • HSV produces protein that inhibits TAP (ER)
  • adenovirus/ cytomegalovirus > reduce MHC I expression
17
Q

What is the difference in antibody production during primary/ secondary responses to viruses?

A
  • Primary Response- activation of naive B cells > production of antibodies specific to epitopes on pathogen
  • Secondary Response (to variant of pathogen)- reactivation of memory B cells > pathogen eradication
  • Original antigenic sin > presence of preformed antibodies inhibits primary response to pathogen > memory B cells not naive B cells
18
Q

What is original antigenic sin?

A
  • Fc regions of antibodies bound to surface of pathogen bind to FcRs on naive B cells > inhibit them from responding to new epitopes
  • no immune response is mounted to each new epitope during subsequent exposures to pathogen until pathogen expresses a significant # of unique epitopes/ memory cells can no longer eradicate pathogen
19
Q

What does the level of host defence to bacterial infection depend on?

A
  • # of organisms entering and their virulence
  • low inocula/ virulence > phagocytes/ nonspecific innate defenses
  • larger inocula/ greater virulence > antigen-specific adaptive responses
20
Q

What is the main mechanism of immunity to extracellular bacteria?

A
  • mainly humoral immune response > antibodies
  • opsonization > antibodies bind to bacterial surface antigens/ act as opsonins
  • complement activation > C3b opsonin/ MAC/ C3a, C5a anaphylatoxins/ chemotactic factors for neutrophils/ macrophages
  • neutralization > antibody binds to bacterial toxin/ neutralizes it
21
Q

What are the 4 primary steps in most bacterial infections?
- host defence mechanisms act at each of these steps > bacteria have evolved to evade

A
  • attachment to host cells
  • proliferation of bacterium
  • invasion of host tissue
  • toxin-induced damage to host cells (some cases)
22
Q

What are some examples of strategies bacteria have evolved to evade host defence mechanisms?

A
  • inhibition of phagocytosis
  • surviving within phagocytic cells ex) block phagosome/ lysosome fusion
23
Q

What are the 2 main types of parasites?

A
  • Protozoan > unicellular
  • Metozoan > helminths/ worms (multicellular)
24
Q

What are some features of protozoan parasites?

A
  • unicellular eukaryotes
  • many progress through multiple antigenic forms/ locations during life cycle in host > most enter intracellular in at least one life cycle stage
  • in bloodstream/ gut/ interstitial fluid > humoral immunity is most effective; however, these stages are very transient/ evasion strategies
  • in intracellular life stages > cell-mediated immunity required; however, these are short stops in parasite life cycle
25
Q

What is the #1 parasitic cause of death worldwide?
- protozoan parasite

A

Plasmodium > Malaria
- poor degree of immunity to infection (evades immune system)

26
Q

What 4 strategies does Plasmodium (protozoan parasite) have to evade the immune system/ cause malaria?

A
  • changes in surface molecules > continual changes in antigens seen by immune system
  • intracellular phases of life cycle > reduces degree of immune activation/ allows organism to multiple shielded from attack
  • short time circulation in blood at most accessible stage
  • sloughing off its surface antigens > antibodies ineffective
27
Q

Apart from malaria (plasmodium), what are 2 other diseases caused by protozoan parasites?

A
  • African sleeping sickness
    > causative trypanosome protozoans evade immune system > up to 1000 variants of protein coat to outrun immune response
  • Leishmaniasis
    > TH1 response limits pathology/ TH2 response leads to progressive disease
28
Q

What are some features of metazoan parasites (helminths/ worms)?

A
  • exclusively extracellular > too big to enter intracellular
  • poor immune reactivity > do not multiply within host
  • too big for phagocytosis > expulsion is best approach
    > not opsonization/ digestion response
29
Q

What is the immune response to metazoan parasites (helminths/ worms)?

A
  • TH2 response > ILC-2s/ IL-4/ TH2/ IgE
  • IgE > mast cell degranulation/ histamine release > muscle contractions and mucus production > diarrhea/ vomiting/ coughing (expulsion)
30
Q

What controls most fungal infections?

A

Innate immunity
- phagocytosis by neutrophils
- commensal organisms control growth of pathogens
- fungal cell wall PAMPs (6-glucans/ mannans/ chitin) recognized by PRRs > complement activation/ phagocytosis

31
Q

What strategies have fungi evolved to evade innate immune responses?

A
  • produce capsule > block PRR binding
  • fungi-induced expulsion from macrophages after phagocytosis
32
Q

What is an example of a fungus?

A

Cryptococcus neoformans (C. neoformans)

33
Q

What is the difference between primary/ opportunistic virulence?
> fungal infections

A
  • Primary > inherently virulent/ infects healthy hosts
  • Opportunistic > low virulence/ infects immunocompromised hosts
34
Q

What mechanism of adaptive immunity controls fungal pathogens?

A
  • cell-mediated rather than humoral
35
Q

What is the difference between emerging/ re-emerging infectious diseases?

A
  • Emerging > arisen/ increased in human population in past 2 decades
  • Re-Emerging > formerly rare (under control) but have recently begun to resurge
36
Q

What are examples of emerging/ re-emerging infectious diseases?

A
  • Emerging > SARS/ Zika
  • Re-Emerging > Tuberculosis/ Measles/ Whooping cough/ Diptheria
37
Q

Why are there re-emerging infectious diseases?

A
  • development of drug resistance
  • acquisition of new virulence factors
  • environmental changes > enhance transmission rates
  • immunosuppressive conditions > AIDS > tuberculosis
  • human contact with wild animals > ebola
  • laxity in vaccination program adherence > diptheria/ whooping cough/ measles
38
Q

What is the culprit for more than 1/3 of all AIDS-associated fatalities?

A

Tuberculosis

PABI 6100 Immunobiology- Exam (6 decks)

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