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KN-Immunology Block 2 > L13: Evasion of Immune Responses > Flashcards

L13: Evasion of Immune Responses Flashcards

1
Q

What is antigenic variation?

A

alteration of epitopes displayed by a pathogen that make the epitopes unrecognizable by an existing immune response

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2
Q

What is antigenic drift?

A

introduction of point mutations that result in minor alterations of the antigenicity of a particular protein

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3
Q

What is antigenic shift?

A

reassortment of genes that results in major changes in the antigenicity of a given protein

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4
Q

What is latency?

A

a state in the life cycle of some viruses during which they do not replicate and remain “hidden” from the immune system

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5
Q

What is a superantigen?

A

molecules that stimulate a subset of CD4 T cells by simultaneously binding to MHC class II molecules and the B-chain of the TCR; these binding interactions are not specific interactions

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6
Q

What are the 3 ways antigenic variation can occur?

A
  1. presence of many infectious agents. The same species organism can infect the same person multiple times with different serotypes
  2. antigenic drift and shift (influenza)
  3. programmed rearrangement of DNA (example: trypanosomes)
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7
Q

What is a trypanosome?

A

insect-borne protozoa that replicates in extracellular tissue spaces in the body and can cause sleeping sickness.
coated with glycoprotein called (VSG), which they change often to evade immunity
Good example of pathogen DNA rearrangement for evasion

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8
Q

How does herpes simplex virus avoid immune responses?

A

it often enters a latency phase and resides in the sensory neurons by incorporating its genome into the host DNA. It then infects epithelial cells when the time is right

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9
Q

What sort of stimuli cause herpes outbreaks?

A

sunlight, bacterial infection, hormonal changes, stress

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10
Q

Why do sensory neurons remain infected by latent herpes virus?

A
  1. virus is quiescent in the nerve, very few viral peptides available for presentation to CTLs.
  2. neurons have very low levels of MHC class I molecules, making it hard for CTLs to recognize them. (They lack them because they do not regenerate and killing them is permanent)
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11
Q

What is varicella zoster?

A

chicken pox. latent virus. After initial episode, virus remains latent in one or a few dorsal root ganglia and can be reactivated by stress or immunosuppression to spread down the nerve and re-infect the skin. The immune response is a characteristic rash (shingles). This usually only happens once in the lifetime of a patient

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12
Q

What is Epstein-Barr virus (EBV)?

A

causes cold-like symptoms in children, but causes infectious mononucleosis in adolescents and adults. The mononucleosis form infects B cells and they proliferate, leading to T cell activation. Infection controlled by CD8 effector cells that kill infected B cells. Becomes latent by inserting its genome into host DNA. Reactivation rarely causes disease symptoms.

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13
Q

What type of pathogens are most likely to subvert immune responses?

A

viruses

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14
Q

How do viruses frequently subvert the immune response?

A
  1. they capture cellular genes for cytokines or cytokine receptors
  2. synthesize complement-regulatory proteins
  3. inhibit MHC class I molecule synthesis
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15
Q

How does mycobacterium tuberculosis trick the immune system?

A

it is taken up by macrophages, but prevents phagosome-lysosome fusion, enabling it to survive inside the phagocyte

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16
Q

What are listeria monocytogenes?

A

a bacterium that can escape from the phagosome and replicate freely in the cytoplasm of the infected macrophage. It is spread via cell to cell contact and can spend its entire life intracellular. Can be cleared by antigen-specific effector CTLs.

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17
Q

What are toxoplasma gondii?

A

protozoan parasites that can generate their own vesicles following phagocytosis. This vesicle isolates the parasite from the rest of the cell, and prevents presentation of parasite-derived peptides. It remains invisible to the immune system

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18
Q

How do staphylococcal bacteria suppress immune responses?

A

either by forming staph enterotoxins or toxic shock syndrom toxin-1 that act as superantigens

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19
Q

What do superantigens do?

A

they induce massive production of cytokines by CD4 cells that somehow induces a state of immune suppression and sometimes systemic toxicity

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20
Q

Do all antigens that bind to MHC class II bind to the binding groove?

A

no. some can bind elsewhere or cross-link

21
Q

What do superantigens bind to?

A

outer surfaces of both MHC class II molecules and the Vbeta region of the TCR (T cell receptor)

22
Q

Will binding both the MHC class II and TCR of a T cell prompt an antigen-specific immune response?

A

No. Instead it will cause massive production of cytokines by CD4 T cells and cause systemic toxicity and/or suppression of immune responses

23
Q

What is leprosy and what causes it?

A

infection by mycobacterium leprae which either causes suppression of cell-mediated acquired responses, or induces a very potent cell-mediated anti-bacterial response.
Can either be lepromatous leprosy or tuberculoid leprosy

24
Q

What are the two forms of leprosy?

A
  1. lepromatous leprosy

2. tuberculoid leprosy

25
Q

What is lepromatous leprosy?

A

cell-mediated immunity is profoundly depressed, and infection is not controlled. The bacteria is highly infectious and replicates in macrophages. There is hypergammaglobuilnemia, low/absent T cell response and immunosuppresion leaves host in anergic state wehre they cannot respond to any antigens

26
Q

What is tuberculoid leprosy?

A

potent cell-mediated immunity with macrophage activation which controls but does not clear infection. Bacteria is not very infectious and only exist in low levels. Granulomas and local inflammation. Normol serum immunoglobulins and T cell responsiveness to M. leprae.

27
Q

What is thought to cause the different modes of leprosy?

A

ratio of TH1 to TH2 cells and cytokine response.

28
Q

Which form of leprosy is characterized by hypergammaglobulinemia?

A

lepromatous

29
Q

Which form of leprosy is characterized by inactive T cells and an anergic state?

A

lepromatous leprosy

30
Q

What is a chemokine?

A

small cytokines that are involved inthe migration and activation of cells (macrophages and lymphocytes)

31
Q

What is seroconversion?

A

the phase of an immune response when antigen-specific antibody production is 1st detectable

32
Q

What is HIV?

A

a lentivirus (lenti=slow) that infects humans and causes acquired immunodeficiency syndrome (AIDS). Characterized by susceptibility to opportunistic infections and is accompanied by a profound decrease in CD4 T cell numbers

33
Q

What are the most notable neoplasms associated with HIV AIDS?

A

Kaposi’s sarcoma and B cell lymphoma

34
Q

What cells does HIV bind to and how does it do it?

A

Its envelope protein complex binds with high affinity to CD4 molecules, which are found on CD4 cells, macrophages, and dendritic cells. Once bound, it interacts with a co-receptor on the host cell (a chemokine receptor) to gain entry

35
Q

What cell type does HIV significantly lower?

A

CD4 T cels

36
Q

What is the primary immune response to HIV?

A

CD8 T cells become antigen-specific effector CTLs and kill infected CD4 T cells

37
Q

When does seroconversion occur after HIV infection?

A

2-6 weeks after infection

38
Q

When does the asymptomatic phase of HIV begin and how long does it typically last?

A

latency phase begins around the same time as seroconversion (2-6 weeks postinfection) and lasts about 10 years

39
Q

What happens at the beginning of the symptomatic phase?

A

the number of functional circulating CD4 cells gets very low. Characterized by high incidence of opportunistic infections

40
Q

What is always the end result of AIDS?

A

death

41
Q

How does HIV evade immune responses and drug therapies?

A

antigenic variation. HIV uses enzyme reverse transcriptase to transcribe its RNA genome into DNA that can integrate into the host cell DNA. It is very error-prone and introduces numerous point mutations druing every replicative cycle. These result in antigenic changes in the envelope protein to facilitate immune evasion. This also helps it develop resistances to viral protease inhibitors and reverse transcriptase inhibitors.

42
Q

What is zidovudine?

A

AZT, a reverse transcriptase inhibitor that HIV takes several months to develop resistance to

43
Q

What is a serotype?

A

form of a bacterial species that has a different surface antigenic composition. Will evade antigen-specific receptors

44
Q

Does the typical disease syndrome resulting from infection with a genetic drift variant of Flu differ from that caused by a genetic shift variant of Flu?

A

YES. Drift variant would cause milder disease because of the existing memory T cell responses in previously infected people. Only point mutations that mess up antibody response.

Antigenic shift is a total change in expressed products of new strain. Will likely wipe out B cell and T cell response.

45
Q

What neuronal structure does the herpes virus latently stay in?

A

trigeminal ganglion

46
Q

What are the two mechanisms human cytomegaloviruses interfere with?

A

Class I MHC antigen loading and NK cell function

47
Q

What is HIV integrase?

A

(p32)

48
Q

Does reverse transcriptase have proof reading ?

A

no. It has a very high error rate that results in antigenic drift

KN-Immunology Block 2 (8 decks)

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