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Immunology Spring 2 > Evasion of Immune Responses > Flashcards

Evasion of Immune Responses Flashcards

1
Q

What 3 methods do pathogens use to evade host immune responses?

A

Antigenic variation, latency, and subversion of host responses/molecular mimicry.

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2
Q

What is antigenic variation?

A

Pathogens display new antigens that are not recognized by immune responses formed in response to previous infection.

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3
Q

That type of immune response does antigenic variation allow pathogens to evade?

A

Pre-formed memory immune responses.

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4
Q

How does Streptococcus pneumoniae utilize antigenic variation?

A

Changes its capsular polysaccharide.

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5
Q

How many distinct serotypes does S. pneumoniae have?

A

84.

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6
Q

What is antigenic drift?

A

Viral genome mutates and changes its particular antigen expression thus not recognized by patient first infected with the non-mutated form.

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7
Q

What is antigenic shift?

A

Two or more different strains of a virus combine to form a new recombinant virus. Upon infection, the patient does not recognize the new recombinant form of the virus.

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8
Q

Which is more serious: antigenic drift or shift? Why?

A

Antigenic shift b/c there are no memory T cells that can recognize the new combination of antigens displayed by the recombinant virus. Note: genetic drift variant causes milder disease b/c of the existing memory T cell responses formed form previous infection.

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9
Q

How do trypanosomes utilize antigenic variation?

A

Trypanosomes possess a cassette gene system of VSGs (variant-specific glycoproteins) containing over 1,000 different glycoprotein genes the organism can express. When the immune system forms a response to one gp, trypanosomes change gp expression resulting in cyclic infections. Termed programmed rearrangement.

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10
Q

What is latency?

A

A state adopted by some viruses in which they have entered cells but do not replicate.

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11
Q

In latency, what usually happens to the viral genome?

A

The viral genome is usually integrated into the host cell DNA.

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12
Q

What 2 viruses are prime examples of latency?

A

Herpes virus and varicella zoster virus.

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13
Q

During the latency phase, where does the herpes virus hide?

A

In nerves (particularly in the trigeminal ganglion?).

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14
Q

What triggers reactivation of the herpes virus leading to a recurrent infection?

A

Stress –> usually herpes blister on lips.

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15
Q

Primary infection of varicella zoster virus causes what?

A

Chickenpox.

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16
Q

Reactivation and recurrent infection of varicella zoster virus causes what?

A

Shingles.

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17
Q

What is unique about the recurrent infection of varicella zoster virus?

A

It occurs only on one side of the body and usually follows nerve pattern.

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18
Q

What virus is a primary example of antigenic shift and antigenic drift?

A

Influenza virus: new strains every year.

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19
Q

What are 2 mechanisms by which CMV subverts immune response?

A
  1. Interrupts loading of MHC Class I molecules

2. Inhibits NK cell recognition of infected cells

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20
Q

How do superantigens initiate massive production of cytokines?

A

Superantigens simultaneously bind to MHC Class II molecules and TCR, thus bypassing antigen-specific T cell recognition and activation.

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21
Q

The massive cytokine production elicited by superantigens results in what?

A

Systemic toxicity and/or suppression of immune response.

22
Q

What are 2 examples of superantigens?

A

SE and TSST-1.

23
Q

Are there antigen-specific responses in the case of a superantigen?

A

No: that’s the whole point of a superantigen.

24
Q

Superantigens bind to which chain of MHC Class II molecules?

A

Alpha.

25
Q

Superantigens bind to which chain of the TCR?

A

Beta.

26
Q

What are 2 enzymes found in the HIV virion?

A

Integrase and reverse transcriptase.

27
Q

Why is HIV prone to undergoing antigenic drift?

A

Reverse transcriptase is sloppy and highly error prone.

28
Q

How does HIV take advantage of human behavior?

A

Sexually transmitted and shared needles.

29
Q

What does the HIV virion bind to?

A

Binds to CD4 and co-receptor on T cell.

30
Q

How does the HIV viral genome enter host cells?

A

Viral envelope fuses with host cell membrane allowing HIV virion to spill its viral genome into the cell.

31
Q

Reverse transcriptase copies viral RNA genome into what and what does that do?

A

Into double-stranded cDNA which enters nucleus and integrates into host DNA.

32
Q

T cell activation induces what of the HIV provirus?

A

Some transcription of the provirus.

33
Q

HIV RNA transcripts are spliced to allow synthesis of what HIV proteins?

A

The early proteins: Tat and Rev.

34
Q

What does Tat do?

A

Tat amplifies transcription of viral RNA.

35
Q

What does Rev do?

A

Rev increases transport of viral RNA to the cytoplasm of the host cell.

36
Q

Gag, pol, and env HIV proteins are made and assembled into what which does what?

A

Packaged into virions which bud from the host cell.

37
Q

What is the ultimate outcome of HIV infection?

A

Depletes CD4+ T cells.

38
Q

Which cells mediate the patient’s anti-HIV immune response?

A

Potent B and T cell mediated responses.

39
Q

How does the patient’s immune response actually help the virus?

A

Immune response provides selective pressure for the HIV virus to evolve.

40
Q

What are the 4 phases of HIV infection?

A
  1. Initial infection
  2. Asymptomatic Phase (latency period)
  3. Symptomatic Phase
  4. Full Blown AIDS (death)
41
Q

What viremia levels are observed in the asymptomatic phase?

A

After initial infection, viremia levels are controlled by host immune response so viremia levels remain low and are variable.

42
Q

What are 3 immune responses the patient forms to control HIV infection?

A
  1. Ab’s against HIV envelope protein
  2. HIV-specific cytotoxic T cells
  3. Ab’s against HIV core protein
43
Q

2-6 weeks post HIV infection, why does the patient present with flu-like symptoms?

A

Due to an initial rapid drop in CD4+ T cells.

44
Q

T or F. Once a patient is infected with HIV, CD4+ T cell levels begin to decline until they are eventually depleted?

A

F: after the rapid drop in CD4+ T cells, levels go back up in the asymptomatic phase then slowly decline until symptomatic phase and full blown AIDS develops.

45
Q

What is the average length of the asymptomatic phase?

A

10 years.

46
Q

What qualifies a patient as a full blown AIDS patient?

A

CD4+ T cell count <200 cell/microliter.

47
Q

What is the eventual cause of death in a terminal AIDS patient?

A

Death by infection due to CD4+ T cells being completely depleted.

48
Q

What does HIV-induced immunodeficiency allow?

A

Opportunistic infections including many species of parasites, bacteria, fungi, and viruses.

49
Q

What malignancies can occur in HIV infected patients?

A
  1. Kaposi’s sarcoma caused by herpesvirus 8
  2. Non-Hodgkin’s lymphoma (including EBV-positive Burkitt’s lymphoma)
  3. Primary lymphoma of the brain
50
Q

What 4 mechanisms does HIV employ to evade immune response?

A
  1. Antigenic drift
  2. Latency
  3. Molecular mimicry
  4. Induction of acquired immunodeficiency (CD4+ T cell depletion leads to death)

Immunology Spring 2 (7 decks)

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