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IMMUNOLOGY: CMOD-Block 2 > (13) Evasion of Immune Responses > Flashcards

(13) Evasion of Immune Responses Flashcards

1
Q

Define Antigenic Variation.

A

Display of New Antigens (by a pathogen) that are not recognized by immune responses formed in response to that pathogen

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2
Q

How do serotypes of Strep. Pneumo. differ?

- what are differences among these serotypes an example of?

A

Strep. Pneumo. uses antigenic variation to evade host defenses different CAPSULE structures allow the bug to evade the antibody made against the previous capsule

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3
Q

What is the advantage to Strep. Pneumo. being able to undergo antigenic variation?

A
  • Same host can be reinfected several times

- NO MEMORY B CELL RESPONSE SO DISEASE CAN SPREAD BEFORE ACQUIRED SYSTEM CAN ATTACK IT.

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4
Q

What are the two primary targets for antibody response to the flu?

A
  1. Neuraminadase
  2. Hemmagglutinin

**Antibodies bind and prevent interaction with host cell receptors

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5
Q

What types of antigenic variation are seen in the flu?

  • which usually leads to more severe disease? why?
  • Relative involvement of B and T cells?
A

2 types:
type 1:
- Flu infects host and begins replicative cycle
- During replicative cycle many mutations occur in the 2 primary antibody targets (Neuraminadase, and Hemagglutinin)
- People who have never been exposed to these Neura. and Hema. isotypes before will be susceptible

***LESS SEVERE, because T CELL response remains relatively the same, only B cell response has changed from altered targets (proteins presented are overall pretty much the same)

type 2:

  • 2 different types of Flu infect a non human host
  • ssRNA that is SEGMENTED in flu viruses shift around and the two different strains can mix segments
  • Neuraminidase and Hemagglutinin proteins are COMPLETELY different now

***MORE SEVERE, because B CELL and T CELL responses from previous infections are evaded because so much variation in proteins

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6
Q

Explain why African sleeping sickness leads to chronic reinfection that ultimately leads to coma?

A
  • Has a Cassette type deal (similar to gonorrhea)
  • 1 protein of the 1000’s that are silent can get put into position to be expressed
  • The body mounts a response against the Variant Specific Glycoprotein (VSG) being expressed at that time however other types are created at low levels and these will be selected for after the other type is wiped out

**Chronic reinfection in African sleeping sickness ultimately leads to neural tissue damage and coma

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7
Q

What is latency?

A

a state adopted by some viruses in which they have entered cells but do not replicated

*Usually because the virus has been integrated into the host’s genome (ON CHROMOSOMAL OR EPISOMAL dna)

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8
Q

T or F: herpes is a latent virus.

A

True, it initially infects the epithelium but later travels up the nerve and integrates into the EPISOMAL DNA in the host’s trigeminal ganglion

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9
Q

When is herpes virus expressed?

- why can it not be eliminated?

A
  • Expressed because of sunlight or mental stressed, travels down from trigeminal and you get herpes lesions on your lip
  • Can’t be eliminated because the latent virus hardly makes any proteins while its integrated in the host’s DNA
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10
Q

What virus causes shingles?

  • clinical signs?
  • where does it reside?
A

Varicella-Zoster Virus causes it

Clinical Signs:
- Unilateral Lesions that correspond to a single nerve or group of nerves in the midline or on the face

Where:
- Resides in DRG

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11
Q

What are 4 general ways in which viruses can subvert human immune responses?

A
  1. Inhibition of Humoral Immunity
  2. Inhibition of Inflammatory Response
  3. Blocking of Antigen Processing and Presentation
  4. Immunosuppression of Host
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12
Q

What are the main ways in which cytomegalovirus can subvert human immune responses?

A
  1. Interfere with Antigen Presentation

2. Interfere with NK cell function

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13
Q

What are superantigens and how do they work?

- outcomes?

A

Superantigen acts as a linker between MHC class II alpha chain and TCR ß-chain

  • This creates a non-specific immune response that can activate 1-20% of the T cell repertoire
  • CAN CAUSE SYSTEMIC TOXICITY RESEMBLING SEPTIC SHOCK

**May also just cause suppression of immune responsivness

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14
Q

What are 2 examples of superantigens?

A

SE and TSST-1

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15
Q

T or F: staphylococcus aureus produces molecules that interfere with neutrophil function, complement cascade, antibody opsonization, and that provide resistance to phagocyte killing.

A

True, if other bugs were studied as closely as staph we would probably find that similar things were happening in them as well.

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16
Q

T or F: evasion mechanisms produced by bugs like staph and strep can completely suppress the response that they interfere with

A

False, they just reduce the efficacy

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17
Q

What Type of Virus is HIV?

- important surface proteins?

A
  • Lentivirus (a type of RETROVIRUS)

Important Surface Proteins:
- gp 160 and transmembrane gp41

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18
Q

In what ways does HIV make its genome maximally efficient?

A
  1. Uses all 3 reading frames

2. Uses alternative splicing to make different transcripts

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19
Q

How does antigenic Variation arise in HIV?

A
  • Reverse Transcriptase has no proof-reading ability so several mutations are created that give rise to antigenic variation
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20
Q

How does HIV gain entry to the host cell?

  • what does it do when it gets there?
  • what does it do when it leaves?
A
  1. Binds to CD4 and Co-receptor on the CD4 T cell
  2. Viral envelope fuses with cell membrane and Viral Genome enters the cell (along with Rev. Trans. and Integrase)
  3. Reverse Transcriptase turns RNA into cDNA
  4. cDNA enters nucleus and become part of the host DNA (with help of the integrase)
  5. KILLS T-cells when it leaves
21
Q

Why can the immune system not clear HIV?

A
  1. Antigenic Variation that results from the error rate of Reverse Transcriptase
  2. Latency: HIV provirus integrates into the host cell DNA and and can remain latent for long periods of time

**IN REALITY WE GENERATE LOTS OF B AND T CELL MEDIATED ANTI-HIV RESPONSES, but this may just help the pathogen evolve

22
Q

When Does HIV become aids?

*what’s the point of HIV killing patients so slowly?

A
  • Patients T cells are depleted to the point where its like they have SCID (=AIDS) - these people are very susceptible to oportunistic infections
  • ALLOWING THE HOST TO LIVE FOR A LONG TIME ON THE WAY TO KILLING IT ALLOWS HIV TO SPREAD TO NEW HOSTS
23
Q

What 3 things make HIV an almost perfect pathogen?

- underlying mechanisms

A
  • Antigenic drift (no proof reading of reverse transcriptase)
  • Latency (allow for lots of spread to new hosts)
  • Induction of acquired immunodeficiency (T cell killing)
24
Q

In what type of pathogen is antigenic variation most advantageous?
- why?

A

Extracellular because the principle immune response against them is Antibodies

25
Q

What 2 distinct mechanisms are used by influenza to assure that it can always infect a new host?

  • how does the rate at which the virus is cleared govern this?
  • Severity of disease that results from use of these two mechanisms?
A

*The flu is cleared quickly so it needs to be able to spread to a wide variety of hosts in order to remain persistent

2 Methods:
Antigenic Drift, point mutations in neuraminidase and hemagglutinin
- disease is usually somewhat similar to what people have experienced before and there is no outbreak

Antigenic Shift, gene reassortment of genes of the -RNA genome
- leads to pandemics because several surface proteins may be altered

26
Q

What antibody type is most important for clearing the flue and what is this antibody typically specific for?

A
  • IgA

- IgA is specific for Neuraminidase and Hemagglutinin

27
Q

What are typanosomes?

- what single type of glycoprotein coats their surface?

A

Insect-borne protozwa that replicate in extracellular tissue spaces of the body causing sleeping sickness.

VSG - varient specific glycoprotein

28
Q

What are the two main ways that the herpes virus remains undetected in host cells?

A
  1. It Latent (no proteins can be presented on MHC I)

2. It lives in neurons, which express very little MHC I to present anything on in the first place

29
Q

What advantage does low expression of MHC I give neurons?

A

They don’t get attacked by CTL’s, this is important because they can’t regenerate

  • This leaves the door open for persistent infections
30
Q

If someone has recurrent shingles what might you assume about their immune status?

A

They may be immunocompromised because immunocompetent people only have 1 recurrence episode at most in their lifetime.

31
Q

What disease state is caused by the Epstein-Barr Virus?

  • what cells does it spread in?
  • how is it ultimately controlled?
A
  • In Children in causes Cold-like symptoms
  • In Adults it causes infectious Mononucleosis

Infects B cells that then proliferated and cause T cell activation

CD8 effector cells eventually come along to kill the infected cells and control the infection

32
Q

How does Mycobacterium TB subvert human immune response?

A

It gets taken into macrophages, then prevents phagolysosome fusion.

33
Q

How does Listeria Monocytogenes subvert human immune response?

A

Escapes the phagosome and replicates freely in the cytoplasm

  • Since the bacteria is spread by cell to cell contact, the entire lifetime of the cell can be intracellular
34
Q

How are Listeria Infections eventually cleared?

A

Macrophage activation by TH1 or Death by CTL

35
Q

What is Toxoplasma Gondii?

- how does it subvert the host immune response?

A
  • Its a protozoan Parasite
  • Following Phagocytosis the parasite generates its own vesicle that isolates it from the rest of the cell and thus its proteins are never presented to the immune system
36
Q

What are 3 general mechanisms used by viruses to subvert the host response?

A
  • Capturing cellular genes for Cytokine or Cytokine Receptors
  • Synthesizing Complement Regulatory Proteins
  • Inhibiting MHC I molecule synthesis or assembly
37
Q

What are the superantigens that staph produces?

A

Staphylococcal Enterotoxins

Toxic Shock Syndrome Toxin-1

38
Q

What binds to the Vß region of MHC II?

- is this in the binding groove of MHC II?

A

Superantigens

  • no, the Vß sequence it binds is located outside the binding pocket
  • This Vß sequence is found on 2-20% of out MHC II
39
Q

T or F: Leprosy causes pathogen induced immunosuppresion

A

True

40
Q

What are the two major forms of leprosy?

- how do they differ in regards to cell mediated immunity?

A

Lepromatous Leprosy:
- Cell Mediated Immunity is profoundly Depressed and the infection is not controlled

Tuberculoid Leprosy:
- Cell mediated immunity is potent which activates macrophages that control but do not eradicate the infection

41
Q

How do Lepromatous Leprosy and Tuberculoid Leprosy Differ in regards to:

  • Infectiousness
  • Replication inside the host
  • Granuloma formation
  • Immunoglobulin levels
  • T cell responsiveness
A

Lepromatous Leprosy:

  • Highly Infectious
  • Replicates Freely in Macrophages
  • NO granumloma formation
  • Crazy High levels of Ig
  • Low of absent T cell Responsiveness

Tuberculoid Leprosy:

  • Not very infectious and is only present at low to detectible levels
  • Granulomas form and prevent Dissemination in the host
  • Normal Levels of Ig (because the bacteria remains in macs)
  • Normal T cell responsiveness
42
Q

T or F: Tuberculoid Leprosy leaves the host in an anergic state and unable to respond to antigens

A

False, Lepromatous Leprosy does this

43
Q

What is believed to lie at the root of the differences between the two types of leprosy?

A

Cytokines and the difference in the ratio of TH1 and TH2 cells

44
Q

What are some notable infections that HIV patients are susceptible to?

A
  • Kaposi’s Sarcoma

- B cell Lymphoma

45
Q

When does seroconversion happen in an aids patient?

A

2-6 weeks post infection

  • This is the time in which Ig’s are build up against the the HIV antigens
  • This corresponds to the act of CD8 T cells becoming activated to kill HIV infected CD4 T cells
46
Q

What is the end result of AIDS?

A

Death, always - however some patients can keep HIV from progressing to AIDS and thus avoid Death

47
Q

When can gp120 and gp24 (core-protein) be detected in an AIDS infection?

A

2-4 weeks Post-Infection

48
Q

T or F: AIDS mutations are extensive and very few are needed to make protease inhibitors drugs ineffective at binding

A

True, the effects of the drugs (if given alone) only last a few weeks

49
Q

What reverse transcriptase inhibitor can act long term (Months) on an HIV virus before enough mutations are made for resistance to be conferred?

A

AZT (zidovudine)

IMMUNOLOGY: CMOD-Block 2 (10 decks)

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