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Immuno block 2 > Evasion immunity > Flashcards

Evasion immunity Flashcards

1
Q

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

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

antigenic shift:

A

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

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4
Q

protein 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

superantigen:

A

molecules that stimulate a subset of CD4 T cells by simultaneously binding to MHC class II molecules and the -chain of the TCR;

these binding interactions are not specific interactions

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6
Q

• there are at least 3 ways that antigenic variation can occur: name them

A
  1. many infectious agents exist in a wide variety of antigenic types
  2. antigenic drift and antigenic shift
  3. programmed rearrangement of DNA by a pathogen
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7
Q

How does a pathogen use many infectious agents that exist in a wide variety of antigenic types?

A

pathogen will use many different types of serotypes which the immune system will recognize but the pathogen also produces many others

this will allow the same pathogen to infect the same host many different times

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8
Q

a single influenza virus type is responsible for most of the infections throughout the world. but the human population gradually develops immunity to this virus type. How?

A

immunity to this virus is primarily mediated by neutralizing antibodies specific for its major surface proteins (hemagglutinin and neuraminidase)

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9
Q

influenza virus has developed 2 distinct mechanisms of changing its antigenic type (to assure
that it will always have unprotected hosts). name them

A

antigenic drift and antigenic shift

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10
Q

What does antigenic drift cause in the influenza viral infection?

A

antigenic drift is caused by point mutations in the genes encoding hemagglutinin and neuraminadase (a second surface protein)

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11
Q

every few years, a variant of influenza arises with mutations that allow the virus to evade neutralization by antibodies in the population (people that survived disease and produced a protective antibody response during previous pandemic). How does the virus evade the host wrt antigenic drift? What are the associated symptoms?

A

other mutations affect epitopes that are recognized by T cells (particularly CTLs), so that cells infected with the mutant virus also escape destruction so ppl with immunity of the old are now susceptible

a new epidemic can now begin; since there is usually considerable cross-reactivity (Ab and T cells) between the old variant and the new variant, most of the population has some level of immunity;

therefore, symptoms associated with the new variant are typically mild

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12
Q

How does a influenza virus spread infection wrt antigenic shift? What are the results ?

A

leads to major changes in the hemagglutinin protein on the surface of the virus

the resulting variant of the virus is recognized very poorly, or not at all, by responses made against the old variant;

therefore, most people are highly susceptible, and severe infection results

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13
Q

What is antigenic shift wrt influenza virus? (nucleic acid type, how it infects)

A

antigenic shift arises through the reassortment of the segmented negative-strand RNA genome (7-8 segments) of influenza virus (and related animal influenza viruses) during co-infection of an animal host

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14
Q

What are trypanosomes? what do they cause?

A

are insect-borne protozoa that replicate in extracellular tissue spaces in the body;

they cause sleeping sickness

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15
Q

What are the trypanosomes covered with that the immune system usually recognizes?

A

trypanosomes are coated with a single type of glycoprotein, the variant-specific glycoprotein
(VSG)

infected hosts produce a potent anti-VSG antibody response that rapidly clears most of the parasites

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16
Q

How do trypanosomes evade the immune system via programmed rearrangement of DNA?

A

trypanosomes have approximately 1000 different VSG genes that each encode a VSG protein that is antigenically distinct

utilize a “cassette system” to express only one of the different VSGs at a time

at least a few of the parasites that express different VSGs can escape the immune response, replicate rapidly, and cause a recurrence of the disease

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17
Q

Why do the trypanosomes eventually lead to sleeping sickness?

A

since this cycle can repeat itself many times, the chronic cycle of immune complex clearance leads
to damage of host tissues, including neurological damage, and eventually resulting in coma (sleeping sickness)

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18
Q

How do viral infections get classified and how do they get removed from the body?

A

usually, viral infections are characterized by rapid production of viral proteins (for replication);

fragments are displayed on the surface MHC class I molecules of the infected cell

recognized by antigen-specific effector CTLs

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19
Q

Describe the latent state of viruses wrt disease caused, growth and immune response

A

viral proteins not produced so no replication occurs

no disease is caused

virally-infected cells cannot be eliminated by CTLs bc there are no viral antigens to flag the presence of viral infection

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20
Q

Describe the herpes virus wrt how and where it infects w/in the body

A

herpes infects epithelia, then spreads to sensory neurons serving the area of infection;

after an effective immune response controls the epithelial infection (cold sores), the virus persists in a latent phase in the sensory neurons by integration of the viral genome into host cell episomal DNA

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21
Q

How can a latent stage herpes virus be reactivated to infect the host?

A

variety of stimuli

  1. upon reactivation, herpes virus travels along the axons of sensory neurons and re- infects the epithelial tissues;
  2. immune responses again control the infection by killing the infected epithelial cells (leaving cold sores);
  3. again the virus persists in the sensory neuron in latency

this cycle can be repeated many times

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22
Q

Wrt herpes infections, what are 2 reasons why sensory neurons remain infected?

A

1) since the virus is quiescent in the nerve, very few viral peptides are available for presentation to CTLs

2) neurons express very low levels of MHC class I molecules, which makes it harder for CTLs to
 recognize infected neurons
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23
Q

What is the good and bad about decreased amount of MHC on neuron cell surface?

A
  • since they can not be regenerated, the lack of MHC I molecules helps to prevent unnecessary killing of the vital cells
  • lack of MHC class I makes neurons extremely susceptible to persistent infections
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24
Q

• varicella zoster (causes chicken pox) is another good example of viral latency. Describe its course of pathogenesis

A

following initial chicken pox episode, virus remains latent in one or a few dorsal root ganglia

•• can be reactivated by stress (or immunosuppression) to spread down the nerve and re-infect
the skin

  • • the immune response to reactivated virus causes a characteristic rash (shingles)
  • • reactivation of varicella zoster usually only happens once in the lifetime of an immunocompetent host
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25
Q

How does EBV present?

A

children=> causes cold-like symptoms in children,

** adolescents and adults upon initial infection** => causes infectious mononucleosis

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26
Q

Describe the pathology caused from EBV in adults/adolescents

A

mononucleosis form of disease is characterized by B cell becoming infected and then proliferating (lots of new virus produced),

leading to activation of T cells.

Ultimately, infection is controlled by CD8 effector cells that kill infected B cells.

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27
Q

After initial infection of EBV, what happens to the virus?

A
  • become latent by inserting its genome into host DNA
  • reactivation rarely causes disease symptoms in immunocompetent people
28
Q

a variety of viral pathogens have evolved mechanisms to subvert various arms of the immune system. Name 3 of them

A
  • •• capturing cellular genes for cytokines or cytokine receptors
  • •• synthesizing complement-regulatory proteins
  • •• inhibiting MHC class I molecule synthesis or assembly
29
Q

Some bacteria “trick” the immune system. How does mycobacterium tuberculosis do this?

A

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

30
Q

How does the listeria monocytogenes escape the immune system? Where is its life cycle?

A

escape from the phagosome and replicate freely in the cytoplasm of the infected macrophage;

since the bacterium is spread via cell to cell contact, its entire life cycle can be intracellular

31
Q

How is listeria infection eventually cleared?

A

listerial infection can be cleared by antigen-specific effector CTLs

32
Q

How does toxoplasma gondii evade the host response?

A

Toxoplasma gondii (a protozoan parasite) can generate its own vesicle following phagocytosis;

this vesicle isolates the parasite from the rest of the cell, and prevents presentation of parasite-derived peptides

remains invisible to the immune system

33
Q

What is the action of superantigens produced by bacterial and viral infections?

A

induce massive production of cytokines by
CD4 cells;

cytokine production somehow induces a state of immune suppression and sometimes systemic toxicity

34
Q

How does staphylococcus suppress the immune system?

A

staphylococcal bacteria produce toxins (staphylococcal enterotoxins and toxic shock syndrome
toxin-1) that act as superantigens

35
Q

Where do superantigens bind?

A

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

36
Q

T/F not all antigens that bind to MHC class II molecules are presented as peptides in the peptide binding groove

A
37
Q

each superantigen can only bind to a few of the many different products of the Vb gene segments (20-50 in humans). What does this mean for immune response stimulation?

A

can only stimulate between 2-20% of all T cells

38
Q

binding of superantigen to both MHC class II and TCR of a T cell (simultaneously) causes what? What is the final result?

A

causes massive production of cytokines by CD4 T cells

cause systemic toxicity and/or suppression of immune responses

39
Q

T/F binding of superantigen to both MHC class II and TCR of a T cell (simultaneously) does not prime an antigen-specific immune response

A

true

40
Q

What is the causal agent for Leprosy?

A

Mycobacterium leprae

41
Q

What are the 2 results from a M. leprae infection?

A
  1. suppression of cell-mediated acquired responses,
  2. induces a very potent cell-mediated anti-bacterial response
42
Q

What are the 2 forms of disease caused by M. leprae?

A

lepromatous leprosy

tuberculoid leprosy

43
Q

Describe the immune response and the quality of it due to lepromatous leprosy

A

cell-mediated immunity is profoundly depressed,

infection is not controlled

44
Q

Describe the pathogenesis of lepromatous leprosy

A
  1. bacteria is highly infectious and replicates freely in macrophages
  2. infection is disseminated widely in the body
  3. hypergammaglobulinemia (elevated levels of immunoglobulins or antibodies in the circulation)
  4. low or absent T cell responsiveness; no response to M.
  5. leprae antigens
  6. the immunosuppression leaves the host in an anergic state;
45
Q

How does the immune system respond to tuberculoid leprosy and what is the result?

A

potent cell-mediated immunity with macrophage activation which controls

does not eradicate infection

46
Q

In tuberculoid leprosy, How does it present in observation and specific immune response?

A

bacteria is not very infectious and are present at low to detectable levels

  • • granulomas and local inflammation are observed
  • • normal serum levels of immunoglobulins is observed
  • • normal T cell responsiveness, and specific responsiveness to M. leprae antigens
47
Q

The difference in the two forms of leprosy is most like what?

A

difference in the ratio of TH1 to TH2 cells

therefore thought to be caused by cytokines

48
Q

chemokine:

A

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

49
Q

seroconversion:

A

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

50
Q

What type of virus is HIV?

A
51
Q

HIV is characterized how? what cells usually accompany it?

A

characterized by susceptibility to opportunistic infections

accompanied by a profound decrease in CD4 T cell numbers

52
Q

In what ways is HIV transmited?

A

sexual activity,

intravenous drug use

via therapeutic use of blood products

53
Q

How does the HIV gain entry into the cell?

A

the envelope protein complex of HIV binds with high affinity to CD4 molecules (on Tcells, macs and DCs)

once HIV has bound to CD4, it must interact with a co-receptor on the host cell (a chemokine receptor) to gain entry into the cell

54
Q

After initial infection, How does HIV affect the immune system?

A

HIV replicates rapidly in the blood causing a marked reduction in circulating CD4 T cell numbers

55
Q

In almost all patients, what occurs to the HIV infection?

A

CD8 T cells are activated to become HIV antigen-specific effector CTLs primed to kill HIV-infected cells (primarily HIV-infected CD4 T cells)

56
Q

Describe seroconversion wrt HIV

A

seroconversion occurs between 2-6 weeks post-infection

57
Q

When does the latency or asymptomatic phase of HIV begin and how long?

A

begins around the same time that seroconversion occurs

lasts approx 10 years

58
Q

What is occuring during the asymptomatic phase?

A

numbers of circulating CD4 T cells rebounds to about 50% of normal numbers;

these numbers gradually decline during the asymptomatic stage of disease

59
Q

When does the symptomatic phase of the disease begin? what is it characterized by?

A

begins when the numbers of functional circulating CD4 cells gets very low

characterized by high incidence of opportunistic infections

60
Q

How is the final stage of HIV clinically defined? What is the result

A

AIDS is clinically defined by very low number of circulating CD4 cells (≤ 200/μl-1)

•• the end result of AIDS is always death

61
Q

Describe the T cell mediated immunity response during an HIV infection

A

T cell mediated immunity is observed very early in infection,

persists throughout the asymptomatic phase of disease,

begins to wane during the AIDS phase of disease

62
Q

What is the initial immune response that is obsrved in HIV infection? How long does it take Ab specific envelope to become detectable?

A

initial immune response that is observed is seroconversion;

antibody specific for the envelope protein and the core protein easily detectable within 4-8 weeks of initial infection

63
Q

HIV has amazing ability to evade immune responses as well as drug therapies. How does it do this?

A

antigenic variation

HIV uses the enzyme reverse transcriptase to transcribe its RNA genome into DNA that can integrate into the host cell DNA

64
Q

What properties of reverse transcriptase allow it to accomplish antigenic variation?

A

reverse transcriptase is very error-prone, and introduces numerous point mutations during every replicative cycle

•• the point mutations result in antigenic changes in the envelope protein that facilitate evasion of immune responses

65
Q

HIV also rapidly acquires resistance to anti-viral drugs. How does it do this?

A

immediately following administration of protease
inhibitors, viral loads decrease rapidly and CD4 cell numbers increase;

within a couple of weeks however, mutant viruses begin to appear and CD4 cell numbers begin to decrease again

66
Q

AZT is a reverse transcriptase inhibitor. How does HIV respond to this?

A

resistance to zidovudine (AZT, a reverse transcriptase inhibitor) takes months to develop because several (3-4) mutations in the reverse transcriptase gene are required to confer resistance

Immuno block 2 (9 decks)

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