Lecture 17 Flashcards

Ch 13 failures of the body's defenses

1
Q

Define immunodeficiency.

A

Failure to protect the host from pathogens or malignant cells

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2
Q

Vaguely explain the difference between a primary and secondary immunodeficiency.

A

Primary- genetic and/or present at birth
Secondary- results from exposure to various agents… acquired

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3
Q

What happens to the innate immune response in a primary immunodeficiency?

A

Defects occur in the following: neutrophils, phagocytes, and complement, leading to increased susceptibility to bacterial infections

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4
Q

A phagocyte defect increases susceptibility to what type of infections?

A

Extracellular bacteria and fungi

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5
Q

A complement defect increases susceptibility to what type of infections?

A

Extracellular bacteria, specifically Neisseria spp

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6
Q

What happens to the adaptive immune response with a primary immunodeficiency?

A

B and T lymphocytes cannot be properly developed and activated

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7
Q

What is the result of a deficiency in T lymphocytes?

A

SCID

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8
Q

What is it called when there is an MHC class I or MHC class II deficiency?

A

Bare lymphocyte syndrome (because no CD8 or CD4 T cells can be activated)

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9
Q

What are some of the defects in cell interaction and signaling between a B cell and T cell?

A

Defects in: JAK-3 pathway, RAG enzymes, expression of MHC class II, bruton’s tyrosine, gamma chain of receptors for IL-2

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10
Q

What is X-linked agammaglobulinemia?

A

It is a primary immunodeficiency where the patient has no gamma globulin, a major Ab fraction of serum, leaving them with few to no mature B cells. It is found on the X chromosome and is therefore X-linked, affecting mostly males.

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11
Q

How does X-linked agammaglobulinemia prevent B cell maturation?

A

Without btk present, phospholipase C cannot activate, and there are no second messengers of DAG and IP3 which prevents maturation of a pro to pre B cell.

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12
Q

How does X-linked agammaglobulinemia function in a female carrier?

A

Since a female has two X chromosomes, she can either be a carrier or have her B-cell development arrested. If the defective X is inactivated, then signaling and maturation will be normal, as opposed to the normal X being inactivated, which would cause the disease.

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13
Q

In normal infants, what Ab is transiently deficient in the first year of life?

A

IgG

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14
Q

What are two ways secondary immunodeficiencies can occur?

A

Malnutrition and agent-induced immunodeficiency

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15
Q

What is affected by malnutrition?

A

Cell-mediated immunity is affected

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16
Q

What are some examples of agent-induced immunodeficiencies?

A

Exposure to chemicals, corticosteroids, immunosuppressive drugs for transplant patients, or radiation/chemotherapy for cancer patients

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17
Q

What causes AIDS?

A

An infection of HIV-1

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18
Q

How was the first group of patients diagnosed with AIDS?

A

Group of patients shows a rare fungal pathogen, had Kaposi’s sarcoma, and decreased CD4+ cell populations

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19
Q

During the global AIDS epidemic, who was affected more: males or females?

20
Q

People living with HIV has increased or decreased over the years?

21
Q

How can HIV be transmitted?

A

Hetero or homosexual intercourse, recipients of infected blood, and passage from mother to infants

22
Q

Why would anal intercourse be more likely for infection versus vaginal intercourse?

A

Microtears/bleeding occurs more easily in the anus than in the vagina

23
Q

In Eastern Europe, what is the biggest mode of HIV transmission?

A

IDU (intravenous drug use)

24
Q

Name at least one prevention intervention of HIV.
Hint: you probably have seen an ad for one on TV

A
  • pre-exposure prophylaxis
  • vaginal and rectal microbicides
  • post-exposure prophylaxis
  • male condom use
  • male circumcision
25
What viral receptor makes HIV so sneaky?
Gp120 on the virus because it can bind CD4 on host cells
26
What else is in the HIV viral envelope that makes it so sneaky?
It contains host proteins like MHC class I and II that can bud off
27
HIV is what type of virus?
Retrovirus
28
What is a provirus?
A DNA copy of the RNA genome in the host cell DNA
29
What happens to the provirus after it becomes integrated into the host cell genome?
It is replicated with the host DNA, new virions get produced, and the host cells lyse, then it buds off and infects another host cell.
30
What structure in retroviruses copies the viral RNA genomes into DS cDNA?
Reverse transcriptase
31
What enzyme integrates the provirus into host DNA?
Integrase
32
What is the role of Tat?
amplifies transcription of viral RNA
33
What is the role of Rev?
Increase transport of singly spliced/unspliced viral RNA to the cytoplasm
34
Can a chemokine receptor bind a chemokine and the virus at the same time?
NO!
35
How can a chemokine potentially block infection?
It can compete with the virus to bind the receptor
36
How is HIV diagnosed?
Early tests for HIV include PCR. Ab usually shows up about 3 months after infection and at this point the patient is "seroconverted".
37
How can AIDS be diagnosed?
presence of Ab, PCR finds viral RNA in the blood, greatly diminished CD4 cells, absent DTH reactions
38
What is considered a dangerously low level of CD4+ T cell count?
Below 200
39
How does the DC become a Trojan horse for HIV?
The DC may pick up the virus and deliver it to a lymph node, which is rich in T cells
40
Describe the progression of HIV infection.
Initial exposure, Ab and CTL keep viral replication in check for a long time until enough infected CD4+ cells are compromised and lymphoid tissue is attacked.
41
What are some ways HIV is treated?
Combination treatment, highly active anti-retroviral therapy, 2 nucleoside analogs, 1 protease inhibitor
42
When using inhibitors, what parts of the infection process can be stopped?
viral entry, reverse transcriptase that makes the cDNA, integrase, and viral assembly
43
What is a potential cell therapy for HIV?
Attempting to replace susceptible cells with resistant cells (knocking out CCR5)
44
What are two other options for treating HIV?
Using autologous genetically engineered T cells with redirected HIV specificity or cells engineered to secrete anti-HIV proteins
45
What is one limitation of the autologous genetically engineered cell treatment?
Clonal exhaustion and viral escape mutations