Lecture 14

Question 1

Is killing the host (or killing him too soon) is advantageous or disadvantageous to the pathogen?

Answer 1

Disadvantageous

Question 2

State the main 2 types of immunodeficiency.

Answer 2

Inherited – lead to susceptibility (individuals who prone to infection)
Acquired – ex. HIV

Question 3

What are the 3 types of antigenic variation?

Answer 3

A variety of serotypes simultaneously in the environment, changes in mutation or gene exchange (Antigenic drift, antigenic shift) and gene conversion/gene rearrangement

Question 4

How many Streptococcus pneumoniae serotypes? What happens with each different serotype in relation with vaccine?

Answer 4

Around 84; each infection with a different serotype is like a new disease, so the vaccine for these diseases is difficult.

Question 5

What is antigenic drift?

Answer 5

Changes by mutation or gene exchange that leaves some epitopes from previous strain. So, previous exposure (immunity) to related strains ease severity of disease.

Question 6

Does antigenic drift still allow the virus to replicate and spread?

Answer 6

Yes.

Question 7

What are epitopes? What happens to the epitopes in antigenic shift?

Answer 7

Surface molecules; they change

Question 8

What is antigenic shift?

Answer 8

Changes by mutation or gene exchange that can create viruses that don’t share epitopes with previous strain (no cross-rxc). So, there is no partial protection from previous infections and disease is much more severe than in years there is only antigenic drift.

Question 9

Give an examples of antigenic shift.

Answer 9

Bird influenza, human influenza virus, the flu pandemic of 1918-19 killed >40,000,000

Question 10

Which is more severe between antigenic drift and shift?

Answer 10

Antigenic shift.

Question 11

Give an example of gene rearrangement or gene conversion.

Answer 11

African trypanosomes (protozoan) cause African sleeping sickness. In terminal stages of the disease there is a severe neurological damage, coma and death.

Question 12

What happens when a virus become latent?

Answer 12

There is no viral replication, no viral proteins made, and no immune response.

Question 13

Give an example of a virus that become latent. Why?

Answer 13

Herpes simplex I becomes latent in nerves because nerves are low in MHC class I.

Question 14

For the herpes I simplex, when immunity is low, virus can emerge from the ________, infect _______, reproduce and spread. ~__% of the population have latent herpes simplex I, which causes ________, but only __% of the population get symptoms.

Answer 14

nerves; epithelia; 90; cold sores/fever blisters; 15

Question 15

IL-10 stops what?

Answer 15

Tends to stop the inflammatory reaction.

Question 16

Superantigen can activate ____ and ____.

Answer 16

T cell; B cells

Question 17

What is the main function of complement?

Answer 17

To lyse bacteria

Question 18

The superantigen binds what?
What happens to T cells in the presence of the superantigen?

Answer 18

To MHC class II and to TRCs that use particular v gene segment.
Any T cell will bind to MHC class II and deliver signals as if it had bound antigen.

Question 19

Why can’t the T cell activated by the superantigen bind to the B cell?
E.g. the B cells binds ______ flagellum and the T cell binds _____________.

Answer 19

Because the B cell is presenting a peptide that is not recognized by this T cell.
e. coli; polio virus capsid

Question 20

Some mice make their own superantigens. This causes all the __ cells that use a particular _ gene to be deleted in the _______. So, they are protected from the _____ (but sacrifice a significant proportion of their T cell repertoire).

Answer 20

T; v; thymus; MMTV

Question 21

MMTV is a _________.

Answer 21

retrovirus

Question 22

Give 4 mechanisms of subversion of host defenses by viruses. Or the viral strategies.

Answer 22

Inhibition of humoral immunity, inhibition of inflammatory response, blocking of antigen processing and presentation, and immunosuppression of host

Question 23

Give 4 inherited immunedeficiencies.

Answer 23

MHC Class I deficiency, Selective IgA, Phagocyte deficiencies, Bloom’s syndrome

Question 24

Immunodeficiencies lead to ___________. What happened in 1952 that helped reveal this?

Answer 24

bacterial infection; antibiotics

Question 25

_____________ is a genetic disorder that makes it hard to fight infections. When does the B-cell development get arrested?

Answer 25

X-linked agammaglobulinemia (XLA); in affected males and carrier females with normal X inactivated

Question 26

Describe the steps of the defects in the complement system.

Answer 26

Classical, mannose-binding lectin and alternate pathway join to go to C3 convertase, then to C3b deposition and then to membrane-attack.

Question 27

What is involved is classical pathway?
C3b convertase? Membrane-attack components? (5)

Answer 27

C1, C2, C4
C3
C5, C6, C7, C8, C9

Question 28

Give 3 severe combined immunodeficiency syndromes.

Answer 28

XSCID, RAG deficiency Omenn syndrome, ADA deficiency.

Question 29

Bone marrow transplants can correct most ___________, but only done in most severe cases because there are big risks. It is also a cure for most ___________.
Mature T cells from the donor _____ (must or mustn’t) be present if a semi allogeneic graft to an immunoincompetent individual is to be successful because the T cell will ___ the host.

Answer 29

immune defects; leukemias

mustn’t; kill

Question 30

For the function of the env (envelope) gene, the transmembrane glycoproteuns ____ binds CD4 and CCR5. While ____ is required for virus fusion and internalization.

Answer 30

gp120; gp41

Question 31

For the function of the env (envelope) gene, the transmembrane glycoproteuns gp120 binds ___ and ____. While gp41 is required for virus fusion and internalization.

Answer 31

CD4; CCR5

Question 32

What are the 2 types of leprosy? Which is low/high infectivity?

Answer 32

Tuberculoid leprosy (low) and lepromatous leprosy (high).

Question 33

The severity of leprosy depends on what?

Answer 33

Whether the immune system responds to infecting bacteria with a TH1 or TH2 response.

Question 34

What does MHC 1 affect (susceptibility)?

Answer 34

Chronic lung and skin inflammation.

Question 35

What does selective IgA affect (susceptibility)?

Answer 35

Respiratory infection.

Question 36

What does phagocyte deficiencies affect (susceptibility)?

Answer 36

Extracellular bacteria and fungi.

Question 37

What does Bloom’s syndrome affect (susceptibility)?

Answer 37

Respiratory infections.

Question 38

List some defects in phagocytic cells.

Answer 38

Prevent adhesion and migration, respiratory burst defect, chronic TH1 stimulation, and vesicle fusion defect.

Question 39

What is the treatment of severe combined immuodeficiency syndromes?

Answer 39

Bone marrow transplants.

Question 40

List some opportunistic infections and cancers.

Answer 40

Parasites, intracellular bacteria, fungi, and viruses.