HIV

Question 1

What type of conditions can manifest in AIDS?

Answer 1

Lecture 20, slide 6

Question 2

What is the structure of HIV-1? What Baltimore group does it belong to?

Answer 2

Lecture 20, slide 11

Question 3

What structure proteins do HIV-1s open readings frames encode? What regulatory and virulence factors do they encode?

Answer 3

Lecture 20, slide 12-13

• structural protein: Pol
• virulence factors

Question 4

How does HIV-1 engage with host cell receptors and enter host cells? What is the rest of its replication cycle?

Answer 4

Lecture 20, slide 14-15

Question 5

What is the viral cellular tropism of HIV-1?

Answer 5

Lecture 20, slide 16

Question 6

What are some viral antagonists of cell restriction factors?

Answer 6

Lecture 20, slide 17

Question 7

What are the two cellular ways that HIV-1 can spread?

Answer 7

Lecture 20, slide 18

Question 8

What is the natural progression (without treatment) of HIV-1 infection? What are the characteristics of HIV-1 infections that diverge from this progression to AIDS?

Answer 8

Lecture 20, slide 20-21

Question 9

Why is the experimental pathogenic SIV infection (in macaques) a better model for HIV-1 infection than natural SIV infection?

Answer 9

Lecture 20, slide 22-23

-the experimental model correlates better to HIV than the natural infection model

Question 10

Compare healthy gut-associated lymphoid tissue (GALT) with HIV-infected GALT.

Answer 10

Lecture 20, slide 24

Question 11

How do CD4+ T cells die in an HIV-1 infection?

Answer 11

Lecture 20, slide 25

Question 12

What causes AIDS?

Answer 12

Lecture 20, slide 26

Question 13

Where are the viral reservoirs made in an HIV-1 infection?

Answer 13

Lecture 20, slide 28

-memory T cells and maybe macrophages

Question 14

What potential cures for HIV-1 infection may there be?

Answer 14

Lecture 20, slide 29

Question 15

What are the events following HIV-1 transmission? What is the immune response to transmission?

Answer 15

Lecture 21, slide 4-5

Question 16

What are the early innate immune responses to HIV-1 infection?

Answer 16

Lecture 21, slide 6

Question 17

What are the T cell responses to HIV-1 infection?

Answer 17

Lecture 21, slide 7

Question 18

What are the antibody responses to HIV-1 infection?

Answer 18

Lecture 21, slide 8

Question 19

What is the major immune evasion mechanism of HIV-1 and how is it done? What are some nAb evasion mechanisms of HIV-1?

Answer 19

Lecture 21, slide 9-10

Question 20

What are the two major vaccine approaches for HIV-1? What are the disadvantages and advantages of each approach and the combination of both approaches?

Answer 20

Lecture 21, slide 12-13

Question 21

What is the aim of CTL-based vaccines? What vectors are being tested?

Answer 21

• adenovirus vectors

- CTL-based approaches have not yet worked in humans

Question 22

What is the rationale of neutralizing antibody vaccines?

Answer 22

-they aim to completely prevent infection

Question 23

What HIV-1 epitopes do bNAbs recognise? How can we elicit bNAbs in people?

Answer 23

Lecture 21, slide 18-19

Question 24

How can HIV-1 replication cycle be therapeutically targeted?

Answer 24

Lecture 21, slide 21

Question 25

What is the structure and function of the reverse transcriptase enzyme? How can it be therapeutically inhibited? Give named examples of drugs.

Answer 25

Lecture 21, slide 22-23

Question 26

What is the structure and function of HIV-1 integrase? How can it be therapeutically inhibited? Give a named example of a drug.

Answer 26

Lecture 21, slide 24

Question 27

What is the structure and function of HIV-1 protease? How can it be therapeutically inhibited?

Answer 27

Lecture 21, slide 25

Question 28

What types of treatments and prevention for HIV-1 infection exist? What drug combinations are used and how successful are the treatments and prevention methods?

Answer 28

Lecture 21, slide 26

Question 29

How does HIV-1 kill cells?

Answer 29

HIV-1 induces cell death in both uninfected (bystander) and infected CD4+ T cells. - Bystander cells may be killed by aberrant caspase-dependent apoptosis, e.g. induced by upregulation of death ligands (e.g. Fas ligand). - Infected cells may be killed by pyroptosis (e.g. due to the accumulation of unintegrated reverse transcripts), caspase-dependent apoptosis, etc