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Virology > HIV > Flashcards

HIV Flashcards

1
Q

What type of conditions can manifest in AIDS?

A

Lecture 20, slide 6

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2
Q

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

A

Lecture 20, slide 11

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3
Q

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

A

Lecture 20, slide 12-13

  • structural protein: Pol
  • virulence factors
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4
Q

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

A

Lecture 20, slide 14-15

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5
Q

What is the viral cellular tropism of HIV-1?

A

Lecture 20, slide 16

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6
Q

What are some viral antagonists of cell restriction factors?

A

Lecture 20, slide 17

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7
Q

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

A

Lecture 20, slide 18

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8
Q

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?

A

Lecture 20, slide 20-21

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9
Q

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

A

Lecture 20, slide 22-23

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

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10
Q

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

A

Lecture 20, slide 24

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11
Q

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

A

Lecture 20, slide 25

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12
Q

What causes AIDS?

A

Lecture 20, slide 26

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13
Q

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

A

Lecture 20, slide 28

-memory T cells and maybe macrophages

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14
Q

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

A

Lecture 20, slide 29

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15
Q

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

A

Lecture 21, slide 4-5

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16
Q

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

A

Lecture 21, slide 6

17
Q

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

A

Lecture 21, slide 7

18
Q

What are the antibody responses to HIV-1 infection?

A

Lecture 21, slide 8

19
Q

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

A

Lecture 21, slide 9-10

20
Q

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?

A

Lecture 21, slide 12-13

21
Q

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

A
  • adenovirus vectors

- CTL-based approaches have not yet worked in humans

22
Q

What is the rationale of neutralizing antibody vaccines?

A

-they aim to completely prevent infection

23
Q

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

A

Lecture 21, slide 18-19

24
Q

How can HIV-1 replication cycle be therapeutically targeted?

A

Lecture 21, slide 21

25
Q

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

A

Lecture 21, slide 22-23

26
Q

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

A

Lecture 21, slide 24

27
Q

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

A

Lecture 21, slide 25

28
Q

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?

A

Lecture 21, slide 26

29
Q

How does HIV-1 kill cells?

A

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

Virology (7 decks)

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