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IMIN 324 > HIV/AIDS > Flashcards

HIV/AIDS Flashcards

1
Q

What does AIDS stand for?

A

Acquired immunodeficiency syndrome

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2
Q

What kind of virus is HIV, what is it’s tropism?

A

virus = retrovirus
tropism = T-lymphotrophic

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3
Q

What are the two groups of HIV?

A

HIV-1 and HIV-2

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4
Q

What are the four subtypes of HIV-1? Briefly describe what each subtype stands for and its prevelance. Where is HIV-2 mostly found?

A
  1. group M (major)
    - pandemic strain
  2. group O (outlier)
    - <10% of infections, restricted to West-Central Africa
  3. group N (non-M. non-O)
    - very rare, only in Cameroon
  4. group P (alphabet)
    - only 2 cases both in Cameroon

HIV-2 is mainly in west africa

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5
Q

Describe the interspecific transfer of SIV/HIV that lead to HIV-2

A

SIVsmm in sooty mangabey -> HIV-2 in humans

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6
Q

Describe the interspecific transger of SIV/HIV that lead to HIV-1 M and N

A

SIVcpz in chimps -> HIV-1 M and N in humans

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7
Q

Describe the interspecific transger of SIV/HIV that lead to HIV-1 O and P

A

SIVcpz in chimps -> SIVgor in gorillas -> HIV-1 P and O in humans

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8
Q

Describe how SIV affects monkeys

A
  1. each monkey contains its own SIV
    - don’t make a significant problem in monkeys
  2. SIVcpz is highly pathogenic to chimps
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9
Q

How did spillover from monekys to humans likely happen?

A

hunting monkeys and apes -> likely blood transfer -> infection

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10
Q

Where is most SIV found in wild chimps and gorillas?

A

chimps = Cameroon and democratic republic of Congo

gorillas = Cameroon

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11
Q

Describe the origin and diversification of HIV-1 M (where did it originate and where was it amplified/diversified and spread?)

A

originate: chimp -> human transfer = Southeast Camerooon

amplification, diversification and spread = Kinshasa

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12
Q

Describe how SIVcpz is deterimental to chimps, and what did this provide evidence for?

A
  • high mortality and AIDS-like immunopathology in wild chimps infected with SIVcpz (sig difference in death rates of chimps who are infected vs healthy)

evidence = chimps get AIDS and die from it -> evidence that the interspecific jumps to chimps happened close (before) it jumped to humans

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13
Q

What other monkey/ape has a pathogenic SIV?

A

gorillas

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14
Q

What are restriction factors? Describe some properties of restriction factors

A

restriction factors = species-species barriers

properties:
- host proteins that inhibit virus replication
- expression is increased by IFN
- often antagonized by viral proteins

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15
Q

Name 3 human restriction factors against HIV-1, their mechanism of action, and the HIV-1 antagonist

A

Restriction factor: APOBEC3G
- mechanism: deamination of proviral DNA
- antagonist: vif (virion infectivity factor)

Restriction factor: Trim5a
- mechanism: premature capsid uncoating
- antagonist: capsid protein mutations

Restriction factor: tetherin
- mechanism: inhibits release of budded virion
- antagonist: vpu (Nef in many SIVs)

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16
Q

Describe the APOBEC3G mechanism of action, how vif antagnoizes it, and state whether it was barrier to chimp-human transmission or not.

A

Mechanism:
1. APOBEC3G hitchhikes into budding virions
2. deaminates cytosine -> uracil
3. impedes reverse ts
4. genome is degraded

Vif mechanism:
1. ubiquitylates A3
2. A3 is degraded

A3G was not likely a barrier because vif works well against it

17
Q

Describe the Trim5a mechanism of action, how HIV antagnoizes it, and state whether it was barrier to chimp-human transmission or not.

A

Mechanism:
1. recognizes the capsid
2. destroys the capsid or
3. causes ubiquitylation by E3 ligase -> immune response

HIV mechanism:
1. human trim5a recognizes HIV-1 capsid poorly

Trim5a was not likely a barrier because human Trim5a does not work well against HIV-1

18
Q

Describe the capsid of HIV (symmetry, and number of hexamers and pentamers)

A

fullurene cone: 250 hexamers and 12 pentamers

19
Q

Describe the tetherin mechanism of action, how vpu/nef antagonize it, which protein does SIVcpz use, and state whether it was a barrier to chimp-human transmisson or not and why

A

Mechanism:
1. located on the cell surface and both ends are anchored to the p.m
2. extracellular domain allows tetherin-tetherin dimerization
3. either tethers virion to cell surface or connexts virions to each other

Vpu mechanism:
1. binds the tetherin transmemb domain
2. retains newly made tetherin to the GA
3. redirects it to lysosomes

Nef mechanism: (SIVcpz)
1. binds tetherin cytoplasmic domain
2. leads to clathrin-dependent endocytosis

Tetherin was likely a barrier to chimp-human transmisson because humans have a 5a.a del in the cytoplasmic domain of thetherin which prevents SIVcpz Nef (and Vpu) from binding tetherin

20
Q

How did HIV overcome tetherin?

A

HIV-1 group M and N has “regained” the ability to antagonize tetherin

21
Q

What is the other critical function of Vpu besides antagonizing tetherin? Which HIV-1 subtypes Vpu has this function? Which subtype has a fully functional Vpu and what is the consequence of this?

A

function = downregulation of surface CD4, which is required for efficient virus release

subtypes = M and O

fully functional Vpu = M -> allowed M to take off and become pandemic

22
Q

Describe the long-term course of HIV-1 infection in untreated humans (describe the different phases)

A

Acute phase:
- large drop in the number of CD4+ T cells in the blood and GIT
- driven by the cytotoxic effects of HIV-1 and killing by anti-HIV CTLs

Asymptomatic phase:
- viral load decreases due to the immune response
- CD4+ T cell numbers in blood and GIT continue to decline

AIDS phase:
- no CD4+ T cells
- virus wins the battle

23
Q

What are CD4+ T cells required for?

A
  1. optimal Ab responses
    - especially class switching
  2. activation and growth of CD8+ T cells
  3. activating antibacterial functions of macrophages
  4. maintaining lymph nose structure and function
    - especially the fibroblast reticular cell network
24
Q

How does early and persistent immune activation help drive progression to AIDS? Describe what causes it, what it affects, and what it leads to

A

caused by:
- breached intestinal barrier (from destruction of GALT) -> bacterial products (LPS) find their way into blood
- inflammatory cytokines produced by infected CD4 T cells, macrophages and DCs

affects:
- all immune cells (not just HIV-1 infected cells)

leads to:
- immune cell exhaustion (anergy)

25
Q

Describe the standard anti-HIV triple therapy

A

2 nucleoside reverse transcriptase inhibitors + 1 non-nucleoside RT inhibitor OR 1 integrase inhibitor OR 1 protease inhibitor

26
Q

Why would we target HIV’s protease in anti-HIV therapy?

A
  1. prevents from making HIV-1 infectious
  2. prevents maturation
27
Q

Describe how anti-retroviral therapy (ART) affects viral load and CD4+ T cell levels

A
  • viral load becomes undetectable (still there)
  • full recovery of blood CD4+ T cells
  • GIT CD4+ T cells do not fully recover
28
Q

Describe why ART is not a cure for HIV?

A
  1. does not eliminate HIV-1 from latently infected, long-lived CD4+ T cells (reservoir) -> virus rapidly rebounds when therapy is discontinued
  2. immune activation persists for at least a decade after ART is initiated
  3. lymph node damage (loss of FRC network and appearnace of fibrosis) that occured before treatment persists
  4. GALT doesn’t fully recover
  5. people on ART are at risk for a number of ageing-related conditions
29
Q

What ageing-related conditions can develop while on ART?

A
  1. cardiovascular disease
  2. osteoporosis
  3. certain cancers
30
Q

What is one major therapeutic goal to treat HIV and what are a couple of approaches?

A

goal = purge latent HIV-1

approach =
- shock latently infected T memory cells to reactivate the virus -> cell killed by HIV or by anti-HIV CTLs
- use gene editing to inactivate the latent provirus

31
Q

What are the reactivation strategies to reactivate latent HIV-1?

A
  1. histone deacetylate inhibitors
    - convert silent chromosomal regions into active ones
  2. HIV therapeutic vaccines
    - most of the latently infected T memory cells are HIV-specific
    - activating the memory cell by exposure to HIV Ag activates the virus
32
Q

What are some reamining challenges surrounding HIV treatment?

A
  1. increasing the availability of ART in developing countries
  2. prevention
33
Q

What are some prevention strategies?

A
  1. effective vaccines
  2. safe sex
  3. injection drug use - safe injection sites and avoid sharing needles

IMIN 324 (14 decks)

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