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Hugh's Intersystems > HIV > Flashcards

HIV Flashcards

1
Q

What is the function of HIV Rev protein?

A

It stabilised and transports unspliced and partially spliced RRE+ HIV RNA to the cytoplasm

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1
Q

What does Vif protein do?

A

Degrades APOBEC3

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1
Q

What does Pneuocystis jirovecii cause?

A

Pneumonia

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2
Q

What does TRIM5a do?

A

A endogenous human protein that destabilises the viral capsid

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2
Q

What viral protein is required for reactivation of transcription after a peroid of latency?

A

Tat

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2
Q

Apart from depleting T cells, what other effects does HIV infection have on the immune system in general?

A

Reduces neutrophil killing of bacteria

Increase B cell production of antibodies, including autoantibodies

Decrease macrophage phagocytosis, chemotaxis and killing

Decreases NK function

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3
Q

Which does HIV preferentially bind to early in infection, CCR5 or CXCR4?

A

CCR5

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3
Q

Why has vaccine development been so difficult?

A

Because envelope gp120 is highly variable

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4
Q

Which nucleoside is acyclovir an analogue of?

A

Guanosine

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5
Q

Is T cell depletion only caused by direct destruction of infected cells?

A

No, indirect destruction of uninfected cells also occurs.

eg Via incorporation of uninfected cells into syncitia

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5
Q

What adverse consequences of infection are seen despite viral control with HAART?

A

HIV-associated metabolic syndrome

Excess pathogens

Loss of Tregs

Microbial translocation through gut

CVS disease

Liver disease

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6
Q

How is it possible for HIV RNA production to occur in patients on HAART?

A

Latency in CD4+ T cells - particularly memory T cells

Replication in sanctuaries away from HAART therapy ie Brain, testis and gut

Replication in immunologically privileged sites

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7
Q

What type of virus is HIV?

A

Lentivirus

Icosahedral capside

Enveloped

+ssRNA

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8
Q

What is ribavirin?

A

A guanosine analogue that can target multiple viruses

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9
Q

What is the name of the viral protein that drives membrane fusion?

A

gp41

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11
Q

What does the HIV provirus’ promoter respond to?

A

Viral Tat protein

NFcappaB - a transcription factor involved in T cell activation

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12
Q

At mutation in delta32 CCR5 confers what for the human?

A

Homozygous confers resistant

Heterozygous confers slowed disease progression

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13
Q

Which has phosphate groups, nucleosides or nucleotides?

A

Nucleotides

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14
Q

What does the gag gene encode for?

A

Matrix

Capsid

Nucleocapsid

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15
Q

What long does primary HIV last?

A

1-4 weeks

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17
Q

What does APOBEC3G do?

A

It is an endogenous human protein that induces lethal hyper-mutations

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18
Q

What are some strategies HIV uses to block the expression of MHC-1?

A

Lysosomal degradation of MHC-1 by Nef and Vpu

Directing MHC-1 into the proteosome by Vpu

Tat inhibiting MHC-1 gene transcription

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19
Q

What causes chronic immune-activation? What is the consequence of it?

A

Lost of gut mucosal barrier > microbial products leak into systemic circulation > PAMPs stimulate immune cells > pro-inflammatory cytokines are elevated

  • CD4+ T-cells enter cell-cycle and die
  • CD8+ T cells become trapped in lymph nodes
  • B-cells make auto-Ab
20
Q

Why must you use 3 drugs in a combination therapy?

A

The chance of spontaneous viral mutation to evade 3 antivirals is highly improbable

21
Q

Is decline in CD4 cells faster or slower with hepatitis G co-infection?

A

Slower

22
Q

What is required for maturation of the viral particular after budding?

A

Activity of viral protease

23
Q

What is the incubation period of primary HIV infection?

A

2-4 weeks

23
Q

Why don’t most antibodies to the HIV env neutralise the virus?

A

It is highly glycosylated

23
Q

Why does acyclovir only target viral DNA replication?

A

Because it requires viral thymidine kinase to add the first phosphate group

25
Q

What is the presentation of primary HIV infection?

A

Flu-like illness

  • Fever
  • Myalgia/arthralgia
  • Nausea/vomiting/diarrhoea
  • Weight loss
26
Q

What is Kaposi’s sarcoma caused by?

A

Infection by human herpesvirus 8

27
Q

What does HAART stand for?

A

Highly active anti-retroviral therapy

27
Q

How does Raltegravir work?

A

Inhibits integrase to block strand transfer

29
Q

Where is the sequence variation highest in the HIV-1 genome?

A

In the env V region

30
Q

How often to nucleotide changes occur to transcription of DNA from RNA?

A

Once per genome replication

31
Q

How is viral fusion/entry inhibited by antivirals?

A

Coreceptor antagonists

  • For CCR5 = Maraviroc
  • For CXC4 = AMD-11070

Preventing unfolding

  • Enfuvirtide
32
Q

How do the protease inhibitors of HIV maturation work?

A

They have analogous regions that maturation enzyme will bind to instead of the viral target

34
Q

What does Vpu do?

A

Facilitates the release of fully infectious virions and counteracts innate immunity factors (degrades CD4, antagonizes tetherin, inhibits surface expression of CD1d)

36
Q

Describes HIV’s structure in terms of its layers

A

Outer bilipid membrane

Matrix protein beneath, complexing with the envelope

Capsid

Nucleocapsid contain the RNA genome

37
Q

What percentage of T-cells are lost within primary HIV-1 infection?

A

>60% of mucosal T-cells

38
Q

What do nucleoside analogues lack that prevents them from being added to the growing DNA chain by polymerase?

A

3’ OH

40
Q

Via what mechanism does HIV get from a local infection into the blood?

A

Virus infection dendritic cells > these fuse with CD4+ T cells > both travel to regional lymph nodes > HIV is spread to activated CD4 T cells > those infected cells enter the bloodstream

41
Q

What is the of the coreceptors that HIV binds to after initially binding to CD4?

A

CCR5

CXCR4

42
Q

Which can be detected first, HIV antigen or anti-HIV antibody?

A

HIV p24 Antigen

44
Q

Which strain of HIV-1 is transmitted between people?

A

R5

45
Q

What does tetherin do?

A

It is a endogenous human protein that inhibits virus release

46
Q

Which protein is required for the maturation of HIV particles?

A

Gag-Pol precursor protein

47
Q

What structural property do all nucleoside reverse transcriptase inhibitors share?

A

They lack the 3’ OH

48
Q

What is the limitation of targeting coreceptors with antagonists?

A

The other coreceptor is selected for

49
Q

Why is the function of the long terminal repeat?

A

Acts as the HIV gene promoter once the provirus have been integrated into the host genome

50
Q

What viral ligand binds CD4 of T cells and macrophages?

A

gp120

51
Q

Which coreceptor is associated with greater pathogenicity?

A

CXCR4

53
Q

Epidemiologically, how does the distribution of HIV infection differ in Australia compared to the rest of the world?

A

In Australia homosexual male are predominantly affected while in worldwide it is predominantly heterosexual women

54
Q

Where does reverse transcription occur?

A

Within the viral capsid when it is in the cytoplasm of the infected cell

55
Q

How is the long terminal repeat created?

A

Duplication of the end of the viral RNA sequence

56
Q

In general, how do non-nucleoside reverse transcriptase inhibitors work?

A

Directly inhibit the reverse transcriptase enzymes by some mechanism

Hugh's Intersystems (15 decks)

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