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BIOL2022 Past Papers > HIV Part 1 > Flashcards

HIV Part 1 Flashcards

1
Q

AIDS (Aquired Immunodeficieny Syndrome)

A
  • HIV + Opportunistic infections
  • Immunocompromised individuals
  • Low levels of CD4 T helper cells
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2
Q

HIV (Human Immunodeficiency Virus)

A
  • HIV-1 and HIV-2 subtypes
  • Vaccines against all sub types is important
  • High mutation rates- variants
  • Variants- changes to which cell type they infect
  • All similar structure and replication process
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3
Q

HIV structure

A
  • Retrovirus (Lentifamily)
  • 2 single stranded RNA- bound by molecule of reverse transcriptase
  • In genome - p10 protease and p32 integrase
  • Surrounded by nucleocapsid - inner layer of protein p24, outer layer of protein p17
  • > p24 = core antigen capsid protein
  • > both: Gag (group specific antigen) polyprotein complex)
  • Outer most portion- lipid membrane derived from host cell
  • > contains gp120 and gp41 = envelope proteins
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4
Q

What are its viral envelop proteins?

A

g120
gp41

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5
Q

What proteins make up the nucleocapsid?

A

Inner = p24
Outer=p17

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6
Q

p24 and p17 form what complex?

A

GAG polyprotein complex

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7
Q

What proteins what in the genome of HIV?

A

p10- protease
p32- integrase

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8
Q

What does GAG encode for?

A
  • Created as a larger molecule =p53 = GAG precursor polyprotein
  • To become function its broken down by protease to produce -Structural capsid proteins
  • > p24 = core antigen capsid protein
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9
Q

p17

A

Matrix protein - 131 amino acids

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10
Q

p7

A

Nucleo-capsid protein - 55 amino acids

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11
Q

Role of the GAG protein

A
  • outermembrane
  • assemby of new HIV virus particles
  • Brings viral RNA and viral proteins and host proteins together
  • triggers process of forming new virus particles
  • breaks awat from host cell surface
  • infect other cells
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12
Q

What side chains are found on gp120?

A

Glycans

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13
Q

What receptor does HIV target and where is it expressed?

A
  • CD4+ receptor
  • On CD4+ T helper cells, some on monocytes and dentritic cells
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14
Q

2 stages of HIV viral infection

A
  1. Binding - gp120 (viral envelope) to CD4+ receptor
  2. Fusion
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15
Q

What type of receptors are CD4+ Receptor

A

Glycoproteins
* Co-receptor of T cell receptor (TCR)

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16
Q

Upon viral recognition of CD4+ R, what it secreted to fight off infection?

A
  • B cells
  • T killer
  • CD4+ T helper (HIV target)
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17
Q

Normal function of CD4

A
  • Major histocompatability complex II (MHCII) molecules on antigen presenting cell
  • Present antigen (piece from bacteria)
  • CD4+ and TCR bind to MHCII at different region
  • Brings it closer- enabled Lck kinase to phosphorylate ITAMS on CD3 complex on TCR.
  • Phosphorylated ITAMS recruit ZAP70 enymze
  • Activates downstream signal transduction via tyrosine phosphorylation in T cell
  • > phorphorylation of proteins
  • NF-Kappab (NK-kb) activation
  • Leads to T cell activiation- immune response against presented antigen
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18
Q

Possible diagram question- Life Cycle of HIV

A

1). Binds to CD4 +ve cells through gp120 to CD4; interactions between virus and chemokine co-receptors.
2). Nucleocapsid enters the cell, unfolds, releasing viral RNA, which is reverse-transcribed to DS DNA.
3). The viral DNA integrates in the host genome, where it lies dormant as a provirus.
4). Following cell activation, viral DNA directs the transcription of viral RNA.
5). Viral proteins are translated from the RNA.
6) Viral proteins and single-stranded viral RNA assemble to form new viral particles.
7). Virus buds from the cell, picking up some of cell membrane, complete viral particles can infect other cells.

19
Q

When gp120 binds to CD4+ what other co-receptor is involved?

A

Chemokine co-receptor

20
Q

What is the virus called when its genetic material integrates with host genome?

A

Provirus

21
Q

The provirus is said to be what before activated?

A

Dormant

22
Q

What is the specific chemokine co-receptor associated with CD4+TCR?

A

CCR5

23
Q

Hijacks immune cell- HIV circumvents normal Dendritic Cell -T cell inter

Explain the viral strategy for efficient transmission of viral particles upon dendritic infection?

A
  • Dendritic shoot out thin appendages - filopodia
  • Rearrangement of actin filaments
  • Relatively fast
  • Carries the viral particle to T cells
  • Waving arc motion
  • Efficient viral transmission
24
Q

Old Model HIV Binding

Explain HIV binding

A
  • gp120 binds to co-receptor CD4+ on TCR
  • gp41 bind to a second protein = chemokine co-receptor on TCR
  • 2 types of co-receptor depending on HIV Variant
25
Q

Old model HIV bonding

M-tropic variant

A

M-tropic variant
* gp41 brinds to b-chemokine co-receptor = CCR5
* Present: CD4+ T cells, Monocytes and Dendritic cells

26
Q

Old model HIV binding

T-tropic variant

A

T-tropic variant
* a-chemokine co-receptor= CXCR4
* Only on CD4 T cells
* Not expressed on monocytes
* Not expressed on Dendritic cells

27
Q

HIV Binding (New model)

Explain the new model for HIV model in detail?

A
  • gp160= precursor fusion glycoprotein
  • > fuse viral and host membrane
  • Spike formation - trimer (3 molecules) of gp120 come together
  • Cleaved -> gp4(transmembrane) + gp120(surface)
  • gp120: binds to CD4+ co-receptor
  • > structural change, binds to chemokine receptor (CXCR4 or CCR5)
  • > Acitvates gp41 (high energy state)
  • > buried fusion peptide (linked amino acids) extends
  • Bridges gap between viral membrane and host cell membrane
  • For viral content to enter host cell
28
Q

How can HIV entry be inhibited?

A
  • Downregulating the expression of chemokine receptor expression
  • > reduces entry points for the virus
  • saturating chemokine receptors with their natural ligand-> chemokine
  • > prevent HIV entry
29
Q

Chemokine exression

M tropic HIV susceptibility

A
  • Binds to CCR5 chemokine receptor
  • Mutation -> CCR5(change)32
  • > 32 base pair deletions
  • Renders receptor non-functional
  • Protection to individuals against M tropic HIV variants
  • Virus difficulty entering cells that express mutated CCR5 receptor
  • Prevelant Europe and North Amerca
  • Rare in Indian populations
30
Q

What is MIP-1a?

A
  • Macrophage Inflammatory Protein 1alpha
  • Ligand to CCR5
  • 1 in 5 Indians
31
Q

T-tropic HIV variant susceptibility

A
  • Binds to CXCR4 chemokine receptor
  • Ligand= SDF-1 (stromal cell derived factor-1)
  • Mutation leads to: Guanine -> Adenine (point mutation)
  • Present in 40% in Healthy Asian individuals
  • Interfers ability for the HIV virus to bind
32
Q

Why is mutated CCR-5 gene results in delayed progression to AIDS?

A
  • CCR5 - 2 alleles
  • > function/mutation
  • 10% of Northern Europeans- mutation - non functionable
  • delayed AIDs progression -ineffective binding M tropic variants
33
Q

1% of caucasians have 2 copies of the CCR-5 gene mutated. What does this mean in terms of HIV infection? Consider expression of CXCR-4 in your answer.

A
  • Resistant to HIV
  • As CCR5 is primary viral entry
  • But still express- CXCR4 (T tropic variant)
  • Suggesting M tropic variant is initial infection entry
34
Q
A
35
Q

How can be rapid progression of AIDs be determined?

A

Emergence of T tropic variant

36
Q

Explain the steps of HIV replication in detail?

A
  • Upon HIV entry into T cell -> nucleocapsid removed
  • Reverse transcriptase: Viral ssRNA -> dsDNA
  • > error prone process, 10mistakes/replication
  • > high mutation rate
  • dsDNA integrated into host genome (integrase)
  • > Provirus (dormant/latent) -inactive for long periods of time
  • RNA template degraded by Rnase H enzyme

T cell activation
* upregulation of NF-kb
* >triggers initiation of virus production from provirus DNA
* Transcribes into viral RNA-> (translated) Viral proteins
* Assembled -> new virus particles that bud from the host cell
* >acquires portion of host cell membrane
* >Viral envelope
* Cycle repeats to infect other cells

37
Q

What is the role of the endoplasmic reticulum in the T cell?

A
  • Processing and packaging of proteins
  • Glycosylation
  • > add carbohydrated molecules to protens
  • Significance to protein function, structure and stability
38
Q

What are the 3 clinical course of HIV infection?

A
  • Infection
  • the ‘latent’ stage
  • Development of AIDS
39
Q

Development of AIDs graph

A
  • progressive loss of CD4 T cell function
  • severe immune supression
  • susceptible to opportunistic infections
40
Q

Infection

A
  • Most people no symptoms immediately after infection
  • 15% : symptoms of influenza
  • > fever, malaise, aching muscles, soar throat, swollen lymph nodes
  • Development of swollen lymph nodes - no other clinical symptom identified
  • Production of antibodies against HIV antigen
  • > process called seroconversion
  • Detection of antibofies to HIV- test for infection
41
Q
  • asymptomatic
  • 33% swollen lymph nodes
  • 10 years (AIDs development)
  • Extremely variable
A
42
Q

Development of AIDs is clinically defined by?

A

appearance of major opportunistic infections or by a drop in the CD4 T cell count to** below 200 cells/µl of blood**

43
Q

AIDs symptoms

A

weight loss, night sweats, fever and diarrhoea

44
Q

Opportunistic infection in HIV (AIDs)

A

BIOL2022 Past Papers (10 decks)

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