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Virology > HIV > Flashcards

HIV Flashcards

1
Q

How many people are infected with HIV and how many deaths each year

A

37 million affected
1.8 million new infections each years
1 million die

New infections fallen by 11% since 2011

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2
Q

What are the 4 types of HIV

A

HIV M, N, O, P

HIV M, N, O and are from Chimps, HIV P Is from gorillas

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3
Q

What did HIV N Cause

A

Only caused 13 infections

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4
Q

What did HIV O Cause

A

Circa 1920, caused tens of thousands of infections

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5
Q

How many subtypes of HIV 1 and HIV 2 are there

A

HIV 1 - 9 subtypes

HIV - 2 8 subtypes

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6
Q

Describe the genome organisation fo HIV

A

9700 nucleotides long

LTR at each end which are important for replication

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7
Q

Describe the HIV Genes

A

GAG: Capsid, Nucelopcapsid, Matrix
Pol: Reverse transcriptaes, Integrase, Protease
Env: Envelope glycoproteins GP120 and GP41

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8
Q

What are the regulatory auxillary proteins

A

Tat - stimulates processive transcription

Rev - binds RRE and facilitates nuclear export of unspliced or singly spliced RNA

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9
Q

What are the accessory auxillary proteins

A

Nef - can decrase expression of MHC, CD4 and CD8 receprots

Vif - antagonist of cellular protein APOBEC3G

Vpu - can cause G2 arrest –> facilitating entry of the pre-integration complex

Vpu - affects viral release as can disrupt the Env-CD4 complex

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10
Q

What is the target of nAB in HIV

A

The envelope glycoprotein is the only target

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11
Q

What is the structure of the envelope gylcoprotein

A

It is trimer of heterodimers of gp120 and gp41

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12
Q

What is involved in the reverse transcriptase complex

A 
2xssRNA genomes
tRNA primers
viral protease
reverse transcriptase
protease
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13
Q

What is involved in the pre-integration complex

A 
dsDNA
Protease
Integrase
reverse transcriptase
Matrix proteins
Vpr
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14
Q

What are some key factors for integration

A

Emerin
Lens-Derived Epithelium Growth Factor (LDECF)
Barrier to autointegration factor (BAF)

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15
Q

What binds to HIV when latent

A

Nf-kB, HDACI and p50

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16
Q

In the active state how is HIV activated

A

Stimulation, i.e. TNF, induces the removal of HDACI and p50
Replaced with CBP/p300 –> causes acetylation
Tat interacts with the pTEFb complex –> comprised of CDK9 and cyclin T1 –> this recruits the stem loop structure TAR which acts as a promoter element in the viral LTR leading to production of full length transcripts

17
Q

What cells does HIV infect

A

Infects cells of mucosal and cutaneous immune system
M cells - bowel epithelium
Dendritic cells - cervical and vaginal epithelium
Activated T Cells - genital sores, particularly HSV2

18
Q

what is the major site of initial HIV infection

A

The GALT

19
Q

What are the proposed mechanisms of CD4+ T Cell depletion

A

Direct killing by HIV (Fas mediated apoptosis, VPr induced apoptosis of G2 arrest, disruption of cell membrane integrity, accumulations of unintegrated DNA, integration of the provirus)

Killing of infected cells by HIV-1 specific CD8+ T cells
Extensive bystander immune activation
Antibody mediated cellular toxicity

20
Q

What are the consequence of persistent immune activation

A

Increased cell turover
Skewign lymphoctes
Induction of cellular exhaustion, sensecence and low renewal potential
The regenerative capacity is progessively lost

21
Q

Describe the characteristics of the children with HIV who were ‘elite controllers’

A

Low expression of CCR5
Low frequency of PD1+ T Cells
Low immune activation even with high l evels of viral replication

22
Q

What mechanisms contribute to persistent

A

1) Regulation of gene expression –> i.e. acetylation at HIV promoter and chromatin remodelling etc
2) Immune activation –> periodic activation of target cells, upregulation of molecules modulating T cell survival e.g. PD1, decreased ability of immune system to recognise and destroy HIV infected cells
3) Specific HIV infected T cell subsets may be important
4) Pathways promoting lifelong memory may promote persistent infection
5) Cellular and tissue sources of persistence

23
Q

Strategies to elimnate persistently affected cells

A

1) Deliberate infuction of viral gene expression
2) Recognising surface antigens on infected cells and targeted cell destruction
3) develop therapeutic vaccine to enhance immune mediated clearance of cells
4) Antibody production to control cell-cell virus transmission
5) Immune based therapeutics to reduce chronic immune activation

24
Q

What is CD32a

A

Recently discovered on D4+ T cells harbouring latent HIV genomes
It is a receptor for IgG Fc
It is not present on normal CD4+ cells, but is on monocytes and platelts
THIS COULD BE A POTENTIAL TARGET TO DESTROY LATENTLY INFECTED CELLS! But it may only mark cells circulating in the blood

Virology (6 decks)

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