HIV Flashcards

(36 cards)

1
Q

What does Gag do

A

Gag: group specific antigen.

Viral core proteins: MA (matrix), CA (capsid), NC (nucleocapsid) - formation of the inside part of the virus

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2
Q

What does Pol do

A

Pol: polymerase
Enzymes: PR (protease), RT (reverse transcriptase), IN (integrase) - converting viral RNA into double stranded DNA

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3
Q

What does Env do

A

envelope glycoprotein

Su (surface), TM (transmembrane) - interaction with hsot receptors and infection into the cell

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4
Q

What does reverse transcriptase do

A

copying of an RNA template (the viral genome) into a double stranded DNA copy

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5
Q

What is integration

A

covalent insertion of viral cDNA into the genome of the infected cell, to form the provirus

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6
Q

What is the consequence of integration

A

an infected cell cannot be cured of retroviral infection, other than by killing that ell. This makes it impossible to eradicate naturally an infected animal or a retroviral infection

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7
Q

What is the outer layer of the HIV virus

A

lipid bilayer with protruding Env spikes (heterodimer of trimers SU3TM3). Surface and transmembrane proteins.

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8
Q

What is the inner layer of the HIV virus

A

Gag proteins. In the immature particle, Gag itself forms a single shell.

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9
Q

What is the the mature particle

A

MA associates with the membrane, CA forms the conical capsid, and NC coats the viral RNA genome. The core contains two genomic RNA strand, tRNALys3, and about 50 copies of each viral enzyme (PR, RT and IN)

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10
Q

Describes the steps of viral replication

A

Attachment and receptor binding. CD4 and co receptors CXCR4 and CCR5
Membrane fusion - allow entry of the core of virus
Uncoating and reverse transcription - minimise immune response
Nuclear import
Integration of DNA into genome
Allows transcription of viral genes and RNA processing
Nuclear export
Translation
Assembly
Budding
Maturation

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11
Q

What does CD4 binding cause

A

conformational rearrangement of the protein to revela co-receptor binding site. New binding sites can be used for HAART.
After co receptor binding, more rearrangement. Fusion peptide inserts into viral membrane. Creates 6-helix bundle formation to allow membrane fusion

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12
Q

What is reverse transcriptase

A

heterodimer of p66 and p51
RT displays three distinct enzymatic activates:
RNA dependent DNA polymerase - coverts viral RNA into cDNA
RNAasH (cleaves RNA from RNA/DNA hybrid)
DNA-dependent DNA polymerase - makes double strand.

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13
Q

What clade dominates in southern afria

A

Clade C

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14
Q

What clade dominates in europe

A

Clade B

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15
Q

What clade dominates in northern africa

A

Clade A

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16
Q

What does APOBEC do

A

converts cytosine to uracil within RNA leading to additional mutations. This is an anti-viral strategy as stop codons could be made.

17
Q

What is the in-vitro ranking of HIV-1 regulatory proteins

A

Tat/Rev>Vif>Nef>Vpr/Vpu

18
Q

What does tat do

A

Potent activator of viral transcription

19
Q

What does rev do

A

mediates unspliced RNA nuclear export

20
Q

What does vif do

A

critical regulator of virus infectivity. Acts against APOBEC gene. Stops introduction of additional mutations.

21
Q

What does nef do

A

immune modulator, T-cell activation, virus infectivity. Remove CD4 from surface of the cell.

22
Q

What does vpu do

A

immune modulator, virus release. Tetherin prevents virus from being released. Vpu marks tetherin for destruction.

23
Q

What does vpr do

A

ell cycle, virus nuclear import

24
Q

What does SAMHD1 sdo

A

suppresses RT in myeloid cells by hydrolysing dNTPS

25
What does SERINC do
Interfere with viral entry
26
What is the most common combination of HAART
2* NRTI and 1 NNRTI or Protease inhibitor
27
What are latent viral reservoirs
barrier to an HIV cure is the integrate provirus. ART prevents new cell infection Some cells don't die and fall back to a resting state - not actively producing virus but have HIV genome introduced. Have silent HIV transcription. Latent pool persists in the presence of drugs. After drug removal, there is activation stimulus so there will be viral rebound.
28
What is associated with elite control
HLA B57 or B 27 - HLA molecule has mutation in tail region so nef can't remove it from the cell surface
29
What are CRR5 inhibitors
(chemokine receptor antagonist) - Maraviroc
30
What are fusion inhibitors
Enfurvitide. Targets envelope protein once it's bound to CD4.
31
What are RT inhibitors
nucleoside analogues reverse transcriptase inhibitors (NRTI) - no 3'OH leads to chain termination (e.g. Zidovudine; Lamivudine. Non-nucleoside reverse transcriptase inhibitors (NNRTI) - Allosteric RT inhibitors - do not bind to active site. Blocks initiation of RT e.g. Efavirenz and nevirapine.
32
What are integrase inhibitors
raltegravir - blocks strand transfer reaction
33
What is acute infection controlled by
Acute infection is controlled by a strong CD8 T cell response Then produce non-neutralising anti-Env antibodies Then neutralising anti-Env antibodies Because virus is mutating at such a fast rate, it prevents the antibodies from working
34
How is HIV diagnosed
ELISA test for presence of anti-p24 antibodies in the serum. Only detects individuals who have seroconverted A positive sample is retested using a different ELISA or Western Blot Confirmation by quantitative reverse transcription linked polymerase chain reaction to detect HIV genomic RNA in the blood
35
What is one of the most common causes of cancer in people with HIV
Kaposi's Sarcoma - herpes virus 8, fungal pneumonia, toxoplasmosis
36
What is a major target in acute HIV-1 function
Gut-associated lymphoid tissue is the major target tissue in the acute HIV-1 function HIV spreads rapidly to the CD4 T cells in the lymphoid tissue of the guy GALT is virtually denuded of T cells Immune integrity of GALT never recovers, even during therapy