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22 Cards in this Set

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NEF (Negative factor)

- enhances what viral factors x2
Infectivity

Pathogenicity
T/F - NEF is essential for replication.
False
In general, list all the functions of NEF in terms of downregulating?

If possible specify mechanism of each.

Specificy results of each
Downregulate MHC-I
- endocytosis
- makes cell invisible to CD8 CTLs

Downregulate MHC-II
- mechanism unk
- prevents cell activation

Down regulate IL-2R
- impairs at gene level and prevents cellular response to IL-2
- Impairs cell function and proliferation

Downregulates CD4
- Removes CD4 at cell surface, then combines with proteosome for degradation pathway.
- Prevents superinfection
- Prevents APC (MHC-II) interaction
- Enhances viral release
In general, list all the functions of NEF in terms of kinases?

If possible specify mechanism of each.

Specificy results of each
1. Binds with PAK protein kinase
MECHANISM
Binds PAK
Causes release of NFkB in to nucleus
NFkB binds to U3 in LTR
RESULTS:
Provirus activation

2. Binds to Ick and TYR PKs
MECHANISM
Just binds to them
RESULTS:
1. Interferes with signal transduction
2. Prevents cell activation
In general, list all the functions of NEF in terms of viral spreading?

If possible specify mechanism of each.

Specificy results of each
Mechanism:
Increases DC-SIGN in dendritic cells by blocking endocytosis

Results:
More HIV-1 will attach to DC, causing more to arrive at local lymph node where a lot more cells can be infected.
In general, list all the functions of NEF in terms of Macrophages?

If possible specify mechanism of each.

Specificy results of each
Mechanism #1:
Induce macrophage to produce MIP1alpha and MIP1beta.

Results #1:
Attract more CD4 cells T-cells via chemotaxis

Mechanism #2:
Induces macrophage to produce more Factor X

Results #2:
Cell activation for replication permissitivity
In general, list all the functions of NEF in terms of apoptosis?

If possible specify mechanism of each.

Specificy results of each
Mechanism #1:
Binds to p53, reducing its half life

Mechanism #2:
Binds to ASK1, inhibiting the FAS and TNF apoptosis pathway

Mechanism #3:
Binds to PI3-K, which inactivates BAD, which increases Bcl-2 (anti-apoptic protein)

Results:
Prevent/block Apoptosis
In general, list all the functions of NEF in terms of trafficking?

If possible specify mechanism of each.

Specificy results of each
Mechanism:
Binds to cellular trafficking proteins.

Results:
Disrupts trafficking
Describe all the functions of TAT and include the mechanisms if possible. x11
1. Anti-Terminator of transcription
(binds to TAR & RNA PY II)

2. Upregulates transcription
(binds to U3)

3. Co-receptor expression inducer in UNINFECTED cells
(TAT is secreted to uninfected cells)

4. Trigger-Activation Promoting Replication in UNINFECTED cells
(TAT is secreted to uninfected cells)

5. Collagenase IV stimulator
(role in KS)

6. Angiogenesis stimulator
(role in KS)

7. Neurotoxin per se
(degrades MAP2, collapse of cytoskeleton filaments)

8. Apoptosis Inducer

9. IFN Blocker
(Binds to RNA-dependent PK - elF2alpha)

10. Downregulates MHC-1 and other genes
(Binds to TAFII250)

11. Upregulates cytokine genes such as IL-1, TNFalpha, TNFbeta, TGFbeta
(can activate provirus)
REV proteins regulate what?

REV essential for what?

REV mediates transition of?

REV functions x2
(include mechanism)
expression of virion proteins

virus production

early to late phase

1. "Nuclear shuttle protein"
(binds to RRE on mRNA, then transports these to cytoplasm for translation)

2. Retards splicing
(binds to splicing machinary)
What is the criteria for mRNA in order for RRE to bind to it?

Is there an exception to the rule?

What are all the mRNAs without RRE's on it?
must be unspliced or spliced once

Yes, VPR can be spliced twice

NEF, TAT, REV
VPR functions x4
Apoptosis Inducer

Transports preintegration complex to nucleus

Arrests infected cells at G2 phase
(inhibits activity of p34-cdc2-cyclin B kinase complex)

Gene expression stimulation
(driven by HIV LTR)
VPR is required for what?

Does this how?
Replication in non-dividing cells (monocytes/macrophages)

Allow ENTRY into nucleus
T/F - VIF is required for replication?
False
VIF:

- where is it
- important factor in what? x2
- major function
In the virion

Tropism
Efficient replication
(increases maturity and assembly)

Prevents incorporation of cellular enzyme, cytidine deaminase (APOBEC3G) into virion.
In what type of cells are VIF proteins essential in?
Non-permissive cells
(CD4 T-cells, macrophages)
expressing cytidine deaminase (APOBEC3G).
What happens in a non-permissive cell infected with a VIF-deletion mutant? x3
Great reduction in infectious virions.

Degradation of provirus

Particles made are NOT infectious.
What does the cytidine deaminase (APOBEC3G) do?

What does this result in? x2
This is a editing enzyme that cause mutations in the MINUS provirus DNA.

It makes C's into U's, leading to hypermutant provirus.
In the end, the G's are A's on the plus viral (+)RNA strands.

RTase second strand DNA synthesis greatly diminished

Increases lability of viral genome
Why does cytidine deaminase (APOBEC3G) target provirus DNA?
B/c it is MINUS single stranded. The repair done to the MINUS strand would make the mutation permanent.

It would not work on double stranded DNA b/c of the repair mechanisms associated with dsDNA would fix the original mutation.
T/F - VPU is essential for replication.
False
VPU:

- found where x2
- functions x2
- mechanism
Golgi and PM

1. Enhance virus release
2. Degrades CD4

Binds cytoplasmic tail of CD4 and Ub-mediated proteolysis in proteosome.
What inhibition would block VPU mediated degradation of CD4?
Inhibit proteosome