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4 PID Unit > 43 RETRO > Flashcards

43 RETRO Flashcards

1
Q

T-F– Retroviruses are naked? What shape are they?

A

False- enveloped

-Icosahedral

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2
Q

What type of genome does a retrovirus have?

A

single stranded, diploid (+) RNA

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3
Q

What is the retrovirus genome transcribed by?

A

virus encoded, vision associated reverse transcriptase

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4
Q

T-F–most retroviruses cause cell death.

A

False

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5
Q

What type of retrovirus is a virus of vertebrates? what does it cause?

A
  1. Oncoretrovirus

2. Cancers-sarcoma, leukemia, carcinoma

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6
Q

What type of virus is a slow virus? What ties of cells does it effect?

A
  1. Lentivirus
  2. cells of immune system- macrophages and lymphocytes
    [HIV1-2]
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7
Q

What type of retrovirus causes characteristic changes in tissue culture where the cells fill up with vacuoles? What disease are they associated with?

A
  1. Spumavirus

2. not associated to date

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8
Q

What 2 human retroviruses cause disease?

A
  1. Human T-cell leukemia HTLV (4 groups)

2. Lentivirus

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9
Q

Is HIV-1 or 2 more virulent?

A

HIV 1 - 2 has west african origins

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10
Q

What HIV-1 group causes most human disease? What is the US sub type?

A

Group M- sub type B

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11
Q

The glycoprotein of retroviruses are made up of what 2 proteins?

A

gp 120- SU VAP

gp 41- TM fusion

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12
Q

What virally encoded enzymes are found in retroviruses?4

A

Reverse transcriptase
ribonuclease
integrase
protease

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13
Q

What 2 receptors does HIV entry require?

A

CD4 and CCR5 or CXCR4 [gp120 binds both]

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14
Q

What HIV glycoprotein mediates fusion after it is exposed?

A

41

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15
Q

What is found at either end of the reverse transcribed DNA?

A
  1. long terminal repeats—required to work with integrase as it is inserted into DNA
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16
Q

How are different viral proteins created from a cellular RNA polymerase that creates a SINGLE full length transcript of the integrated virus?

A

Splicing!

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17
Q

There are 3 polyproteins translated from HIV- what does gag get cleaved into?

A

capsid p24 and other capsids

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18
Q

There are 3 polyproteins translated from HIV- what does pol get cleaved into?

A

PR, RT and IN

protease, reverse transcriptase, integrase?

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19
Q

There are 3 polyproteins translated from HIV- what is env cleaved into?

A

gp120 and gp41

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20
Q

During assembly budding and maturation of the retrovirus–what all accumulates and associates in the cytoplasm?

A

full length (unspliced) viral protein, gag and pol polyproteins

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21
Q

Where do viral glycoproteins (env) go?

A

made on ER/golgi and incorporated into plasma membrane

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22
Q

Where does assembly of the vision occur?

A

at plasma membrane

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23
Q

Does retrovirus bud from cell in a cytolytic manner?

A

No

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24
Q

What processes gag and pol polyproteins to generate mature viral particles that is infectious?

A

virally encoded protease

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25
Trans-species transfer of SIV sm from primate to man resulted in which HIV?
HIV-2 (west africa)
26
Trans species transfers (at least 3) of SIVcpz resulted in what>
HIV-1
27
T-F-- with RT there is abundant genetic variation on which selective pressures drive evolution?
True- this is why there are so many sub types
28
T-F-- subtypes don't have much variation?
False- tons---ESPECIALLY C
29
What does all this variability do?
Create severe problems for vaccine design and anti-viral therapy
30
Infections of all types accounts for how many deaths %?
26%
31
Can HIV be passed from mother to child via breast milk?
Yes
32
Order the transmission rates of heterosexual contact, male-to-male, and injection drugs from highest to lowest?
male-male, injection drugs, heterosexual
33
What cells express CCR5?
monocytes/macrophages & memory T cell
34
What cells express CXCR4?
CD4 effector T cell subset
35
Viral persistence of HIV is due to what?
latent / slow persistent infection of long lived tissue macrophages and memory CD4 t cells
36
CD4 T cells have effects on what other cells?
``` CD8 B cells Macrophages NK Cells [ that is why when you take out CD4 T cells you elicit immunopathogenesis] ```
37
T-F--HIV disease progression occurs despite antibodies and cellular immune response?
True
38
What 2 types of killing take place in CD4 t cell depletion?
Direct killing | indirect killing
39
What 2 principals are behind indirect killing (CD 4 depletion)?
1. immune clearance (bystander T cell killing) | 2. Syncytium formation producing giant cells
40
What are the 2 key indicators for speed of progression to symptoms?
1. Virus Load | 2. CD4 T cell count
41
There are different viral factors leading to variability of disease progression- what 2 things may change this variability in regards to polymorphism?
1. strains may differ in virulence | 2. strains may differ in immune evasion
42
T-F CCR5 tropic strains are more rapid CD4 killers?
False- the CXCR4 strains are
43
T-F- syncytium formation results in a decrease in the rate of progression?
False- an increase
44
Homozygous CCR5 mutations causes what?
resistance to progression of HIV | [heterozygosity causes delay of progression]
45
What are the 3 things that promotes resistance of HIV progression?
1. CCR5 mutation 2. CCR5 promote mutation 3. MHC class I alleles
46
Primary HIV infection presents in what 2 ways ?
1. asymptomatic frequently | 2. mononucleosis like syndrome
47
Early symptomatic HIV phase presents how?
lymph node swelling, thrush, fever, weight loss and shingles
48
Late phase HIV presents with what?
numerous opportunistic infections and cancers
49
AIDS is defined as what?
seropositive for HIV with either 1. CD4<200 or 2. one or more aids indicator diseases [encephalopathy, opportunistic infection, unusual malignancy]
50
HIV lab diagnosis starts with initial screening by ELISA or latex agglutination for p24 capsid---what is the confirmation for this?
Western blot gp 120
51
Why is PCR required for detection of neonatal HIV?
no robust antibody response to detect
52
What is quantifiable HIV RNA PCRs good for?
1. Prognostic indicator | 2. response to therapy
53
What do the nucleoside inhibitors inhibit? Non-nucleside inhibitors?
Both inhibit RT
54
What does the infusion inhibitors bind to?
gp41 and thus prevents fusion
55
What is the goal of HIV treatment?
reduce viral load to as low as possible, lower levels lead to less virus replication and less evolution
56
How many antivirals are used in HAART?
3 or more
57
T-F HAART therapy wipes out HIV?
FAlse-- does reduce morbidity, but ongoing detectable levels of viremia still exist
58
What if we discontinue HAART?
resurgence of viral replication and progression to AIDS
59
What happened to marrow transplant patient receiving CCR5 mutated bone marrow?
low to no virus levels
60
All vaccine attempts have focused on what?
subunit vaccines- remains unclear if either broadly neutralizing antibodies or broadly reactive T cells can be generated by HIV vaccines
61
IS mounting T cell responses sufficient for protection?
No- demonstrated by Merck/NIH study focusing on T cell responses
62
T-f--- there are many conserved sites on glycoprotein that have been identified and bind/neutralized by Abs?
False- very few-- all sites of Ab are conformationally dependent epitopes.
63
Have microbicides been proven to be effective in preventing HIV?
Yes- tenofovir (RT inhibitor)
64
What do we use for post exposure prophylaxis?
RT and protease inhibitors | [perinatal antiviral treatment, healthcare workers]
65
Where is HTLV-1 found?
tropical areas- southern japanese islands, and carribean etc.
66
How is HTLV-1 transmitted?
Same as HIV
67
What two diseases do we see from HTLV-1?
1. Adult T cell leukemia/lymphoma | 2. Peripheral neuropathy
68
Does viral protein TAX appear to promote the progression of HTLV-1 disease?
No but promotes the initial formation of the malignancy
69
Is there a HTLV vaccine? IS treatment very effective?
``` No Not really (chemo for adult T cell leukemia, slow growing slightly responds to RT inhibitor) ```

4 PID Unit (6 decks)

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