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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
Q

Trans-species transfer of SIV sm from primate to man resulted in which HIV?

A

HIV-2 (west africa)

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26
Q

Trans species transfers (at least 3) of SIVcpz resulted in what>

A

HIV-1

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27
Q

T-F– with RT there is abundant genetic variation on which selective pressures drive evolution?

A

True- this is why there are so many sub types

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28
Q

T-F– subtypes don’t have much variation?

A

False- tons—ESPECIALLY C

29
Q

What does all this variability do?

A

Create severe problems for vaccine design and anti-viral therapy

30
Q

Infections of all types accounts for how many deaths %?

A

26%

31
Q

Can HIV be passed from mother to child via breast milk?

A

Yes

32
Q

Order the transmission rates of heterosexual contact, male-to-male, and injection drugs from highest to lowest?

A

male-male, injection drugs, heterosexual

33
Q

What cells express CCR5?

A

monocytes/macrophages & memory T cell

34
Q

What cells express CXCR4?

A

CD4 effector T cell subset

35
Q

Viral persistence of HIV is due to what?

A

latent / slow persistent infection of long lived tissue macrophages and memory CD4 t cells

36
Q

CD4 T cells have effects on what other cells?

A 
CD8
B cells
Macrophages
NK Cells
[ that is why when you take out CD4 T cells you elicit immunopathogenesis]
37
Q

T-F–HIV disease progression occurs despite antibodies and cellular immune response?

A

True

38
Q

What 2 types of killing take place in CD4 t cell depletion?

A

Direct killing

indirect killing

39
Q

What 2 principals are behind indirect killing (CD 4 depletion)?

A
  1. immune clearance (bystander T cell killing)

2. Syncytium formation producing giant cells

40
Q

What are the 2 key indicators for speed of progression to symptoms?

A
  1. Virus Load

2. CD4 T cell count

41
Q

There are different viral factors leading to variability of disease progression- what 2 things may change this variability in regards to polymorphism?

A
  1. strains may differ in virulence

2. strains may differ in immune evasion

42
Q

T-F CCR5 tropic strains are more rapid CD4 killers?

A

False- the CXCR4 strains are

43
Q

T-F- syncytium formation results in a decrease in the rate of progression?

A

False- an increase

44
Q

Homozygous CCR5 mutations causes what?

A

resistance to progression of HIV

[heterozygosity causes delay of progression]

45
Q

What are the 3 things that promotes resistance of HIV progression?

A
  1. CCR5 mutation
  2. CCR5 promote mutation
  3. MHC class I alleles
46
Q

Primary HIV infection presents in what 2 ways ?

A
  1. asymptomatic frequently

2. mononucleosis like syndrome

47
Q

Early symptomatic HIV phase presents how?

A

lymph node swelling, thrush, fever, weight loss and shingles

48
Q

Late phase HIV presents with what?

A

numerous opportunistic infections and cancers

49
Q

AIDS is defined as what?

A

seropositive for HIV with
either 1. CD4<200 or 2. one or more aids indicator diseases [encephalopathy, opportunistic infection, unusual malignancy]

50
Q

HIV lab diagnosis starts with initial screening by ELISA or latex agglutination for p24 capsid—what is the confirmation for this?

A

Western blot gp 120

51
Q

Why is PCR required for detection of neonatal HIV?

A

no robust antibody response to detect

52
Q

What is quantifiable HIV RNA PCRs good for?

A
  1. Prognostic indicator

2. response to therapy

53
Q

What do the nucleoside inhibitors inhibit? Non-nucleside inhibitors?

A

Both inhibit RT

54
Q

What does the infusion inhibitors bind to?

A

gp41 and thus prevents fusion

55
Q

What is the goal of HIV treatment?

A

reduce viral load to as low as possible, lower levels lead to less virus replication and less evolution

56
Q

How many antivirals are used in HAART?

A

3 or more

57
Q

T-F HAART therapy wipes out HIV?

A

FAlse– does reduce morbidity, but ongoing detectable levels of viremia still exist

58
Q

What if we discontinue HAART?

A

resurgence of viral replication and progression to AIDS

59
Q

What happened to marrow transplant patient receiving CCR5 mutated bone marrow?

A

low to no virus levels

60
Q

All vaccine attempts have focused on what?

A

subunit vaccines- remains unclear if either broadly neutralizing antibodies or broadly reactive T cells can be generated by HIV vaccines

61
Q

IS mounting T cell responses sufficient for protection?

A

No- demonstrated by Merck/NIH study focusing on T cell responses

62
Q

T-f— there are many conserved sites on glycoprotein that have been identified and bind/neutralized by Abs?

A

False- very few– all sites of Ab are conformationally dependent epitopes.

63
Q

Have microbicides been proven to be effective in preventing HIV?

A

Yes- tenofovir (RT inhibitor)

64
Q

What do we use for post exposure prophylaxis?

A

RT and protease inhibitors

[perinatal antiviral treatment, healthcare workers]

65
Q

Where is HTLV-1 found?

A

tropical areas- southern japanese islands, and carribean etc.

66
Q

How is HTLV-1 transmitted?

A

Same as HIV

67
Q

What two diseases do we see from HTLV-1?

A
  1. Adult T cell leukemia/lymphoma

2. Peripheral neuropathy

68
Q

Does viral protein TAX appear to promote the progression of HTLV-1 disease?

A

No but promotes the initial formation of the malignancy

69
Q

Is there a HTLV vaccine? IS treatment very effective?

A 
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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