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x Virology Term 2 Post-quiz Jen > HIV/AIDS > Flashcards

HIV/AIDS Flashcards

1
Q

What is the structure of the HIV virion?

A

enveloped, two identical strands of +ssRNA.

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2
Q

does the virion carry enzymes?

A

Yes, carries 3 enzymes: reverse transcriptase, integrase, protease.

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3
Q

List the life cycle steps of the HIV life cycle

A

attachent, co-receptor binding, fustion, reverse transcription, integration, transcription, translation, clevage of precursor proteins, nucleocapsid assembly, budding, virion maturation.

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4
Q

HIV: tropism?

A

HIV likes to infect host’s CD4+ cells.

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5
Q

Is binding to CD4 antigen alone enough to permit entry of HIV into host cells?

A

NO, must interact with host cell co-receptor, usually CCR5. Then fusion of the viral envelope occurs, resulting in nucleocapsid entry.

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6
Q

Once the HIV nucleocapsid is inside the host cell, what happens?

A

The HIV/s reverse transcriptase uses a host tRNA as a primer, and makes a sDNA copy of the RNA genome. Eventually yields a linear dsDNA copy of the HIV genome.

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7
Q

what helps HIV integrate into the host cell genome?

A

HIV integrase enzyme

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8
Q

For replication to occur, what needs to happen to the integrated HIV genome?

A

must be translated by host cell RNA polymerase to make HIV mRNA that can be translated into proteins.

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9
Q

what activates the expr of HIV mRNA from the integrated HIV genome?

A

activated CD4 cells

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10
Q

what does the HIV protease do?

A

cleaves HIV precursor proteins into mature HIV products.

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11
Q

How are new HIV virions formed?

A

by budding out of the capsid via a modified host cell plasma membrane. virion at this point is NOT fully mature

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12
Q

Does the reverse transcriptase that makes the DNA copy of HIV have proofreading functions? what is the result of this

A

NO: these replication enzymes are error prone. effect is that HIV mutates frequently. A billion HIV mutants are made daily.

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13
Q

DNA: transmission route?

A

sexual contact, infected blood

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14
Q

a higher risk of transmission can be attributed to what?

A

higher concentration of HIV aka viral load

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15
Q

Routes of transmission: (3+)

A

IV drug use
sex (vag, anal: receptive partner is at higher risk)
other includes transplacental, perinatal, breastfeeding, blood transfusions, needle stick

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16
Q

Prevention strategies for HIV: (3)

A

condoms
circumcision (in some popns)
microbicidal creams

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17
Q

Early HIV infection: what does it appear as?

A

Acute infection. can look like mono, fever, lymph nodes, fatigue

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18
Q

what is the level of viremia during this early phase?

A

extremely high.

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19
Q

what happens to the number of CD4+ t cells during acute HIV infection?

A

dramatic decrease

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20
Q

what does an infected person do in response to acute HIV infection?

A

mounts a robust immune response. following this response, viral load decreases, and the number of CD4+ t cells is partially restored back to normal

21
Q

at what point does the HIV load attain its set point?

A

after the acute infection and subsequent immune response

22
Q

does the immune system ever clear the HIV infection?

A

NO

23
Q

what other virus does the body not ever clear?

A

Some of the Hep viruses: Hep A and E are cleared, Hep B can be but may not be, Hep C is not usually cleared, Hep D can be, herpes NOT cleared.

24
Q

What is a predictor of progression of HIV to AIDS?

A

viral load

25
Q

what is a proxy for the level of immunosuppression of the body in HIV/AIDS?

A

CD4+ counts

26
Q

Measles does what to T cells?

A

puts them in an anergic state

27
Q

IF you get a PPD test after you have just been infected with measles, will it be positive or neg? why?

A

negative (even if you have Tb), because the T cells are anergic and will not respond

28
Q

Measles: trophism?

A

pantrophic

29
Q

what 3 viruses are most concerning if they are transmitted transplacentally?

A

Rubella, CMV (1st tri is worst), parvo (problem at any point).

30
Q

The decrease in viral load correlates with what

A

seroconversion

31
Q

during chronic infection, HIV replication is extensive in what tissue

A

lymphoid

32
Q

how do we diagnose chronic HIV infection?

A

HIV serology: ELISA, western blot

33
Q

during chronic infection, what is happening to the immune system?

A

slow relentless decline in CD4+ T cell count

34
Q

what does HIV do to evade immune response?

A

mutates in process called viral escape

35
Q

what is one key mechanism underlying disease pathogenesis?

A

chronic activation of the immune system. leads to decreased ability to control infection, promoges HIV rep in CD4+ t cells

36
Q

what predicts the rate of progression to AIDS?

A

the HIV viral load set point that is established following acute infection

37
Q

How is AIDS defined?

A

presence of one of 27 conditions indicative of severe immunodeciciency
HIV infection in person with a CD4+ count less than 200 cells/mm3 OR CD4+ T cell less than 15% of lymphocytes

38
Q

What other infections are often seen with AIDS?

A

Kaposi’s sarcoma (associated with HHV-8)
Burkett’s lymphoma (asociated with EBV)
Cervical/anal cancers (assocd with HPV)

39
Q

HIV infectd people are at risk for what other viral infections?

A 
Hep B
Hep C
HSV
CMV
reactivated EBV (oral hairy leukoplasia)
40
Q

The mutation rate of HIV means what for treatment?

A

it can mutate and become resistant to all known drug classes.

41
Q

what does HAART stand for

A

highly active antiretroviral therapy

42
Q

what does HAART consist of?

A

3 antiretroviral drugs of at least 2 different classes. (class = mechanism of action)

43
Q

what is immune reconstitution syndrome?

A

may occur in some patients after HAART is initiated. due to rapid expansion of CD4+ T cells that increase inflammatory response if there is a co-infection.

44
Q

Nucleoside Reverse Transcriptase Inhibitors (nRTI). what do they look like? what do they do, biochemically?

A

They look like nucleosides, and they terminate the growing HIV DNA chain

45
Q

Non-nucleoside Reverse Transcriptase Inhibitors (nnRTI). what do they look like, what is the mechanism of action?

A

do not look like nucleosides. mech: inhibit reverse transcriptase enzyme activity, block synthesis of HIV DNA

46
Q

Protease Inhibitors. mechanism?

A

block the protease activity of HIV protease. therefore prevent production of infectious HIV virions

47
Q

CCR5 antagonists. mechanism?

A

block HIV virion binding to co-receptor, CC5R. prevents HIV from infecting cells

48
Q

Fusion inhibitors. mech?

A

interfere with formation of gp41 fusion complex. block fusion of viral envelope with the host cell plasma membrane. HIV fails to infect cells

49
Q

Integrase inhibitors. mech?

A

block integrase, prevent integration of HIV proviral DNA. virus production cannot occur.

x Virology Term 2 Post-quiz Jen (4 decks)

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