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Infect & Immune 2 AW, DJT & ISB > AW L1 HIV > Flashcards

AW L1 HIV Flashcards

1
Q

HIV infection has slowed recently due to….

A

policy, knowledge, reducing risk factors.

Not drugs.

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2
Q

HIV primarily infects …………. cells

A

CD4+ T cells

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3
Q

What receptor on the HIV binds first?

A

GP 120

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4
Q

Coreceptors on HIV… (2)

A

CCR-5
CXCR4
(usually uses one or the other)

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5
Q

Co receptor binding causes a conformational change in order to….

A

bring GP41 closer to the surface - binding the membrane fusion - single stranded RNA from virus enters

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6
Q

HIV is super smart becuase

A

it uses the host cell machinery to replicate its DNA

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7
Q

HIV is characterised by …….

A

chronic immune system activation leading to dysfunction

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8
Q

HIV results in increased expression of ………. on ……. and …… cells

A

CD38 on CD4 and CD8 cells

also increased T cell proliferation

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9
Q

What is the best correlation for progression of the disease….

A

levels of CD38 expression on CD4 and CD8 cells

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10
Q

Despite immune deficiency virtually all components of the immune system show activation, including (4)

A

B cells
NK cells
T cells
macrophages

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11
Q

Mutation in europeans means….

it inactivates….

A

resistance as the particle cannot enter the T cells.
inactivates CCR-5
(related to primary spread of the virus rather than enhanced immune response)

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12
Q

CD4 and CD8 expression is ……………. in HIV

A

elevated

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13
Q

Increased levels of pro inflam cytokines such as ………….. in HIV

A

IFN-a, TNF-a, IL6

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14
Q

Elevated CD4 T cells but CD4 t cells depletion, why?

A

only infected T cells stimulated to proliferate - defective as viral DNA has been introduced

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15
Q

Opportunistic infections in HIV e.g. (5)

A 
Candida
Cytomegalovirus
Herpes simplex
TB
Mycobacterium avium complex
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16
Q

What used to be the most common cause of death amongst AIDs patients

A

TB

- increases the likelihood that infection with m. tuberculosis will lead to TB disease

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17
Q

How does the presence of TB affect the HIV infection

A

allows more rapid progression of the HIV

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18
Q

Most HIV drugs have been developped against what target?

A

reverse transcriptase and protease (AZT)

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19
Q

Virus undergoes mutations which is a problem with treatment becuase

A

develops resistance

20
Q

Why treat in combination….

A

treatment with a single drug tends to select mutant strains

21
Q

5 classes of HIV drugs

A
  1. NRITIs
  2. NNRTIs
  3. Protease inhibitors
  4. Entry/fusion inhibitors
  5. Integrase inhibitors
22
Q

Gerneally HARRT treatment involves …………… different antiretrovirals from at least ………… classes

A

3 different drugs

2 classes

23
Q

HAART stands for

A

Highly active antiretroviral therapy

24
Q

NRTI stands for

A

nucleoside reverse transcriptase inhibitors

25
Q

NRTIs mode of action

A

act as chain terminators or inhibitors at the substrate binding site of reverse transcriptase

26
Q

NNRTIs stands for

A

Non-nucleoside reverse transcriptase inhibitors

27
Q

NNTRIs mode of action

A

bind to allosteric non-bonding site of reverse transcriptase, causing conformational change in active site - inhibit viral DNA replication

28
Q

Protease inhibitors mode of action:

A

non-scissible substrate analogue for HIV protease

Protein does not get chopped up so the new virus is not viable

29
Q

during reproductive cycle of HIV a specific protease is needed to

A

process GAG and POL polyproteins into mature HIC components

30
Q

PI contain a ………. bond instead of a ………. bond

A

hydroxyethylene bond instead of a peptide bond

31
Q

Fusion inhibitor e.g.

A

fuzeon (36 amino acid peptide produced synthetically)

32
Q

Fuzeon mode of action

A

blocks entry of HIV into cells (CD4 or T cells)

33
Q

Fuzeon works by mimicking….

A

components of GP41

34
Q

Why is fuzeon super-dooper awesome?

A

Targets the virus so less toxic & prevents infection in the first place

35
Q

Entry inhibitors e.g.

A

Maraviroc

36
Q

Maraviroc inhibits …..

mode of action….

A

CCR5

Blocks HIV attachment to CCR5, halting HIV replication.

37
Q

Maraviroc is only effective against….

A

HIV that uses the CCR5 receptor site (HIV using CXCR4 is unaffected)

38
Q

The process of HIV using host cells’ genetic material to makes its own DNA is called….

A

reverse transcription

39
Q

Integrase enzyme has what function

A

integration of genetic material into the genetic material of the host cell

40
Q

Mode of action of integrase inhibitors

A

Block integrase, preventing the virus from adding its DNA to the host DNA in CD4 cells - prevents replication and making new viruses

41
Q

e.g. of integrase inhibitor

A

Raltegravir

42
Q

What are fixed dose combinations?

A

Combination of 2 or more medications from one or more different classes - one pill

43
Q

HARRT is just a way of using the same drugs more effectively, does it alter progression or mortality?

A

Fewer mortalities

No change in progression

44
Q

4 Challenges to HAART therapy

A

Intolerance and long term tox
Lack of adherence
Co-morbidities
Increasing drug resistance

45
Q

Barriers to adherance

A
  • frequency and severity of ADR
  • conflict with daily routine
  • dietary requirements
  • frequency of medications
  • number and dosage of medications
  • psychosocial factors
  • pharmacy refills
  • physiological needs
46
Q

Major cause of mortality (4)

A

Liver disease (related to hepatotropic viruses)
CV complications
Renal disease
Non-HIV related malignancies

47
Q

Future of HAART:

A
  • improve current drug tolerability & convenience
  • preserve hepatic function
  • overcome resistance

Infect & Immune 2 AW, DJT & ISB (9 decks)

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