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Andy Watts Flashcards

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1
Q

What is the HIV mechanism of infection?

A

HIV primarily infects CD4+ T cells of the immune system.

  1. HIV gp120 protein binds to CD4 receptors.
  2. Co-receptors CCR-5 and CXCR4 are involved.
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2
Q

What HIV protein binds to CD4 receptors?

A

gp120

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3
Q

What occurs once gp120 + CD4 binding has occurred?

A

Conformational change occurs and gp120/CD4 binds to either CCR-5 or CXCR4.

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4
Q

What is a HIV infection characterised by? [3]

A
  1. Chronic immune activation.
  2. CD4 T cell depletion.
  3. Dysfunction of the immune system.
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5
Q

What is the importance of the CCR-5 receptor?

A
  1. Co-receptor involved in HIV entry to cells.
  2. Mutations that inactivate it are found and individuals homozygous for the CCR-5 mutation are very resistant to HIV infection.
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6
Q

What co-receptors are involved in HIV infection?

A

CCR-5
CXCR4
Some HIV will only use one or the other, some will use both.

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7
Q

What opportunistic infections may someone with HIV develop? [5]

A
  1. Candidiasis
  2. Cytomegalovirus (CMV)
  3. Herpes Simplex Virus (HSV)
  4. Tuberculosis (TB)
  5. Mycobacterium avium complex (MAC or MAI)
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8
Q

In what ways can the immune activation associated with HIV infection be manifested? [2]

A
  1. T cell proliferation

2. Increased expression of CD38 on CD4/CD8 T cells.

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9
Q

What occurs after gp120/CD4 has bound to either CCR-5 or CXCR4?

A

gp41 membrane penetration and then fusion occurs.

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10
Q

What is the most potent factor known to increase the risk of progression from M.tuberculosis infection to disease?

A

HIV.

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11
Q

What does current HIV treatment involve?

A

Combinations of drugs acting at different targets. Treatment with a single drug has short term benefit, but long term only serves to select resistant mutants,

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12
Q

What are NNRTIs?

A

Non-nucleoside reverse transcriptase inhibitors.

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13
Q

What are the six classes of current HIV anti-virals?

A
  1. NRTIs
  2. NNRTIs
  3. Protease inhibitors (PI)
  4. Fusion inhibitors
  5. Integrase inhibitors.
  6. CCR5 antagonists
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14
Q

What is HAART?

A

Highly Active Anti-Retroviral Therapy.

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15
Q

What is HAART composed of?

A
  1. 3 different antiretroviral drugs
  2. From at least two different classes.
  3. Reduces incidence of resistance.
  4. Can reduce toxicity/side effects by lowering dose.
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16
Q

What are NRTIs?

A

Nucleoside/Nucleotide Reverse Transcriptase Inhibitors.

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17
Q

How do NRTIs function?

A

Act as chain terminators or inhibitors at the substrate binding site of RT.
Didanosine.
Zidovudine.
Lamivudine.

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18
Q

What examples of NRTIs are there?

A

Didanosine, Zidovudine, Lamivudine.

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19
Q

What are NNRTIs?

A

Non-nucleoside analog reverse transcriptase inhibitors. Bind allosterically, causing a conformational change.
Nevirapine, Delavirdine, Efavirenz.

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20
Q

What is Nevirapine?

A

NNRTI

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21
Q

What is Delavirdine?

A

NNRTI

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22
Q

What is lamivudine?

A

NRTI - chain terminator/inhibitor at active site.

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23
Q

What is Efavirenz?

A

NNRTI

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24
Q

What is didanosine?

A

NRTI - chain terminator/inhibitor at active site.

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25
What are three NNRTIs?
1. Efavirenz 2. Nevirapine 3. Delavirdine.
26
How do protease inhibitors function?
Inhibit HIV protease which is need to process GAG and POL polyproteins into mature HIV components. All PIs contain a hydroxyethylene bond instead of the normal peptide bond. Lopinavir
27
What bond do all PIs contain that allows them to inhibit HIV protease?
Hydroxyethylene bond instead of normal peptide bond. | Lopinavir
28
HIV protease normally processes what into mature HIV components?
GAG and POL polyproteins. | Lopinavir.
29
What is Lopinavir?
Protease inhibitor.
30
What is fuzeon?
New class: fusion inhibitors. 36 amino acid peptide. Produced synthetically. Rationally designed to mimic components of GP41 and displace them.
31
Fuzeon was rationally designed to mimic what?
New class: fusion inhibitors. 36 amino acid peptide. Produced synthetically. Rationally designed to mimic components of GP41 and displace them.
32
What is Maraviroc?
CCR5 inhibitor. Block attachment of HIC to the CCR5 receptor. Only effective in people whose HIV only uses the CCR5 receptor for replication, not ones that use both (CCR5 + CXCR4) or those that only use CXCR4.
33
For which patients can Maraviroc be prescribed?
CCR5 inhibitor. Block attachment of HIC to the CCR5 receptor. Only effective in people whose HIV only uses the CCR5 receptor for replication, not ones that use both (CCR5 + CXCR4) or those that only use CXCR4.
34
Against which receptor is Maraviroc targeted?
CCR5 inhibitor. Block attachment of HIC to the CCR5 receptor. Only effective in people whose HIV only uses the CCR5 receptor for replication, not ones that use both (CCR5 + CXCR4) or those that only use CXCR4.
35
An antiviral targeted for the CCR5 receptor:
Maraviroc. CCR5 inhibitor. Block attachment of HIC to the CCR5 receptor. Only effective in people whose HIV only uses the CCR5 receptor for replication, not ones that use both (CCR5 + CXCR4) or those that only use CXCR4.
36
What is Raltegravir?
Integrase inhibitor.
37
What are fixed dose combinations?
Antiretrovirals which are combinations of 2 or more medications from one or more different classes. These antiretrovirals are combined into one single pill with specific doses of these medicines.
38
NNRTI-based HAART consists of:
Tenofovir/Emtricitabine + Efavirenz
39
Protease inhibitor-based HAART consists of:
Tenofovir/Emtricitabine + Ritonavir + Atazanavir OR | Ritonavir + darunavir.
40
Integrase strand transfer inhibitor based HAART consists of:
Tenofovir + (AND) + Emtricitabine + Raltegravir.
41
What are the main challenges to HAART?
1. Intolerance and long-term toxicity 2. Lack of adherence 3. Co-morbidities 4. Increasing drug resistance 5. Liver disease
42
What is our initial response to influenza infection?
NFKB transcription and thus pro-inflammatory cytokine gene expression of TNFa, IFNB and IL-8. TH1 response.
43
What is our long-term response to influenza infection?
IFNgamma boosts chemokine gene expression, activation of macrophages, antigen presentation and continual development of specific-cell mediated immunity. TH2 response. Long term protection against similar strains.
44
What is an antigen?
Molecule that provokes a specific immune response may be components of microorganisms.
45
What are the key influenza antigens?
HA
46
What is the primary immune response?
First encounter with a foreign antigen. Only a few B or T cells can recognise the antigen.
47
What is the secondary immune response?
Second exposure to a foreign antigen. This time there is a large clone supply of memory cells that can recognise the antigen. Immune response is more effective (antigen specific antibodies)
48
What is the difference between vaccines for influenza and drugs for influenza?
Drugs will be active against all strains and serotypes but not confer long lasting protection. Can be stockpiled. Vaccines provide protection, which can be long term, against infection but need to be produced ahead of time. A specific vaccine is required for each serotype of influenza.
49
How are Influenza subtypes distinguished?
The antigenic properties of HA and NA.
50
How many HA subtypes are found in influenza type A viruses that exhibit human-human spread?
3. H1 H2 H3
51
How many NA subtypes are found in influenza type A viruses isolated from infected humans?
2. N1 N2
52
What is antigenic drift?
Gradual accumulation of mutations that allow the hemagglutinin to escape neutralising antibodies. Epidemic strains are thought to have changes in three or more antigenic sites.
53
What is pandemic influenza?
Occurs when a NEW strain of virus is formed, often origination from another species. No immune history so no natural protection. Impossible to predict the nature of the strain or when it will emerge. Can be highly pathogenic and result in high rates of mortality
54
What is a trivalent vaccine?
Contains three inactivated vaccines, given IM
55
How are vaccines prepared?
Chicken eggs
56
What are the critical factors relating to influenza vaccine manufacturing? [4]
1. Growth potential of seed virus. 2. Timing of strain selection. 3. Potency test reagents. 4. Timing of Annual Licence Supplement Approval.
57
What are the two classes of influenza antiviral drugs?
``` 1. M2 inhibitors. Adamantanes: Amantadine. Rimantadine. 2. NA inhibitors. Oseltamivir. Zanamivir. ```
58
Oseltamivir and Zanamivir are which class of influenza antiviral?
NA inhibitors.
59
Amantadine and rimantadine are examples of which class of influenza antiviral?
M2 inhibitors,
60
How does amantadine function?
Interferes with the transmembrane domain of the M2 protein. | Prevents virus assembly.
61
What are the problems with Amantadine?
90% of clinical isolates showed resistance.
62
What is Rimantadine?
1. Less toxic alternative to amantadine. 2. Similar mechanism of action. 3. Not NICE recommend.
63
How do NA inhibitors work?
Competitive inhibitors that compete with the natural receptors for access to the NA active site.
64
What are the advantages of NA inhibitors?
Active against all strains of influenza (ABC) and all serotypes.
65
Why are NAi preferred to M2 inhibitors?
Active against all strains of influenza (ABC) and all serotypes. M2 only against A.
66
What is Nevirapine?
Non-nucleoside analog reverse transcriptase inhibitors. Bind allosterically, causing a conformational change. Nevirapine, Delavirdine, Efavirenz.
67
What is Delavirdine?
Non-nucleoside analog reverse transcriptase inhibitors. Bind allosterically, causing a conformational change. Nevirapine, Delavirdine, Efavirenz.
68
What are nevirapine, delavirdine and efavirenz all examples of?
Non-nucleoside analog reverse transcriptase inhibitors. Bind allosterically, causing a conformational change. Nevirapine, Delavirdine, Efavirenz.
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