Antivirals Flashcards

1
Q

What are the stages in the pathogenesis of HIV

A

1) HIV contracted
2) Primary infection
3) host immune system contains it
4) latent phase
5) overtime CD4 falls as does the immune function.
6) symptoms occur
7) Initially non- specific.

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2
Q

How is HIV contracted

A

mother to baby, sex or IV

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3
Q

Drug used for HIV

A

T3-3 Drugs in one.

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4
Q

What type of viruses cause acute infection.

A

RNA viruses

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5
Q

Examples of acute infections

A

Influenza, measles, mumps, hepatitis A virus.

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6
Q

What type of viruses cause chronic infection

A

DNA viruses

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7
Q

2 types of chronic viral infection.

A

Latent- come out under stress.

Persistent-replicate all the time and are found in blood- HIV, Hep B.

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8
Q

What does viruses consist of

A

nucleic acid- DNA or RNA
protein coat
lipid envelope derived from the cells they grow in.

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9
Q

why don’t viruses which infect the GI tract have an envelope

A

to withstand the ph- envelope proteins would otherwise be destroyed.

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10
Q

which 2 gene types make up a virus

A

Structural- make virus

Non-structural- take over host machinery.

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11
Q

Mechanism of viral replication

A

1) virus attaches to a cell
2) cell entry
3) virus uncoating
4) early proteins produced.
5) Replication
6)Latent transcription and translation
7)virus assembly
virus release

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12
Q

Prime target of antivirals

A

Polymerases.

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13
Q

How does AZT (azidothymidine) work

A

mimics the binding blocks used for DNA and RNA synthesis.

changes OH group to NH3 on bases.

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14
Q

what type of antiviral is AZT

A

Nucleoside reverse transcriptase Inhibitor.

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15
Q

2 types of NRTI’s

A

Pyrimidine analogues.- C an T

Purine analogues.- A and G.

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16
Q

Thymidine analogues

A

zidovudine

17
Q

Cytosine analogue

A

Lamivudine

18
Q

Adenine and Guanidine analogues

A

Abacavir

Tenofovir

19
Q

NRTI’s active against HBV

A

Lamivudine

Tenofovir

20
Q

Examples of non- nucleoside reverse transcriptase (NNRTI’s)

A

Efavirenz

Nevirapine.

21
Q

How do NNRTI work

A

Bind to different parts of the polymerase and inhibit it.

22
Q

Examples of protein inhibitors.

A
Atazanavir
Darunavir
Fospamprenavir
Lopinavir
Nelfinavir
Ritonavir*- now used to boost the level of other protein inhibitiors which are brokendown by liver enzymes.
Saquinavir
Aspartate protease
23
Q

How does fusion inhibitors work and a example

A

block virus fusing with membrane- given IM

Enfuviritide

24
Q

How do Intergrase inhibitors work

A

prevents virus incorporating in the host genome. Not toxic.

25
Q

How do  Chemokine receptor antagonsits work

A

prevent s entry
HIV requires CC5 to enter the cell as it is a co- receptor.
Maraviroc (CCR-5)

26
Q

What does HAART stand for

A

Highly active antiretroviral therapy

27
Q

What does HAART consist of and what is it’s function

A

– 2 NRTIs + NNRTI
– 2 NRTIs + boosted PI
Aims to switch of virus replication can cause liver toxicity.

28
Q

what mutation arises due to resistance to Lamivudine

A

M184V

29
Q

What mutation provides resistance to HIV.

A

CCR5 delta 32 - chnage in CCR5 means that HIV cannot bind

30
Q

2 drugs which sure Hep C

A

Interferons and ribavirin

31
Q

How long do interferons need to be given for

A

3-12 months.

32
Q

Important antivirals

A
Aciclovir- HSV and VZC
Ganciclovir- CMV
Oseltamivir and Zanamavir- (neurainidase inhibitors)- flu
Ribavirin- Hep C and RSV
Interferons- Hep C and B.