8.14_Antivirals Flashcards

1
Q

Targets of antivirals

A

penetration, uncoating, genome replication, RNA synthesis, protein synthesis, re-assembly, release from host

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2
Q

Common Herpes Rash

A

presents with a vesicular rash on an erthematous base

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3
Q

Acyclovir

A

treats HSV-1 and 2 well, is also drug of choice for VZV, is an analogue of deoxyguanosine and will be incorporated into genome as replication occurs therefore ending the replication,

it is activated in a cell with virus by a viral thymidine kinase that phosphorylates it, this is what makes it specific to viral cells
It also has greater affinity for viral polymerase

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4
Q

What is more toxic antibiotics or antivirals?

A

Antivirals are more toxic because virals use so much of host cell machinery that it is hard to differentiate or be specific in attack

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5
Q

Valacyclovir and Famciclovir

A

These are two modifications of acyclovir and are used for oral therapy. They have modification that makes them have a much higher bioavailability and be better absorbed in GI tract, these are considered a prodrug while acyclovir is not

Often used for prophylaxis and treatment but severe infections need acyclovir too

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6
Q

How to treat latent herpes viruses?

A

These cannot be treated with acyclovir or the others because there is nothing replicating. Latency means the virus is hanging out in a nerve cell and not doing anything so antivirals have no effect, must wait until prodromal phase reappears

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7
Q

Ganciclovir

A

Similar to ancyclovir, but phosphorylated by a cellular kinase so it is less specific. used in treatment of cytamegalovirus, also has a pro drug called valganciclovir

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8
Q

Resistance to Herpes virus Antivirals

A

Can occur due to mutations in the viral thymine kinase or the viral polymerase, but in regular immuno patients it is uncommon,

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9
Q

Adamantanes

A

group of antiinfluenze drugs, this group inhibits the M2 protein that is in charge of uncoating the virus when it enters a host, these are good for flu A but not flu B

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10
Q

Adamantanes examples

A

Amantadine and Rimantadine are both examples of an adamantane, they target the M2 and prevent uncoating and release of virus in a cell

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11
Q

Neuraminidase inhibitors

A

class of anti influenzas that target the enzyme neuraminidase which helps cleave the virus from the cyalic linkage to the host when it is trying to leave, so if inhibited you will get a collection of viruses attached to outside of host

Target flu A and B

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12
Q

Neuraminidase examples

A

Oseltamivir and Zanamivir Peramivir and Laninamivir

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13
Q

Resistance to Neuraminidases and side effects

A

very easy for cells to make new neuraminidases so they drugs do not work anymore, side effects often include some neuropsych issues

These also dont provide a great reduction in duration of disease only about 1.3 days and fever also down for only about 1 day

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14
Q

Ribavirin

A

Nucleoside analogue with antiviral activity, used to treat infants with RSV through aerosol treatment, can also treat some funky things like lassa fever, side effect is anemia

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15
Q

What does a retrovirus need to bring into a host?

A

A reverse transcriptase to make the DNA intermediate

A viral polymerase to transcribe

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16
Q

Classes of antiretroviral agents

A

Nucleoside reverse transcriptase inhibitors
Nucleotide RT inhibitors
Non nucleotide RT inhibitors
Protease inhibitors
Fusion/entry inhibitors
Integrase inhibitors-inhibits DNA from being inserted into host

17
Q

Challenges of HIV therapy

A

successful therapy for decades with minimal toxicity
eradication or functional cure
effective prevention of HIV from mother to child and sexually spread
Vaccine?

18
Q

PEP versus PrEP

A

Post-Exposure prophylaxis is when you start treatment right after likely infected

Pre Exposure prophylaxis is when you start when you think there is a high risk of infection but not sure if infected

19
Q

Resistance to antiretrovirals

A

has a wild polymerase that leads to lots of resistance through high mutation rates

to combat we hope patients ahere to medication guidelines and can genotype the viral gene and also watch phenotype or how virus functions

20
Q

What type of therapy is best for HIV

A

This is measured with CD4 counts and plasma levels of HIV1RNA
Highly Active Antiretroviral Therapy HART is best

21
Q

Monotherapy CD4 and HIVRNA info

A

CD4 will rise and HIV RNA decreases but converges back in middle showing resistance

22
Q

Double RTI Therapy CD4 and HIV RNA info

A

CD4 rises and HIV RNA decreases and they start to come back together but do not completely converge, so some better than monotherapy

23
Q

HART or Highly active Antiretroviral Therapy CD4 and HIVRNA

A

CD4 continuously increases and HIVRNA decreases, they do not show any signs of converging, so best therapy

Even have combination drugs that can be given once daily now so less toxic and easier adherence