Virology - Antivirals

Front 1

Antiviral
-mechanisms

Back 1

-ion channel blockers
-polymerase inhibitors
-post-translational modification

Front 2

Disinfection
-definition

Back 2

virus inactivation on surface

Front 3

Disinfection
-why is it important

Back 3

-1st line of defense

Front 4

Disinfection
-effectiveness of a disinfectant is dependent on

Back 4

-presence or absence of an envelope
-composition of nucleic acids
-other factors

Front 5

Why do we study viruses?

Back 5

They are the one diagnosis that we as vets can catch and spread

Front 6

Common disinfectants

Back 6

-alcohol
-bleach
-Quaternary ammonium compounds
-Irradiation
-Autocleaving

Front 7

What is a gold standard for viral toughness?

Back 7

-parvovirus

Front 8

What should you never forget to do when using an antiviral compounds?

Back 8

-don't forget to read the product insert

Front 9

Ideal properties of antiviral compounds

Back 9

-broadly effective against a variety of viruses within the same group
-minimal toxicity to the host
-minimal side effects
-minimal appearance of resistanct viruses after a wide-spread use

Front 10

Why are many antivirals not used widely

Back 10

-afraid of resistance and the possibility of zoonotic viruses becoming resistant in humans

Front 11

Amantidine
-use

Back 11

-effective in protecting birds from avian influenza
-not recommended to be used

Front 12

Amantadine
-mechanism of action

Back 12

-blocks the pore formed by the M2 protein in the surface of the viral cell
-doesn't allow H+ to be pumped into the cell
-uncoating and release of genomic RNA does not occur

Front 13

Amantadine
-originally developed as

Back 13

-drug to treat parkinsons

Front 14

Amantadine
-side effects

Back 14

CNS
-nervousness
-anxiety
-agitation
-insomnia
-difficulty concentrating

Front 15

Amantadine
-reason for side effects

Back 15

-dopaminergic activity
-adrenergic activity
-anticholinergic activity

Front 16

Acyclovir
-mechanism of action

Back 16

target genome replication of herpesvirus
-nucleoside analog taken up by cells
-conversion to acyclovir monophasphate by herpesvirus-encoded thymidine kinase
-monophosphate form converted to ACTVP by cellular enzymes
-ACTVP acts as an analog of deoxyguanosine triphosphate (dGTP) for incorporation into copies of the viral genome by a viral-encoded DNA polymerase
-dsDNA chain termination due to absence of 3' hydroxyl group

Front 17

Acyclovir
-step of herpesvirus replication being inhibited

Back 17

-progeny DNA replication

Front 18

2 things that DNA polymerases look for

Back 18

-template to copy from
-free 3' hydroxyl group to form a bond with the next nucleoside incorporated into the growing chain

Front 19

Acyclovir
-therapeutic properties

Back 19

-only active in an infected cell
-high therapeutic ration because of a higher affinity for viral DNA polymerase
-irreversible inhibition (chain termination of viral DNA)
-low toxicity to non-virus infected cells (ACVMP & ACVTP not exported from cells)

Front 20

Acyclovir
-resistance due to

Back 20

mutation related to TK
-TK-negative/low mutants (substitution of a less efficient host cell thymidine kinase)
-TK mutation that doesn't bind drug

Front 21

Retrovirus drugs
-3 classes

Back 21

-nucleoside analog RT inhibitors
-non-nucleoside analog RT inhibitors
-protease inhibitors

Front 22

Retrovirus drug
-reason for target

Back 22

-target reverse transcriptase because it is unique to the virus
-no host cell has reverse transcriptase

Front 23

AZT
-function

Back 23

-nucleoside RT inhibitor

Front 24

AZT
-mechanism of action

Back 24

-imported into the cell in a non-phosphorylated form then becomes phosphorylated and acts as a chain terminator

Front 25

AZT
-acts on

Back 25

-Reverse transcriptase
-host polymerase (high conc.)