Acyclovir Flashcards
What are they key differences between small and large viruses
Small viruses have less nucleic acid material and hence encode fewer virus-specific genes.
Larger viruses have more nucleic acid material and hence many more virus-specific genes. Therefore, the bigger the virus the more proteins that differ from the host, the more potential targets for drug intervention.
What are the properties of viruses
They are obligate parasites- inject DNA or RNA into host cell to take over their cellular machinery. Acellular No nucleus or organelles Microscopic Cannot reproduce outside host cell.
Describe the life cycle of a virus
Entry into host cell DNA replicated DNA translated to make host protein Formation of new viruses Cell lysis Drugs aim to prevent these processes.
How do drugs not effect cell systems
They take advantage of structural differences between viral isoforms of a protein from the cell’s own isoform.
What are the key characteristics of the Herpes Simplex Virus
Fairly large virus and hence it can synthesise its own isoform of thymidine kinase and DNA polymerase.
Difference between acyclovir and deoxyguanosine
No 3’-OH group on acyclovir.
What is acyclovir
A nucleoside analogue.
What happens when acyclovir enters the host cell.
Viral thymidine kinase phosphorylates acyclovir, forming acylo GMP.
Acyclo GMP — Acyclo GDP ( host guanylate kinase)
Acyclo GDP — Acyclo GTP ( host phophotransferase)
Acyclo GTP is the active ingredient.
What is the role of acyclo GTP
It acts as an analogue, it has a higher affinity for viral DNA polymerase than deoxyguanosine. However acyclo GTP has no 3’-OH group, hence no phosphodiester bond can be formed to the 5’ phosphate group. Viral DNA replication stops, no more virus produced.
Why is acyclovir not a complete cure
the infected cell will still die. It suppresses the virus by reducing the viral load- the host’s immune system can then work to eradicate the virus.
How does acyclovir have selective toxicity
low affinity to host thymidine kinase and DNA polymerase- hence only infected cells are effected.
What are the opportunities of resistance to acyclovir
Mutated thymidine kinase which cannot metabolise acyclovir. Mutated DNA polymerase which does not stop at acyclo-GTP. However these are lethal mutations and so would not be passed on.
What else can acyclovir be used to treat
EBV, Chicken Pox, HSV types I and II.
