prevention and treatment of viral disease

Question 1

Define prophylaxis and therapy.

Answer 1

Preventing the diseases before the aetiologic agent is acquired, by vaccination or giving the drug before infection.

Therapy: is treating the disease after the host has been infected.

Question 2

What allowed smallpox to be eradicated?

Answer 2

• No animal reservoir
• easily recognised disease
• vaccine works against all strains
• no latent or persisten infection
• vaccine properties- low cost etc

Question 3

What are the four broad types of virus vaccines?

Answer 3

Live Attenuated Virus e.g. Polio, influenza
Inactivated virus e.g. Rabies
Purified Subunit e.g. influenza
Cloned subunit e.g. Hep B and HPV

Question 4

Describe each of the types of virus vaccines.

Answer 4

Live Attenuated – live virus has its virulence reduced and then is administered to the patient Inactivated – the virus is taken from teh parental virus and its genome is destroyed so that it is still stimulates a response but can no longer be infectious – given with adjuvant Purified Subunits – the viral genome is taken and treated with proteases which chops it into small pieces. These subunits have antigens that can trigger an immune response. Cloning – viral genome is cloned in a bacterium and the copies of the genome are either: Injected into people Put into virus-like particles A new virus is made with a little segment of virulent material from the original virus

Question 5

State what type of vaccine has been produced for each of these diseases:
Polio
Smallpox
Rubella
Hep B
Influenza
HPV

Answer 5

Polio – inactivated + live attenuated
Smallpox – live attenuated 
Rubella – live attenuated 
Hepatitis B – cloned subunit
 Influenza – purified subunit + live attenuated 
HPV – cloned subunit

Question 6

How are Live Attenuated Vaccines made?

Answer 6

The virus is passed through the wrong type/wrong species of cells this makes the virus evolve and change its virulence e.g. if a virus is passed through monkey cells then it will become a monkey virus and it will no longer be as virulent to humans

Question 7

What are some differences between live attenuated vaccines and inactivated vaccines?

Answer 7

Live attenuated vaccines give rapid, broad, long-lived immunity, dose sparing Inactivated vaccines often require boosters, high doses needed, safe

Question 8

What types of vaccines exist for influenza and what does it include inside?

Answer 8

Purified subunit vaccine: contains only of the spike proteins (HA)
Live-attenuated (nasal spray): cold adapted, can replicate at 32 not 37 degrees

Question 9

What types of vaccines exist for polio?

Answer 9

SALK – inactivated: virus treated so no longer can replicate, require high dose
SABINE – live attenuated: leads to poliomyelitis, should stop using this

Question 10

What 3 genes do virus contain and How are recombinant attenuated virus vaccines made?

Answer 10

-Receptor-binding gene, virulence gene and capsid protein genes
The virulence gene is either mutated or deleted so virus in IMMUNOGENIC but not VIRULENT

Question 11

What type of vaccine does rotavirus have and what do rotavirus cause, also explain at what time it should be given and why?

Answer 11

• Live attenuated reassortant vaccine
• causes dehydration from vomitting and diarrhoea.
• given to babies older than 15 weeks as it causes intussusception (bowel blockage) in babies older than 3 months

Question 12

Give two examples of subunit vaccines.

Answer 12

HPV

Hepatitis B Virus

Question 13

What is the best available broad antiviral therapy and what are the limitations of it?

Answer 13

Interferons – it activates inflammation and fever and can make the patient feel even more ill, but supresses the virus

Question 14

What do antiviral drugs tend to target and how do they work?

Answer 14

Viral enzymes- often by acting as substrate analogues.
nucleoside analogues look like normal bases but have the 3’ hydroxyl group missing- which prevents the RNA chain growing in the Virus

Question 15

What are the two strategies for inhibiting influenza?

Answer 15

-Blocking the M2 channel -Neuraminidase inhibition

Question 16

Describe inhibition of the M2 channel in influenza.

Answer 16

When endocytosed, influenza virus enters the endosome The low pH of the endosome opens the M2 channel allowing protons to move into the endosome and break the bonds holding together the protein capsid of influenza This allows influenza to uncoat and release its contents into the cytoplasm of the cell Adamantes: (rimantadine and amanatadine) can fit in the M2 channel and prevent protons from moving in, thus meaning that the influenza is locked in its protein shell

Question 17

What are adamantanes and does it work?

Answer 17

Cyclic amines- by products of petrol refinement

-single point mutation will mean that it no lomger fit in M2 channel: now all human influenza are resistent to this

Question 18

Describe neuraminidase inhibition in influenza.

Answer 18

Neuraminidase is usually produced by influenza to destroy sialic acid on the surface of the host cell thus meaning that the virus doesn’t bind to the same cell again By blocking neuraminidase you can limit the spread of the virus to other cells

Question 19

Give two examples of neuraminidase inhibitors.

Answer 19

Oseltamivir (Tamiflu) Zanamivir (Relenza)

Question 20

Give eight examples of HIV drugs.

Answer 20

Nucleoside reverse transcriptase inhibitor:
Zidovudine 
Stavudine 
Non-Nucleoside reverse transcriptase inhibitor:
Efavirenz 
Viramune 
Integrase inhibitor:
Raltegravir
Entry inhibitors:
Maraviroc - blocks gp120
Enduvirtide- binds to gp41- prevents membrane fusion
Protease inhibitors:
-Atazanavir

Question 21

State two treatments for Hepatitis C.

Answer 21

Interferons Ribavirin

Question 22

how does acyclovir work?

Answer 22

Acyclovir is a nucleoside analogue. It is given to the patient in an unphosphorylated (inactive) form, a prodrug, that means it cannot yet be used as a substrate in DNA replication. It’s specificity comes from the fact that it is only converted into its active form inside a cell that is already infected by herpes virus. This is because the virus encodes an enzyme thymidine kinase that can phosphorylate the drug. Once acyclovir triphosphate is incorporated into the growing DNA chain in the herpes virus genome, it terminates the reaction because it lacks the OH
groups by which the next nucleoside would normally be attached.