Viruses

Question 1

What does polyoma middle and large t antigen target?

Answer 1

L - Rb

M - Src, PI3K, PP2A

Question 2

What do SV40 and adenovirus oncoproteins target?

Answer 2

Large t - Rb, p53
Small - PP2A

E1A - Rb
E1B - p53

Question 3

What are LTRs?

Answer 3

Duplication of specific sequences at 5’ and 3’ ends –> integration signals, promoter elements, enhancer elements, polyadenylation sites.

Question 4

How do slow transforming viruses mediate their effects?

Answer 4

Virus integrates next to protooncogene - then overexpressed due to adjacent LTRs (long terminal repeat).

Question 5

How does MMTV induce tumours?

Answer 5

Slow transforming virus 
Favoured integration sites = (INT-1) wnt1 and (INT-2) FGF3 
Random integration at these sites rare.
Monoclonal tumour (recruits transformed cells to tumour as result of horizontal spread from cell to cell by infection).

Question 6

Give an example of an acute transforming virus. How does it differ to slow?

Answer 6

RSV

oncogene tagged onto end of viral genome (doesn’t disrupt genes required for replication)

Question 7

What are replication defective viruses?

Answer 7

Acute transforming but oncogene disrupts replication genes

Helper virus needed to provide missing gene products (slow transforming)

Question 8

Why is v-src an oncogene gene?

Answer 8

C-src is PO

V-src has point mutations and rearrangements (Tyr527 deletion / polyoma middle T binds Tyr527)

Question 9

How does HTLV-1 transform and what is it?

Answer 9

Only example of a human retrovirus
Extra viral Tax gene
Activates other TFs e.g.NFkB and induces IL2 and IL2-R expression.
Binds and inactivates p16 and MAD1

Question 10

What are the high risk strains of HPV?

Answer 10

16, 18, 31, 33
Vaccine against 16 and 18

Low risk are 6 and 11.