1. Chapter 6
Virus and cancer
Prepared by:
Miss Putri Shareen Binti Rosman

2. Cancer
• Activated oncogenes transform
normal cells into cancerous cells.
• Transformed cells have increased
growth, loss of contact inhibition,
tumor specific transplant and T
antigens.
• The genetic material of oncogenic
viruses becomes integrated into the
host cell's DNA.

3. Oncogenic viruses
• that produce tumors in their natural hosts or in
experimental animals . induce malignant
transformation of cells on culture.
• Transformation
• changes that accompany the conversion of a
normal cell into malignant cell.

4. Oncogenic Viruses
• Oncogenic DNA
 Oncogenic RNA
Viruses viruses
 Retroviridae
– Adenoviridae
– Herpesviridae  Viral RNA is
– Poxviridae transcribed to DNA
– Papovaviridae which can integrate
– Hepadnaviridae into host DNA
 HTLV 1
 HTLV 2

5. Oncogenic viruses

6. Oncogenic viruses
Brief background on cell cycle factors
Rb and E2F example
Enquist et al., Principles of Virology, ASM, 2004
Example: DNA damage during G1
P53 recognizes DNA damage and activates P21 (p53 recognizes
certain types of DNA mismatches)
P21 binds and inactivates the cyclin-CDK complex which has
already begun to be produced in response to different signals
DNA repaired, p53 decreases, P21 no longer blocks cyclin-CDK,
cell cycle progression

7. • Coming out of G1 phase and entering S.
•E2F: important transcriptional activator
•Enters the nucleus and binds upstream of important
nucleotides.
•Bound to retinoblastoma protein
•Keeps the E2F from entering the nucleus and acting
as an important activator.
•Cdk2/cyclin A
•Phosphorylates Rb causing the release of e2f.
•Allows the cell to enter S phase.
• DNA damage
•Any double stranded DNA breaks causes the dna
polymerase to fall off terminating trascritipion.
• P53
•P53 act as a checkpoint controller to stop cell-cycle
progression
•If DNA is damaged this protein activates p21
preventing the cell from entering S phase.
•P21- blocks the cyclin dependent reaction.
•Central player in the decision to commit to S phase.

8. Inactivation of p53 by papillomavirus proteins
HPV
n
Enquist et al., Principles of Virology, ASM, 2004

9. Chapter 6
Novel acellular
infectious agent

10. Prions
•Prions are “infectious
proteins”
• They are normal body
proteins that get
converted into an
alternate configuration by
contact with other prion
proteins
• They have no DNA or
RNA
•The main protein involved
in human and mammalian
prion diseases is called
“PrP”

11. How a Protein Can Be Infectious
Figure 13.22

12. Prion Diseases
•Prions form insoluble
deposits in the brain
•Causes neurons to
rapidly degeneration.
•Mad cow disease
(bovine spongiform
encephalitis: BSE) is an
example
•People in New Guinea
used to suffer from
kuru, which they got
from eating the brains
of their enemies

13. Prions
• Inherited and transmissible by ingestion,
transplant, & surgical instruments
• Spongiform encephalopathies: Sheep
scrapie, Creutzfeldt-Jakob disease,
Gerstmann-Sträussler-Scheinker
syndrome, fatal familial insomnia, mad cow
disease

14. Viroids
•Small, circular
RNA molecules
without a protein
coat.RNA does not
code any protein.
•Infect plants
•Resemble introns
cut out of
eukaryotic

15. Treatment for Viral
Disease

16. Vaccines
• An attenuated virus is a weakened, less
vigorous virus
• “Attenuate" refers to procedures that
weaken an agent of disease (heating)
• A vaccine against a viral disease can be
made from an attenuated, less virulent
strain of the virus
• Attenuated virus is capable of stimulating
an immune response and creating
immunity, but not causing illness

17. Other Viral Treatments
•Interferon are naturally
occurring proteins made
by cells to fight viruses
•Genetic altering of
viruses (attenuated
viruses)
•Antiviral drugs (AZT)
•Protease inhibitors –
prevent capsid formation

18. Antiviral Treatment Strategies
• Inhibitors of viral replication
– every step in viral replication is potentially a target
– targeting host cell functions is generally not
feasible (toxicity)