Q33 (a)

Criteria	Marks
Explains the link between inserted viral DNA and protein production through transcription and translation; describes effects on host-cell regulation, repair or apoptosis; and links these to uncontrolled proliferation.	6
Describes transcription and translation of the viral protein; explains disruption of cell-cycle control, including p53, and links this to uncontrolled proliferation.	5
Briefly describes transcription and translation in viral-protein production and outlines effects on p53.	4
Briefly describes transcription and translation and an effect on p53, or describes effects on host-cell processes linked to proliferation.	3
Briefly refers to transcription and translation and identifies a p53 role, or outlines effects on p53.	2
Provides some relevant information.	1

Sample answer:

High-risk HPV strains, such as HPV-16 and HPV-18, are responsible for most cases of cervical cancer. When these viruses infect cervical epithelial cells, they integrate their DNA into the host cell's genome. This leads to the expression a viral oncoproteins, E6.

The viral gene will use the hosts RNA polymerase to produce E6 mRNA. RNA polymerase adds complementary free RNA nucleotides (adenine, uracil, cytosine, and guanine) to the growing RNA strand.
This mRNA molecule is converted into a sequence of amino acids to build an E6 protein.
Ribosomes bind and move along the mRNA. Transfer RNAs (tRNAs) bring amino acids to the ribosome based on the codons in the mRNA.
Amino acids are added to the growing polypeptide chain through peptide bond formation. This continues until a stop codon is reached.
The newly synthesized polypeptide undergoes folding to adopt its functional three-dimensional structure of the E6 protein.

Once synthesised, the E6 oncoprotein targets a cellular protein called p53. P53 is a tumor suppressor protein that plays a critical role in regulating the cell cycle, DNA repair, and apoptosis (programmed cell death) in response to DNA damage.
P53 tumour suppressor gene
Cell cycle regulation – monitors the cell cycle, the process by which cells replicate and divide. If DNA damage is detected, p53 can halt the cell cycle at various checkpoints, giving the cell time to repair the damage before proceeding with division.
Apoptosis – If DNA damage is too severe to be repaired, p53 can trigger apoptosis, a process in which the cell undergoes programmed cell death. This eliminates cells with irreparable damage and prevents them from becoming cancerous.
DNA Repair – p53 can also stimulate the repair of damaged DNA by activating certain genes involved in DNA repair mechanisms. This helps maintain the integrity of the genome and reduces the likelihood of mutations that could lead to cancer.
By promoting the degradation of p53, E6 prevents the cell from effectively responding to DNA damage, increasing the risk of uncontrolled cell division leading to cancer.