Viruses, individually or synergistically, have developed unique mechanisms for hijacking or inhibiting the tumour suppressive functions of wildtype p53.23 Since there were direct relationships between the p53 gene, miR-21 and miR-200c in terms of viral infection, the higher expression of the p53 gene (tumour suppressor) in participants with EBV and HPV mono-infections could be an immunologic response to higher miR-21 and miR-200c (oncogenes) among participants with mono-infection. Here, TP53 is linked to infection.