Human Papillomavirus (HPV) and Hepatitis B virus (HBV) are known aetiology of cervical and hepatocellular carcinoma, respectively. Both diseases share a similar clinical course, that is, the vast majority of those infected by these two viruses can eradicate the viruses spontaneously. A small sub-group who fails to clear the virus becomes chronic carrier and can progress to carcinoma many years later. We postulated that patients with pre-malignant or malignant cervical lesion are at increased risk of becoming chronic HBV carrier if infected, which may be attributed to inherent immunological deficiency against viral infection. We tested HBV carrier status from 288 patients with cervical carcinoma, 242 patients with high grade cervical intra-epithelial neoplasia (CIN) and 311 women with neither of the above conditions as control subjects. The HBV carrier rate in the Cancer Group, CIN Group and Control Group was 21.4%, 24.1% and 10.6%. The carrier rate was significantly higher in both the Cancer Group (p<0.01) and the CIN Group (p<0.01), compared to the Control Group. Our study suggests that a common immunological mechanism is involved in eradication of HBV and HPV infections and inherent immuno-deficiency might lead to an association of HBV carrier status with cervical carcinoma. Further studies are needed to confirm our findings and delineate the mechanism involved.