Despite cervical cancer being considered a preventable disease, it still remains the second most common malignancy in women worldwide, with a higher incidence in underdeveloped countries. Human papillomavirus (HPV) is considered the causative agent of cervical cancer. The major mechanisms through which HPV contributes to neoplastic initiation and progression include the activity of 2 viral oncoproteins, E6 and E7, which interfere with critical cell cycle tumor suppressive proteins, p53 and retinoblastoma (Rb) protein. However, HPV infection alone is not sufficient to induce malignant transformation, and other significant cofactors contribute to the multi-step process of tumor formation, such as individual genetic variations as well as environmental factors. However, these cofactors are not important in the absence of HPV. Papanicolaou testing (Pap smear) and HPV DNA testing are tools used in the screening and diagnosis of cervical neoplastic lesions. Vaccination against HPV appears to be cost-effective in the prevention of HPV infection. A thorough understanding of the mechanisms that underline HPV carcinogenesis may result in the development of sophisticated targeted therapeutic approaches, such as antisense oligonucleotides against HPV oncoproteins.