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Dr. Om Prakash Gupta, Shainda Laeeq* and Dr. Shalini Gupta


HPV enters the skin or mucosa through breaks in the surface (even
those not visible to the naked eye). Once inside, HPV infects
host epithelial cells, it produces new viruses. In the process of healthy
cell replacement, the infected cells are shed, releasing viral particles.
Although this is not a normal part of the HPV life cycle, high risk
strains of HPV can combine viral DNA into the host genome. Infected
host cells get a selective advantage from viral integration leading to a
longer infection time. As long as the infection lasts, the more time
there is for cancer to develop. The human papillomaviruses (HPV)
have a heterogeneous group of more than 130 epitheliotropic
genotypes, 16 of which are considered "high-risk" types and linked
with the development of malignant disease. HPV 16 and HPV 18, are
high-risk types, with the main etiological agents of cervical cancer. HPV 16 is involved in
about half of all cases of cancer.[1] HPV are responsible for approximately half a million new
cervical cancer with Head and neck squamous cell carcinoma as the eighth most common
cancer.[2] Almost 250,000 deaths per year, occur in developing countries.[1]

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