Sera from animals or humans with a history of infection generally react with papillomavirus capsid proteins. Antibodies to the E7 protein of HPV16 and HPV18 are frequently found in sera of patients with cervical cancer. Similarly, antibody titers against the E2, E6 and E7 proteins have been detected in patients' sera.
Infection with the common papillomaviruses of the skin and mucosa often results in a chronic infection. This chronic infection occurs in the immunocompetent host, suggesting that viral antigens are not recognized by the immune system. However, an increased incidence of clinically apparent HPV disease occurs in the immunosuppressed transplant recipient and also in patients with the acquired immune deficiency syndrome (AIDS). These observations indicate that cell-mediated immunity is important in controlling HPV infection. A decrease in the ratio of CD4T (helper) to CD84 (suppressor) T cells has been reported in patients with HPV infection or precancerous cervical intraepithelial neoplasia, which is usually a manifestation of HPV disease.
Natural killer (NK) cells may have a role in the cellular response to HPV infections. Patients with HPV-induced cancerous and precancerous lesions are reported to display decreased NK cell activity, and these NK cells have a restricted responsiveness to immunostimulatory cytokines.
Langerhans cells are specialized cells in epithelial tissues that are potent antigen-presenting cells. In most warts, there is a reduction of Langerhans cells resulting in a local immunodeficiency state in these lesions. Decreased numbers of Langerhans cells have been observed in the HPV precancerous lesions.
Class I iVIHC molecules present viral antigens to T cells. Downregulation of class I MHC and the TAP-1 transporter protein has been reported in HPV-induced cervical lesions and laryngeal lesions. Additionally, an association between certain class II MHC alleles (e.g. DQw3) and susceptibility to cervical cancer and laryngeal papillomatosis has been observed.
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