[Role of macrophages in papillomavirus infections]

Papillomaviruses have naturally a strict tropism to epithelial cells in which they replicate during the cell differentiation. There is no histological evidence of any inflammatory reaction. No leucocyte recruitment is observed and thus, the role of macrophages during the early infectious process in the epithelium remains unknown. This silent, subacute or chronic infectious disease is characterized fundamentally by a dual pathogenic process, including an infectious process leading to the production of infective virus particles during the differentiation of infected epithelial cells, on the one hand, and an oncogenic process due to interactions of viral oncogenes with host cell regulatory proteins after integration of the virus to the cellular genome. The role of activated macrophages on the oncogenic process is clearly established. They contribute to regulate negatively the transcription of the non structural E6 E7 viral oncogenes and have cytotoxic effects to transformed cells by a direct intercellular contact without evidence of an effect due to a soluble factor such as tumor-necrotizing factor (TNF). Macrophages have, hence, a prominent role as cellular effectors of protective immunity against lesions due to papillomaviruses and particularly against the oncogenic process complicating these infections.