Papillomaviruses infect epithelial cells causing mainly benign lesions or warts. In some rare instances, these may progress to malignancy. For example, human papillomavirus type 16 (HPV16) is the causative agent of 60 percent of cases of cervical cancer. The replication cycle of papillomaviruses is intimately linked to epithelial differentiation. In particular, late gene expression is completed exclusively in the upper epithelial layers. Regulation of late gene expression is largely by post-transcriptional means. RNAs encoding the late proteins, the virus capsid proteins L1 and L2, can be detected in the lower layers of infected epithelia but protein is detected only in the upper layers. It is clear that cellular factors mediate this gene regulation. RNA regulatory elements that bind RNA processing factors that mediate post-transcriptional control have been identified in the 3' untranslated regions of a number of papillomaviruses. These elements, the proteins they bind and the mechanisms by which they are proposed to act are discussed. Further understanding of such host-virus molecular interactions may lead to development of novel strategies for abrogating virus infection.