The human papillomavirus (HPV) associated apoptosis can be primarily attributed to some early proteins, such as E2, E5, E6, E7, and so on. Though these proteins have a low molecular size, they are capable to interact with a series of host cellular regulation proteins to induce or inhibit apoptosis. The oncoproteins E6 can inhibit the apoptosis mainly through p53 pathway. The E5 protein can protect cells from tumor necrosis factor-related apoptosis. The protein E2 protein have regulatory functions in viral transcription and induction of apoptosis. The oncoprotein E7 plays the role in both apoptosis activation and inhibition. In addition, the HPV full-length E2 proteins involve in activating or repressing the transcription of E6/E7, so as to regulating the apoptosis caused by E6 and E7. We search major databases (such as Elsevier) with the following selection criteria: HPV, early protein, apoptosis. In this review, we summary the literature related with E2, E5, E6, and E7 proteins, and describe the regulatory principles and specific mechanism by which HPV early proteins can interfere with apoptosis and trigger gynaecopathias for women.