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Abstract
The ability of the host to trigger apoptosis in infected cells is perhaps the most powerful tool by which viruses can be cleared from the host organism. To avoid elimination by this mechanism, human papillomaviruses (HPV) have developed several mechanisms that enable the cells they infect to elude both extrinsic and intrinsic apoptosis. In this manuscript, we review the current literature regarding how HPV-infected cells avoid apoptosis and the molecular mechanisms involved in these events. In particular, we will discuss the modifications in intrinsic and extrinsic apoptotic pathways caused by proteins encoded by HPV early genes. Many of the current efforts regarding anti-cancer drug development are focused on directing tumor cells to undergo apoptosis. However, the ability of HPV-infected cells to resist apoptotic signals renders such therapies ineffective. Possible mechanisms for overcoming the resistance of HPV-infected tumor cells to anticancer drugs will be discussed.
Highlights
Human papillomaviruses (HPV) are small, double stranded DNA viruses that infect epithelial tissues, including those of the anogenital tract
We review the current literature regarding the molecular mechanisms through which HPV-infected cells avoid apoptosis
tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) [12]. Adaptor molecules such as TRADD (Tumor necrosis factor receptor type 1-associated DEATH domain protein) and FADD (Fas-Associated protein with Death Domain) are engaged, and initiator caspases such as procaspase-8 are activated
Summary
Human papillomaviruses (HPV) are small, double stranded DNA viruses that infect epithelial tissues, including those of the anogenital tract. HPV types 6 and 11 are classified as low risk types, and infection with these types results in the proliferation of epithelial cells and manifests as warts or papillomas on the skin These infections are generally self-limiting and do not lead to malignancy. Integration is closely tied to the development of cancer, as most cases of HPV-induced cervical cancer feature an integrated form of the HPV genome Such integration typically leads to an increase in the expression of HPV early proteins, including the E6 and E7 oncoproteins, and a consequential increase in cellular transformation and the probability of HPV induced carcinogenesis [5]. We will discuss the modifications in the intrinsic and extrinsic apoptotic pathways caused by proteins encoded by HPV early genes This has clinical relevance, because many of the current efforts regarding anti-cancer drug development focus on directing tumor cells to undergo apoptosis
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