High-risk human papillomaviruses infect the basal cells of human epithelia. There it deploys several mechanisms to suppress pathogen receptor recognition signalling, impeding the immune system to control viral infection. Furthermore, infected cells become more resistant to type I and II interferon, tumour necrosis factor-α and CD40 activation, via interference with downstream programs halting viral replication or regulating the proliferation and cell death. Consequently, some infected individuals fail to raise early protein-specific T-cell responses that are strong enough to protect against virus-induced premalignant disease and ultimately cancer. Therapeutic vaccines triggering a strong T-cell response against the early proteins can successfully be used to treat patients at the premalignant stage but combinations of different treatment modalities are required for cancer therapy.
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Ma et al. (2017) studied this question.
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