The papillomavirus E5 gene contributes to transformation and tumorigenesis; however, its exact function in these processes and viral pathogenesis is unclear. While E5 is present in high-risk mucosotropic HPVs that cause anogenital and head and neck cancers, it is absent in cutaneous HPVs and the recently discovered mouse papillomavirus (MmuPV1), which causes papillomas and squamous cell carcinomas of the skin and mucosal epithelia in laboratory mice. We infected K14E5 transgenic mice, which express the high-risk mucosotropic HPV16 E5 gene in stratified epithelia, with MmuPV1 to investigate the effects of E5 on papillomavirus-induced pathogenesis. Skin lesions in MmuPV1-infected K14E5 mice had earlier onset, higher incidence, and reduced frequency of spontaneous regression compared to those in non-transgenic mice. K14E5 mice were also more susceptible to cervicovaginal cancers when infected with MmuPV1 and treated with estrogen compared to non-transgenic mice. Our studies support the hypothesis that E5 contributes to papillomavirus-induced pathogenesis.

中文翻译：

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人类乳头瘤病毒16 E5基因增强MmuPV1依赖的发病机理。

乳头瘤病毒E5基因有助于转化和肿瘤发生。然而，其在这些过程和病毒发病机理中的确切功能尚不清楚。尽管E5存在于引起肛门生殖器和头颈部癌症的高危溶血性HPV中，但在皮肤HPV和最近发现的小鼠乳头瘤病毒（MmuPV1）中却不存在E5，后者在实验室中引起皮肤和粘膜上皮的乳头状瘤和鳞状细胞癌老鼠。我们用MmuPV1感染在分层上皮中表达高危溶血性HPV16 E5基因的K14E5转基因小鼠，以研究E5对乳头瘤病毒引起的发病机制的影响。与非转基因小鼠相比，感染MmuPV1的K14E5小鼠的皮肤病变发作更早，发生率更高，并且自发消退的频率降低。与非转基因小鼠相比，当用MmuPV1感染并用雌激素治疗时，K14E5小鼠还更易患宫颈阴道癌。我们的研究支持E5有助于乳头瘤病毒引起的发病机理的假说。