宫颈癌为全球女性常见第二大恶性肿瘤，而人乳头瘤病毒（human papillomavirus，HPV）是98％以上宫颈癌的致病因子。HPV感染后，通过与宿主相互作用成功逃避免疫清除，在生殖道中建立持续感染。信号转导与转录激活因子（signal transducer and activator of transcription，STAT）家族成员是天然免疫应答的重要调节因子，HPV通过抑制STAT1的表达来稳定维持病毒游离基因水平。STAT5是另一重要成员，可调控细胞周期进程。有研究表明，HPV阳性细胞中STAT5被激活对HPV基因组的扩增十分重要[1]。HPV的持续感染与异常表达的STAT蛋白相互作用，可能与宫颈癌的发展密切相关。通过药物靶向这些途径抑制HPV感染，可能为宫颈癌治疗提供新思路。本文就此方面研究进展进行综述。

Human papillomavirus (HPV) is the causative pathogen of over 98% of cervical cancer, which is the second most common cancer in women worldwide. Prior to the development of cancer, HPV establishes persistent infections in the genital tract and successfully evades immune clearance. Members of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) family are important regulators of the innate immune response. HPV proteins can downregulate the expression of STAT1 to allow for stable maintenance of viral episome. STAT5 is another member of this pathway, which plays an important role in controlling cell cycle progression. Several studies reveal that STAT5 is activated in HPV-positive cells and it is necessary for HPV genome amplification. Persistent infection of HPV interacts with abnormal expression of STAT proteins and contributes to the development of cervical cancer. Targeting of these pathways by pharmaceuticals can inhibit HPV infection, which will contribute to the treatment of cervical cancer. The article summarizes the progress on the relationship between HPV and STAT pathway.