Abstract: Objective　To explore the distribution characteristics of protein gene product 9.5 (PGP9.5) in the proximal and distal lesions of liver tissue in patients with alveolar echinococcosis (AE), and to clarify the relationship between the positive nerve fiber density of PGP9.5 in the proximal lesion of liver tissue of patients with AE and clinical pathological features and biochemical indexes. Methods　From July 2019 to July 2022, 59 patients with AE who were hospitalized in the Department of Hepatobiliary Surgery of the First Affiliated Hospital of Xinjiang Medical University were selected, and their liver tissues at the proximal and distal ends of the lesion were collected, and their clinicopathological data and biochemical index information were collected at the same time. Immunohistochemical method was used to detect the density of PGP9.5 positive nerve fibers in the proximal and distal liver tissues of 59 patients with AE, and to analyze the difference between the density of PGP9.5 positive nerve fibers in the proximal and distal liver tissues of patients with AE, and to further analyze the relationship between the density of PGP9.5 positive nerve fibers in the proximal liver tissues of patients with AE and clinicopathological features and biochemical indexes. Results　The nerves in the proximal lesion of the liver tissue in patients with AE increased, mainly distributed in the outer layer of the fibrous capsule enclosing the lesion, and no obvious abnormalities were observed in the distal nerves. The density of PGP9.5 positive nerve fibers in the liver tissue of patients with AE was significantly higher than that in the distal part of the lesion, with statistical significance (Z=-4.237, P<0.05). The density of PGP9.5 positive nerve fibers in the liver tissue of patients with AE was correlated with the increase of liver volume (Z=-2.632, P<0.05). Conclusions　The area of PGP9.5 positive nerve fibers in the proximal liver tissue of patients with alveolar echinococcosis increases, suggesting that PGP9.5 positive nerve is involved in the pathogenesis of AE, and its specific role needs further study.