ObjectiveTo investigate the distribution of HCV genotypes in 383 patients with HIV/HCV coinfection in Guizhou, China and the effect of coinfection on HIV viral load, CD4+ T lymphocytes, and platelet count (PLT), and to provide a basis for individualized treatment of patients with HIV/HCV coinfection. MethodsRelated clinical data were collected from 383 patients with HIV/HCV coinfection who were treated in Guiyang Public Health Clinical Center from March 2015 to December 2019, and HCV genotype, HIV viral load, CD4+ T lymphocytes, and PLT were determined. A total of 1068 patients with HIV alone were enrolled as control. The Kruskal-Wallis H test was used for comparison between multiple groups, the Wilcoxon rank-sum test was used for comparison between two groups, and the Bonferroni method was used for further comparison between two groups; the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. ResultsAmong the 4664 patients with HIV infection, 383 (8.21%) had HCV coinfection, and the main HCV genotypes were genotype 6a (35.51%), genotype 3b (27.42%), and genotype 1b (21.41%), followed by genotypes 3a (1332%), 1a (1.31%), 2a (0.52%), 6n (0.26%), and 6xa (0.26%). The most common route of infection was intravenous drug addiction (72.59%), followed by sexual contact (24.80%). Compared with the patients with HIV infection alone, the patients with HIV/HCV coinfection had a significantly higher HIV RNA load and significantly lower CD4+ T lymphocytes and PLT (Z=6.716, 11.813, and 9.192, all P＜0.05). Among the patients with coinfection, the patients with HCV genotype 3b had the highest HIV RNA load and the lowest CD4+ T lymphocytes and PLT, while the patients with HCV genotype 1a had the lowest HIV RNA load and the highest CD4+ T lymphocytes (all P＜0.05). Among the patients with different clinical stages, the patients with compensated cirrhosis had the highest HIV RNA load, the patients with chronic hepatitis C had the lowest HIV RNA load, the patients with end-stage liver disease had the lowest count of CD4+ T lymphocytes, and the patients with chronic hepatitis C had the highest PLT (all P＜0.05). ConclusionThe distribution of HCV genotypes is diverse in the patients with HIV/HCV coinfection in Guizhou, and HCV strains with genotypes 6a, 3b, and 1b are the main epidemic strains. Intravenous drug addiction is the main route of infection. Coinfection may affect HIV replication and immune status, with a significantly marked effect on HCV genotype 3b and liver cirrhosis or end-stage liver disease.

[摘 要] 目的：探讨CD68+ 肿瘤相关巨噬细胞（TAM）、CD8+ T细胞、Foxp3+ Treg细胞等在肺腺癌（LUAD）组织中浸润分布及其与患者预后的关系。方法：收集2004年9月至2009年4月间在苏州大学附属第三医院手术切除的93例LUAD组织及78例癌旁组织，采用组织芯片（TMA）及多重免疫荧光（mIF）技术检测其中的免疫细胞浸润与分布，Wilcoxon秩和检验比较癌与癌旁组织、癌巢与间质中浸润水平的差异，χ2检验分析其浸润水平及CD8+/CD68+细胞比值与临床病理特征的关系，Kaplan-Meier法和COX模型分析影响患者OS的潜在危险因素。结果：与癌旁组织比较，癌组织中CD68+ TAM、CD8+ T细胞、Foxp3+ Treg细胞浸润水平均显著增加（均P<0.01），间质CD68+ TAM、CD8+ T细胞的浸润水平均显著高于癌巢（均P<0.01）。总CD68+ TAM、癌巢及间质CD68+ TAM浸润水平与淋巴结转移呈正向关联（均P<0.05），癌巢CD68+ TAM浸润水平与T分期呈正向关联（P<0.05），间质CD68+ TAM浸润水平与病理分级呈正向关联（P<0.05）；癌组织中CD8+/CD68+细胞比值与病理分级、淋巴结转移均呈负向关联（均P<0.05）。Kaplan-Meier生存分析显示，LUAD组织中总CD68+ TAM、癌巢及间质CD68+ TAM高浸润患者OS均短于低浸润患者（P<0.05或P<0.01）、癌组织中CD8+/CD68+细胞比值高患者OS显著长于低比值患者（P<0.05）。多因素COX模型分析示，LUAD患者年龄、TNM分期及癌组织中CD8+/CD68+ 细胞比值是影响患者预后的独立风险因素（P<0.05或P<0.01）。结论:高度浸润的CD68+ TAM与LUAD的进展、侵袭、转移和不良预后显著关联，而高CD8+/CD68+ 细胞比值是影响LUAD患者OS的独立保护因素。