Distinct inflammation-related proteins associated with T cell immune recovery during chronic HIV-1 infection. Issue 1 (31st December 2023)

• Record Type: Journal Article
• Authors: Wan, Lin-Yu; Huang, Hui-Huang; Zhen, Cheng; Chen, Si-Yuan; Song, Bing; Cao, Wen-Jing; Shen, Li-Li; Zhou, Ming-Ju; Zhang, Xiao-Chang; Xu, Ruonan; Fan, Xing; Zhang, Ji-Yuan; Shi, Ming; Zhang, Chao; Jiao, Yan-Mei; Song, Jin-Wen; Wang, Fu-Sheng
• Is Part Of: Emerging microbes & infections. Volume 12:Issue 1(2023)
• Publication Date: 2023-12-31
• Subjects: HIV-1 -- Inflammation -- HIV-1 reservoir -- CXCL9 -- CXCL10 -- CXCL11 -- T cell dysregulation; Medical microbiology -- Periodicals; Communicable diseases -- Periodicals; Infection -- Periodicals; 616.9041
• DOI: 10.1080/22221751.2022.2150566
• Languages: English
• ISSNs: 2222-1751

Abstract

ABSTRACT: Chronic inflammation and T cell dysregulation persist in individuals infected with human immunodeficiency virus type 1 (HIV-1), even after successful antiretroviral treatment. The mechanism involved is not fully understood. Here, we used Olink proteomics to comprehensively analyze the aberrant inflammation-related proteins (IRPs) in chronic HIV-1-infected individuals, including in 24 treatment-naïve individuals, 33 immunological responders, and 38 immunological non-responders. T cell dysfunction was evaluated as T cell exhaustion, activation, and differentiation using flow cytometry. We identified a cluster of IRPs (cluster 7), including CXCL11, CXCL9, TNF, CXCL10, and IL18, which was closely associated with T cell dysregulation during chronic HIV-1 infection. Interestingly, IRPs in cluster 5, including ST1A1, CASP8, SIRT2, AXIN1, STAMBP, CD40, and IL7, were negatively correlated with the HIV-1 reservoir size. We also identified a combination of CDCP1, CXCL11, CST5, SLAMF1, TRANCE, and CD5, which may be useful for distinguishing immunological responders and immunological non-responders. In conclusion, the distinct inflammatory milieu is closely associated with immune restoration of T cells, and our results provide insight into immune dysregulation during chronic HIV-1 infection.