Plasma interleukin-7 correlation with human immunodeficiency virus RNA and CD4+T cell counts, and interleukin-5 with circulating hepatitis B virus DNA may have implications in viral control

• Type of Material: Article
• Authors: Jaisheela Vimali, Central University of Tamil Nadu; Yean Kong Yong, Xiamen University Malaysia; Amudhan Murugesan, Government Theni Medical College and Hospital; Kumaran Vishnupriya, Central University of Tamil Nadu; Rajeev Ashwin, Central University of Tamil Nadu; Evangeline Ann Daniel, Indian Council of Medical Research; Pachamuthu Balakrishnan, Saveetha Inst Med & Tech Sci SIMATS; Sivadoss Raju, Directorate of Public Health and Preventive Medicine; Mohamed Rosmawati, Universiti Malaya Medical Center; Vijayakumar Velu, Emory University; Marie Larsson, Linkoping University; Esaki M Shankar, Central University of Tamil Nadu
• Language: English
• Date: 2022-11-03
• Publisher: FRONTIERS MEDIA SA
• Publication Version: Final Published Version
• Copyright Statement: © 2022 Vimali, Yong, Murugesan, Vishnupriya, Ashwin, Daniel, Balakrishnan, Raju, Rosmawati, Velu, Larsson and Shankar.
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.3389/fmed.2022.1019230
• Title of Journal or Parent Work: FRONTIERS IN MEDICINE
• Volume: 9
• Start Page: 1019230
• End Page: 1019230
• Grant/Funding Information: This work was also supported by grants through: AI52731, the Swedish Research Council, the Swedish, Physicians against AIDS Research Foundation, the Swedish International Development Cooperation Agency, SIDA SARC, VINNMER for Vinnova, Linköping University Hospital Research Fund, CALF, and the Swedish Society of Medicine (to ML).; VV was supported by: The NIH Office of Research Infrastructure Programs (P51 OD011132 to ENPRC), and Emory CFAR (P30 AI050409).; This work was supported by funding provided by the Department of Science and Technology-Science and Engineering Research Board, Government of India (CRG/2019/006096) (to ES).
• Keywords: ASSOCIATION; REPLICATION; MARKERS; General & Internal Medicine; HIV-1 INFECTION; Science & Technology; GM-CSF; IL-7; Medicine, General & Internal; viral load; chronic viral hepatitis B; Life Sciences & Biomedicine; HIV; liver enzymes; hepatitis C; IMMUNE-RESPONSES; ACTIVE ANTIRETROVIRAL THERAPY; COLONY-STIMULATING FACTOR; cytokines; SERUM CYTOKINE LEVELS
• Research Categories: Biology, Microbiology

Abstract

Chronic viral infections represent a leading cause of global morbidity and mortality. Chronic HBV, HCV, and HIV infections result in cytokine perturbations that may hold key implications in understanding the complex disease mechanisms driving virus persistence and/or resolution. Here, we determined the levels of various plasma cytokines using a commercial Bio-Plex Luminex cytokine array in chronic HBV (n = 30), HCV (n = 15), and HIV (n = 40) infections and correlated with corresponding plasma viral loads (PVLs) and liver parameters. We observed differential perturbations in cytokine profiles among the study groups. The cytokines levels positively correlated with PVL and liver transaminases. The monocyte-derived cytokines viz., MIP-1β, IL-8, and TNF-α, and Th2 cytokines like IL-4, IL-5, and IL-13 showed a better correlation with liver enzymes as compared to their corresponding PVLs. Our investigation also identified two cytokines viz., IL-5 and IL-7 that inversely correlated with HBV DNA and HIV PVLs, respectively. Regression analysis adjusted for age showed that every increase of IL-5 by one unit was associated with a reduction in HBV PVL by log10 0.4, whereas, every elevation by a unit of IL-7 was associated with decreased HIV PVL by log10 2.5. We also found that IL-7 levels correlated positively with absolute CD4+ T cell counts in HIV-infected patients. We concluded that plasma IL-5 and IL-7 may likely have a key role on viral control in HBV and HIV infections, respectively. A noteworthy increase in cytokines appears to bear protective and pathological significance, and indeed is reflective of the host’s versatile immune armory against viral persistence.