HBV and HIV/HBV Infected Patients Have Distinct Immune Exhaustion and Apoptotic Serum Biomarker Profiles

Pathogens & Immunity
Mohamed T ShataKenneth E Sherman

Abstract

Hepatitis B virus (HBV) infection is a leading cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma worldwide. Due to their shared routes of transmission, approximately 10% of HIV-infected patients worldwide are chronically coinfected with HBV. Additionally, liver disease has become a major cause of morbidity and mortality in HBV/HIV coinfected patients due to prolonged survival with the success of antiretroviral therapy. The relationship between immune exhaustion markers (PD-1/PD-L1) and apoptotic markers such as Fas/FasL, TGFβ1, TNF-α, and Th1/Th2 cytokines are not clearly delineated in HBV/HIV coinfection. Levels of soluble Fas/FasL, TGFβ1, TNF-α, and sPD-1/sPD-L1 as well as Th1 and Th2 cytokines were evaluated in the sera of HBV-monoinfected (n = 30) and HBV/HIV-coinfected (n = 15) patients and compared to levels in healthy controls (n = 20). HBV-monoinfected patients had significantly lower levels of the anti-inflammatory cytokine IL-4 (P < 0.05) and higher levels of apoptotic markers sFas, sFasL, and TGFβ-1 (P < 0.001) compared to healthy controls. Coinfection with HIV was associated with higher levels of sFas, TNF-α, and sPD-L1 (P < 0.005), and higher levels of the pro-inflammatory cytokines IL-6, IL...Continue Reading

Citations

Mar 7, 2020·Current Opinion in HIV and AIDS·Jennifer Audsley, Joe Sasadeusz
May 1, 2021·International Journal of Clinical Practice·Muhammed BekçibaşıMustafa Kemal Çelen
May 25, 2021·Journal of Immunoassay & Immunochemistry·Oluwadamilola Gideon OsasonaOluwatosin Oluwagbenga Oguntoye
Jun 4, 2021·Frontiers in Immunology·Shu YuanZi-Lin Li
Jul 30, 2021·Biochimica Et Biophysica Acta. Reviews on Cancer·Keerthi KurmaPatrick Legembre

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Methods Mentioned

BETA
ELISA
PCR

Software Mentioned

Bio
SAS
Plex Manager
R

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis