Serum cytokine/chemokine profiles predict hepatitis B reactivation in HBV/HCV co-infected subjects receiving direct-acting antiviral agents

J Formos Med Assoc. 2022 May;121(5):920-929. doi: 10.1016/j.jfma.2021.09.002. Epub 2021 Sep 15.

Abstract

Background/purpose: Direct-acting antiviral agents (DAAs) have revolutionized the paradigm for HCV treatment. However, patients with HBV and HCV co-infection receiving DAAs are at significant risk of HBV reactivation, with limited literature addressing the roles of serum chemokines/chemokines. We aimed to explore the profiles and predictive value of serum cytokines/chemokines regarding HBV reactivation in this clinical setting.

Methods: From 2017 to 2019, 25 patients with HBV and HCV co-infection scheduled for DAA therapy were prospectively enrolled. At enrolment and after DAA treatment, serial serum cytokine/chemokine levels were examined. The baseline and dynamic levels were compared between those with versus without HBV virologic (defined by an increase of serum HBV DNA to >10 times) and clinical reactivation (defined by > 1.5-fold elevated ALT level than nadir and >100 U/L; or > 2-fold increase from nadir and greater than the upper normal limit, in addition to virologic reactivation).

Results: There were 20 patients (80%) experiencing HBV virologic reactivation and 6 patients (24%) experiencing clinical reactivation. Patients with clinical reactivation had higher pre-treatment TNF-alpha (27.93 versus 18.85 pg/mL, P = 0.015), lower week-4 IFN-gamma (1.07 versus 8.74 pg/mL, P = 0.020) levels and significant declines of CCL2 and TNF-alpha (P < 0.05). Single or combination of these cytokines helped predict clinical reactivation (all P < 0.05).

Conclusion: Higher serum TNF-alpha at baseline and lower IFN-gamma at week 4 were associated with mild clinical reactivation of HBV in patients with HBV/HCV co-infection receiving DAAs. Combination of these cytokines reliably predicted HBV reactivation early.

Keywords: Acute flare; Co-infection; C–C motif chemokine ligand 2; Interferon-gamma; TNF-alpha.

MeSH terms

  • Antiviral Agents / adverse effects
  • Chemokines
  • Coinfection* / drug therapy
  • Cytokines
  • Hepacivirus
  • Hepatitis B virus / physiology
  • Hepatitis B* / drug therapy
  • Hepatitis C* / drug therapy
  • Hepatitis C, Chronic* / drug therapy
  • Humans
  • Tumor Necrosis Factor-alpha
  • Virus Activation

Substances

  • Antiviral Agents
  • Chemokines
  • Cytokines
  • Tumor Necrosis Factor-alpha