Immune drivers of HBsAg loss in HBeAg-negative CHB patients after stopping nucleotide analog and administration of Peg-IFN.
Hepatol Commun
; 7(5)2023 05 01.
Article
em En
| MEDLINE
| ID: mdl-37102765
ABSTRACT
BACKGROUND:
The stoppage of nucleoside analog (NA) can lead to immune flare and loss of HBsAg in a proportion of HBeAg-negative chronic hepatitis B (CHB) patients. HBsAg loss could be improved by instituting Peg-Interferon therapy in those who show an immune flare after the stoppage of NA. We investigated the immune drivers of HBsAg loss in NA-treated HBeAg-negative CHB patients after stopping NAs and administration of Peg-IFN-α2b therapy.METHODS:
Fifty-five NA-treated eAg-ve, HBV DNA not detected CHB patients were subjected to stopping NA therapy. Twenty-two (40%) patients relapsed (REL-CHBV) within 6 months (HBV DNA ≥2000 IU/mL, ALT ≥2XULN) and were started on Peg-IFN-α2b (1.5 mcg/kg) for 48 weeks (PEG-CHBV). Cytokine levels, immune responses, and T-cell functionality were assessed.RESULTS:
Only 22 (40%) of 55 patients clinically relapsed, of which 6 (27%) cleared HBsAg. None of the 33 (60%) nonrelapsers cleared HBsAg. REL-CHBV patients had significantly increased IL-6 (p=0.035), IFN-γ (p=0.049), Th1/17 (p=0.005), CD4 effector memory (EM) (p=0.01), Tfh1/17 (p=0.005), and mature B cells (p=0.04) compared with CHBV. Six months after Peg-IFN therapy, immune resetting with a significant increase in CXCL10 (p=0.042), CD8 (p=0.01), CD19 (p=0.001), and mature B cells (p=0.001) was observed. HBV-specific T-cell functionality showed increased Tfh-secreting IFN-γ (p=0.001), IL-21 (p=0.001), and TNF-α (p=0.005) in relapsers and IFN-γ-secreting CD4 T cell (p=0.03) in PEG-CHBV.CONCLUSIONS:
Stopping NA therapy induces flare in about 40% of HBeAg-negative patients. Peg-IFN therapy given to such patients causes immune restoration with HBsAg loss in one fourth of them.
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Hepatite B Crônica
/
Antígenos de Superfície da Hepatite B
Limite:
Humans
Idioma:
En
Revista:
Hepatol Commun
Ano de publicação:
2023
Tipo de documento:
Article
País de afiliação:
Índia