Please use this identifier to cite or link to this item: http://localhost:8080/xmlui/handle/123456789/9536
Title: Higher hepatitis B core-specific T cell response is associated with a lower risk of clinical relapse after discontinuation of oral antiviral treatment
Authors: Tseng, Tai-Chung
Cheng, Huei-Ru
Su, Tung-Hung
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Keywords: HBV
Immunity
HBsAg
HBcrAg
Immunotherapy
Issue Date: Oct-2024
Publisher: Journal of Microbiology, Immunology and Infection
Series/Report no.: Original Article;700-708
Abstract: Background: Hepatitis B virus (HBV)-specific T cell response is a major host immune response to control the virus. However, it is still unclear how it affects long-term outcomes of chronic hepatitis B patients, especially those who stop nucleos(t)ide analogue (NA) therapy. We aimed to explore whether the HBV-specific T cell response at the end of treatment (EOT) was associated with clinical outcomes. Methods: In a prospective cohort study, 51 HBeAg-negative patients who discontinued NA therapy were enrolled. Results: In amean follow-up of 25.3months, 25 patients developed clinical relapse.We found that a stronger hepatitis B core (HBc)-specific T cell response at EOTwas associated with a lower risk of clinical relapse. Compared to the low-response group, the high-response group had a lower risk of clinical relapsewith hazard ratio of 0.21 (95% CI: 0.05e0.88). The high HBc-specific Tcell response was associated with reduced surge of HBV DNA and HBcrAg during the first year of follow-up. The T cell response at EOTwas comparable between different NA treatments. Notably, the overall HBVspecific T cell response could be partially restored along with clinical relapse; however, such reinvigorated T cell response was not associated with HBsAg seroclearance. Conclusions: A higher HBc-specific T cell response at EOTwas associated with lower risk of clinical relapse and reduced surge of HBV DNA and HBcrAg levels off NA therapy.
URI: http://localhost:8080/xmlui/handle/123456789/9536
ISSN: 1684-1182
Appears in Collections:Vol. 57 No. 5 (2024)

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