Objective: To analyze the characteristic of T cell response to specific antigen proteins in patients with hepatitis B virus infection.
Methods: 76 cases were recruited, including four groups, acute hepatitis B (AHB), active phase of chronic hepatitis B (CHB), inactive HBV carriers (AsC) and past HBV infection. T cell responses stimulated by 3 antigen specific proteins of HBV were detected using enzyme linked immunospot (ELISPOT) assay.
Results: (1) There were no significant difference in frequencies to HBsAg, HBcAg and HBeAg in AHB and CHB. The frequencies to HBsAg and HBcAg in AsC were lower than that to HBeAg, and the frequencies to HBsAg in group of past HBV infection were significantly lower than that to HBcAg and HBeAg. (2) The frequencies to HBsAg in AHB and CHB both were higher than in group of past HBV infection. The frequencies to HBcAg of AHB, CHB and AsC were higher than that of group of past HBV infection. (3) There were no significant difference in magnitude to HBsAg, HBcAg and HBeAg in AHB and AsC. In CHB, the magnitude to HBsAg was lower than that to HBcAg. The magnitude of in group of past HBV infection were HBcAg > HBeAg > HBsAg. (4) In four groups, the sequence of the magnitude to HBsAg from high to low was AHB, CHB, group of past HBV infection and AsC. The magnitude to HBcAg in of AsC was lower than other three groups. As to the magnitude to HBeAg, the difference was no significant between any two groups except between AHB and CHB.
Conclusions: The T cell responses in group of AsC to HBeAg were the highest, while the T cell responses to HBcAg were the highest in group of other groups.
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PLoS Pathog
January 2025
State Key Laboratory of Virology and Hubei Province Key Laboratory of Allergy and Immunology, Institute of Medical Virology, TaiKang Medical School, Wuhan University, Wuhan, China.
Chronic hepatitis B virus (HBV) infection can significantly increase the incidence of cirrhosis and liver cancer, and there is no curative treatment. The persistence of HBV covalently closed circular DNA (cccDNA) is the major obstacle of antiviral treatments. cccDNA is formed through repairing viral partially double-stranded relaxed circular DNA (rcDNA) by varies host factors.
View Article and Find Full Text PDFRheumatol Int
January 2025
Department of Pathophysiology, National and Kapodistrian University of Athens, Athens, Greece.
Introduction: Hepatitis B reactivation and administration of prophylactic antiviral treatment are considered in patients with autoimmune inflammatory rheumatic diseases (AIIRD) undergoing immunosuppressive/immunomodulatory treatment. Data are more robust for rheumatoid arthritis patients receiving bDMARDs but are limited for other AIIRD and drug categories.
Methods: Adult patients with AIIRD (inflammatory arthritis [IA] or connective tissue diseases [CTD]) and documented chronic or resolved HBV infection (defined as serum HBsAg positivity or anti-HBcAb positivity in the case of HBsAg non-detection respectively), followed-up in six rheumatology centers in Greece and Italy, were included.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
December 2024
Department of Infection and Immunology, Changsha First Hospital, Changsha 410005, China.
Objective To clarify the mechanism that HIV infection mediates mitochondrial damage of CD4 T lymphocytes (CD4 T cells) through mitogen-activated protein kinase (MAPK) pathway. Methods From October 1st, 2022 to March 31st, 2023, 47 HIV-infected people who received antiretroviral therapy (ART) for 4 years were recruited, including 22 immune non-responders (INR) and 25 responders (IR); and 26 sex and age-matched control participants (HC) who were negative for HCV, HBV, and HIV infections. The immune parameters were analyzed by flow cytometry.
View Article and Find Full Text PDFJ Med Virol
January 2025
Center of Infectious Diseases, West China Hospital of Sichuan University, Chengdu, China.
Glucose-regulated protein 78 kDa (GRP78), a key marker of endoplasmic reticulum stress (ERS), is upregulated in hepatocellular carcinoma (HCC) tissues, but its role in hepatitis B virus (HBV)-induced tumorigenesis remains unclear. This study aimed to investigate the contribution of GRP78 to HBV-associated tumor development and explore the ERS pathways involved. The results showed that increased GRP78 expression in patients with HBV-related HCC was associated with a poor prognosis within the first 2 years following diagnosis.
View Article and Find Full Text PDFEmerg Microbes Infect
January 2025
Storr Liver Centre, The Westmead Institute for Medical Research, Westmead Hospital and The University of Sydney, Westmead, NSW, Australia.
Hepatitis B virus (HBV) DNA integration into the host cell genome is reportedly a major cause of liver cancer, and a source of hepatitis B surface antigen (HBsAg). High HBsAg levels can alter immune responses which therefore contributes to the progression of HBV-related disease. However, to what extent integration leads to the persistent circulating HBsAg is unclear.
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