: The natural history of hepatitis B virus (HBV) infection is closely dependent on the dynamic interplay between the host immune response and viral replication. Spontaneous HBV clearance in acute self-limited infection is the result of an adequate and efficient antiviral immune response. Instead, it is widely recognized that in chronic HBV infection, immunologic dysfunction contributes to viral persistence. Long-lasting exposure to high viral antigens, upregulation of multiple co-inhibitory receptors, dysfunctional intracellular signaling pathways and metabolic alterations, and intrahepatic regulatory mechanisms have been described as features ultimately leading to a hierarchical loss of effector functions up to full T-cell exhaustion.
What Is the Current Status of Hepatitis B Virus Viro-Immunology? / Boni, C.; Rossi, M.; Montali, I.; Tiezzi, C.; Vecchi, A.; Penna, A.; Doselli, S.; Reverberi, V.; Ceccatelli Berti, C.; Montali, A.; Schivazappa, S.; Laccabue, D.; Missale, G.; Fisicaro, P.. - In: CLINICS IN LIVER DISEASE. - ISSN 1089-3261. - 27:4(2023), pp. 819-836. [10.1016/j.cld.2023.05.001]
What Is the Current Status of Hepatitis B Virus Viro-Immunology?
Boni C.;Rossi M.;Montali I.;Tiezzi C.;Ceccatelli Berti C.;Montali A.;Schivazappa S.;Laccabue D.;Missale G.;
2023-01-01
Abstract
: The natural history of hepatitis B virus (HBV) infection is closely dependent on the dynamic interplay between the host immune response and viral replication. Spontaneous HBV clearance in acute self-limited infection is the result of an adequate and efficient antiviral immune response. Instead, it is widely recognized that in chronic HBV infection, immunologic dysfunction contributes to viral persistence. Long-lasting exposure to high viral antigens, upregulation of multiple co-inhibitory receptors, dysfunctional intracellular signaling pathways and metabolic alterations, and intrahepatic regulatory mechanisms have been described as features ultimately leading to a hierarchical loss of effector functions up to full T-cell exhaustion.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.