Transmission of a homogenous hepatitis B virus population of A1896-containing strains leading to mild resolving acute hepatitis and seroconversion to hepatitis B e antigen antibodies in an adult

Abstract

Although the molecular biology is reasonably straightforThe pre-core variant, A 1896 , which switches off hepatitis B ward, associations with clinical outcome are less firm. A 1896 e antigen (HBeAg) production, is common in hepatitis B e was first discovered in persons with hepatitis B e antigen antigen antibody (anti-HBe)-positive chronic hepatitis paantibody (anti-HBe)-positive severe chronic hepatitis, 1,2 but tients. It has been observed in occasional case reports of acute was subsequently found in those with mild hepatitis. 7,8 Simihepatitis. However, transmission in the absence of HBeAglarly, the strength of reported associations of A 1896 with fulmiproducing strains, leading to acute nonfulminant hepatitis and nant hepatitis 9 has been diluted by such strains being occaclearance in adults, has not been reported. Here, we show sionally observed in acute, nonfulminant hepatitis, and by a that this event can occur, further confirming that A 1896 strains low incidence in HBeAg-positive fulminant patients. 10

Long-Term Follow-Up of Acute Hepatitis B: New Insights in Its Natural History and Implications for Antiviral Treatment

“…However, its role in HBsAg clearance still needs elucidation. This study demonstrates for the first time the association between the G1896A mutation and a shorter time to HBsAg clearance, extending the observation that it can occur very early after infection (or could indeed be transmitted, as previously suggested [ 33 ]). Although in chronic infection G1896A has been controversially suspected of being related to decompensated cirrhosis or cancer [ 34 , 35 ], in acute hepatitis it could be rather considered as a marker of a potent cytotoxic immune response (at genotype parity), generating more severe liver alterations [ 36 ] but most successful at clearing the infection.…”

Detection and significance of a G1862T variant of hepatitis B virus in Chinese patients with fulminant hepatitis

“…The co-existence therefore of HBeAg- with non-HBeAg-producing variants may be due to the preexistence of the wild-type virus or due to degraded core, released as a result of the extensive liver tissue damage. Anti-HBe has been detected following transmission of the G1896A variant, even though in this case report, HBeAg was not detectable during the acute phase (Mphahlele et al , 1997 ). HBeAg epitopes can therefore be presented to the immune system by degraded core protein, and lead to the production of anti-HBe, in the absence of the authentic protein.…”

Hepatitis B Virus e Antigen Activates the Suppressor of Cytokine Signaling 2 to Repress Interferon Action

“…It is known that HBeAg is not required for HBV replication and its exact function is unclear, but may play a role in chronic HBV infection 17, 18 . The emergence of HBeAg-negative variants correlates with an exacerbation of liver injury in some patients 20, 21 . HBeAg modulates host immune response during CHB progression 22 , suppresses TLR-induced IFN-β and ISG production in liver cells 23 , and inhibits IL-18 signaling and IFN-γ expression in NK and hepatoma cells 36 .…”

“…The emergence of HBeAg-negative variants correlates with an exacerbation of liver injury and even with viral clearance in some patients 20, 21 . HBeAg is responsible for modulation of host immune response during CHB progression, inhibits TLR-2 expression, and abrogates the antiviral activity of TLR signaling via suppressing IFN-β and ISG production 22–25 .…”