Dynamic profile of the HBeAg-anti-HBe system in acute and chronic hepatitis B virus infection: A clinical-laboratory app

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Dynamic profile of the HBeAg-anti-HBe system in acute and chronic hepatitis B virus infection: A clinical-laboratory approach Robério Amorim de Almeida Pondé1,2  Received: 17 September 2020 / Accepted: 1 December 2020 © The Author(s), under exclusive licence to Springer Nature B.V. part of Springer Nature 2020

Abstract Wild-type HBV infection is followed by the blood expression of its widely known serological markers of infection, and designated as, hepatitis B virus surface antigen (HBsAg) and its antibody (anti-HBs), anti-HBc antibodies (IgM/IgG), and hepatitis B virus ‘e’ antigen (HBeAg) and its antibody (anti-HBe). These markers are detected as the infection develops and its kinetic behavior serves as a basis for monitoring the disorder and for diagnosing the clinical form or infection phase. Among these, the HBeAg-anti-HBe system markers demonstrate a dynamic profile whose interpretation, both in the acute or chronic HBV infection context, can offer greater difficulty to the health professionals, due to its particularities. This review offers a revisit to the markers dynamics of this system in the acute and chronic HBV infection and to the clinical and laboratory significance of its expression in these two clinical contexts. Keywords  Hepatitis B virus · HBe Antigen · Anti-HBe antibodies · Acute HBV infection · Chronic HBV infection

Introduction The hepatitis B virus (HBV) has a universal distribution and remains a global health problem, despite the control and prevention measures adopted, and availability of effective antiviral therapy [1]. Its transmission can occur through percutaneous or mucosal exposure to infectious fluids [2, 3], through sexual contact with infected people, and even vertically (from mother to son), from mothers infected with the agent [4]. The vertical transmission from father to infant has also been considered based on the possible integration of HBV/DNA into genes of germ cells (human sperm chromosome) and subsequent infection of the offspring during fertilization [5, 6]. In humans, HBV infection can vary from an unapparent form to the manifest clinical disease, which can progress * Robério Amorim de Almeida Pondé [email protected] 1



Laboratory of Human Virology, Institute of Tropical Pathology and Public Health, Federal University of Goiás, Goiânia, Goiás, Brazil



Secretaria de Estado da Saúde -SES/Superintendência de Vigilância em Saúde-SUVISA/GO, Gerência de Vigilância Epidemiológica-GVE/Coordenação de Análises e Pesquisas-CAP, Goiânia, Goiás, Brazil

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from an acute form to recovery, with long-lasting immunity, or to the chronic carrier state. The signs and infection symptoms development varies according to age, being practically nonexistent in newborns, and slightly more prominent in adults (33–50% of cases), with severity ranging from moderate to fulminant [7]. However, regardless of the clinical characteristics (whether symptomatic or asymptomatic) or the infection clinical phase (whether acute or chronic), the infection with the wild-type HBV is followe