Snapshot A 35-year-old presents to the emergency department due to abdominal pain and malaise. He also reports "yellow-ing" of his skin. Medical history is noncontributory. Social history is notable for intravenous drug use and having multiple sexual partners. Physical examination is remarkable for right upper quadrant tenderness, generalized jaundice, and scleral icterus. Laboratory studies demonstrate the presence of HBsAg and significantly elevated IgM anti-HBc, and HBeAg. Introduction Classification a Hepadnavirus in the Hepadnaviridae family circular, partially double-stranded DNA virus Epidemiology risk factors not receiving hepatitis B virus (HBV) vaccine sexual contact with a person with HBV illicit drug use having HIV and hepatitis C virus Transmission perinatal transmission blood transfusion transplant sexual contact blood exposure Pathogenesis once the HBV is in the bloodstream, it makes its way to the liver, where it replicates within hepatocytes, causing immune-mediated hepatitis via CD8+ T-cells and natural killer cells when HBV is inside the hepatocyte, the viral genome enters the hepatocyte nucleus the positive strand of the HBV DNA is synthesized and is converted to covalently closed, circular DNA (cccDNA) the HBV genome undergoes reverse transcription, creating a pre-genomic RNA, which becomes encapsidated a new negative and subsequent positive strand of the HBV DNA is eventually synthesized the partially double-stranded HBV DNA nucleocapsid can enter more hepatocytes to produce more cccDNA Prognosis most immunocompetent adult patients spontaneously recover 90% of infected adults recover, 10% progress to chronic infection most neonates progress to chronic infection worse prognosis with coinfection with hepatitis D or hepatitis C infection Presentation Symptoms acute hepatitis anorexia nausea right upper quadrant pain chronic hepatitis many are asymptomatic fatigue Physical exam acute hepatitis jaundice and scleral icterus typically resolves in 1-3 months chronic hepatitis normal may have stigmata of chronic liver disease e.g., spider angiomata, ascites, and asterixis extrahepatic manifestations polyarteritis nodosa membranous nephropathy (leading to nephrotic range proteinuria) and less commonly, membranoproliferative glomerulonephropathy aplastic anemia Studies Liver function tests Alanine/aspartate aminotransferases (ALT/AST) Elevation in the acute phase of up to 1,000 to 2,000 U/L Milder elevations or can be normal in the chronic phase Serologic studies HBsAg indicates that there is an HBV infection anti-HBs indicates immunity to HBV infection via prior infection vaccination HBcAg an antigen associated with the core of the HBV anti-HBc IgM antibodies against HBc suggests an acute or recent infection IgG antibodies against HBc suggest a previous exposure or chronic infection during the window period, may be the only positive serologic test suggesting infection HBeAg infected hepatocytes secrete this antigen, suggesting active replication, thus having high transmissibility anti-HBe suggest low transmissibility Differential Hepatitis A infection differentiating factor presence of anti-hepatitis A antibodies in serological testing Hepatitis C infection differentiating factor presence of anti-hepatitis C antibodies in serological testing Treatment Medical vaccination indication as a preventative measure against HBV infection all neonates all unvaccinated infants, children, and adolescents all unvaccinated adults with an increased risk of contracting the infection healthcare personnel a sexually-active person with multiple sexual partners end-stage renal disease HIV infection chronic liver disease tenofovir or entecavir indication monotherapy for acute HBV infection in patients with fulminant infection or severe acute hepatitis (e.g., increased INR) monotherapy for chronic HBV infection with immune-active chronic hepatitis HBeAg-positive HBeAg-negative with elevated viral DNA levels and a transaminitis patients with hepatocellular carcinoma comments acute HBV infection is usually symptomatically treated as most cases self-resolve Complications Superinfection with hepatitis D virus Acute fulminant hepatic failure Cirrhosis Hepatocellular carcinoma