The Discovery of the Hepatitis D Virus: Three Princes of Serendip and the Recognition of Autoantibodies to Liver‐Kidney Microsomes

Abstract

During my university years in Padua, where I followed in the footsteps of William Harvey (Fig. 1), I was fascinated by the emerging discipline of hepatology. In the 1950s, two discoveries opened the way to understanding the new and evolving entity of chronic hepatitis (CH). First was the observation by the Italian clinicians Fernando de Ritis, Mario Coltorti, and Giuseppe Giusti 1 that serum transaminases (or aminotransferases, for the pedants among you) that once were the sole domain of the cardiologists 2 were elevated in patients with hepatitis. Ironically, cardiologists now find that serum alkaline phosphatase and gamma-glutamyl transferase are useful in assessing coronary artery disease. 3 Second was the almost coincident honing of the technique of liver biopsy by Dr. Giorgio Menghini 4 (Fig. 2). The allure of CH was that it seemed to be the missing link between cirrhosis (which had been known since antiquity) and acute hepatitis.

Hepatitis D virus infection: Progress on the path toward disease control and cure

“…It uncovered the global impact of this small virus as a major cause of liver-related morbidity and mortality in people with HBV infection. 2,3 While the epidemiological studies are incomplete in some regions, an estimated 12 million people worldwide are chronically infected with hepatitis B and D, placing them at risk for faster progression to cirrhosis, hepatic decompensation and hepatocellular carcinoma compared to people with HBV alone. For people diagnosed with active HDV infection, effective treatments for hepatitis D virus infection have been elusive, limited to prolonged courses of high-dose interferon alfa.…”

“…However, identifying a novel RNA genome in the chimpanzees carrying the delta antigen led to the designation of this pathogen as the hepatitis D virus. It uncovered the global impact of this small virus as a major cause of liver‐related morbidity and mortality in people with HBV infection 2,3 . While the epidemiological studies are incomplete in some regions, an estimated 12 million people worldwide are chronically infected with hepatitis B and D, placing them at risk for faster progression to cirrhosis, hepatic decompensation and hepatocellular carcinoma compared to people with HBV alone.…”

Clinical andIn SituCharacterization of Hepatitis Delta Virus in Sjogren’s Syndrome

“…Anti-mitochondrial antibodies (AMA) occur in 1.7-13% of Sjogren's syndrome patients and most often in patients with primary biliary cirrhosis (PBC) (29,30). Increased prevalence of anti-mitochondrial antibodies (AMA) has also been reported in PBC (31), but no direct associations between detectible AMA and HDV have been reported. The detected co-localization of HDAg with mitochondria and its potential impact on mitochondrial function and cellular respiration warrants further investigation.…”

Efficacy and safety of bulevirtide in patients with chronic hepatitis D and compensated cirrhosis

“…Результаты исследований продемонстрировали преимущества булевиртида в эффективности по сравнению с тенофовиром и ПЕГ-ИФН и позволили рекомендовать препарат в качестве 1-й линии лечения ХГD [1]. Эффективность лечения повышалась с увеличением длительности лечения с 24 до 48 нед.…”

“…Вирус гепатита D (HDV) -открытый в 1977 г. М. Риццетто дефектный вирус-сателлит вируса гепатита В (HBV), не имеющий собственных ферментных систем (полимераз) и собственной оболочки, использующий для репликации полимеразы клетки, для построения оболочки -HBsAg (поверхностный антиген вируса гепатита В) [1,27]. Распространенность хронической инфекции HDV составляет в среднем 4,5% от HBsAg-позитивных лиц, что соответствует 12 млн инфицированных HDV в мире [2,3].…”