Hepatitis viruses: neurologic complications

Sergio Monteiro de Almeida MD PhD (

Dr. de Almeida of Universidade Federal do Paraná, Brazil, has no relevant financial relationships to disclose.

)
Gabriel LO Salvador MD (

Dr. Salvador of Universidade Federal do Paraná, Brazil, has no relevant financial relationships to disclose.

)
Maria Lucia Alves Pedroso MD PhD (

Dr. Pedroso of Universidade Federal do Paraná, Brazil, has no relevant financial relationships to disclose.

)
Christina M Marra MD, editor. (

Dr. Marra of the University of Washington School of Medicine owned stock in Johnson & Johnson and McKesson within the past 12 months.

)
Originally released February 8, 2015; last updated January 28, 2020; expires January 28, 2023

Overview

Viral hepatitis has emerged as a major public health problem worldwide, affecting several hundreds of millions of people. It is a cause of considerable morbidity and mortality in the human population, both from acute infection and chronic sequelae. Hepatitis viruses encompass a range of diverse and unrelated group of viruses from different families, with the common characteristics of hepatotropism, hepatovirulence, and hepatotoxicity. The hepatitis viruses of neurologic interest primarily comprise RNA viruses, hepatitis A, C, and E viruses (HAV, HCV, and HEV, respectively), and a DNA virus, hepatitis B virus (HBV) (Sellner and Steiner 2014). This article provides a broad overview of the neurologic manifestations and complications of acute and chronic viral hepatitis.

Key points

 

• The most common hepatitis viruses with nervous system involvement are hepatitis C virus and hepatitis B virus.

 

• Hepatitis viruses can affect the entire nervous system, including the brain, spinal cord, motor neurons, peripheral nerves, and muscles.

 

• The most common neurologic manifestation of hepatitis C virus and hepatitis B virus is peripheral neuropathy.

 

• A significant proportion of patients with chronic hepatitis C virus experience cognitive impairment in the absence of advanced liver disease.

 

• Neurologists should be aware of the specific neurologic complications of hepatitis viruses.

Historical note and terminology

There were a number of key milestones in the history of hepatitis viruses during the 20th century. From 1942 to 1950, a series of independent experiments in Europe and the United States confirmed the transmissibility of viral hepatitis A and B and defined their clinico-epidemiological characteristics. However, the individualization of hepatitis viruses only emerged after World War II. In 1947, MacCallum classified viral hepatitis into 2 types, hepatitis A and B. In 1965, Baruch Blumberg identified the hepatitis B surface antigen (HBsAg). Blumberg was awarded the Nobel Prize in Medicine in 1976 for both the description of hepatitis B virus and the notion of the revolutionary first-generation hepatitis B virus vaccine. In 1973, Stephen Mark Feinstone identified the hepatitis A virus using immune-electron microscopy. In 1974, Prince and Feinstone independently described several cases of posttransfusion hepatitis, HBs negative, named non-A non-B hepatitis. However, it was only in 1989 that hepatitis C virus, responsible for 80% to 90% of posttransfusion hepatitis, was identified. The discovery of hepatitis C virus by Choo and colleagues started a new era because it was the first virus identified using a direct molecular approach. Hepatitis E virus was only identified in 1990 by Reyes (Trepo 2014). The neurologic history of hepatitis viruses started in 1943, when Arthur Hurst reported the first case of acute polyneuropathy secondary to hepatitis. Hepatitis C virus sequences in the brain were first reported in 1996 by Bolay and associates (Abutaleb et al 2018). In the beginning of the 21st century, evidence of a cerebral effect of hepatitis C virus was shown for the first time (Forton et al 2001; Forton et al 2004).

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