Hepatitis E Virus and rheumatic diseases: what do rheumatologists need to know?
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Bartolomeo et al. BMC Rheumatology (2020) 4:51 https://doi.org/10.1186/s41927-020-00149-0
REVIEW
Open Access
Hepatitis E Virus and rheumatic diseases: what do rheumatologists need to know? Salvatore Di Bartolomeo1,2* , Francesco Carubbi1,2 and Paola Cipriani1 Abstract Background: Hepatitis E virus (HEV) represents the most common cause of acute hepatitis and jaundice in the world. About 2 million of infection cases occur each year in Europe, mainly as autochthonous anthropozoonosis, and HEV can be transmitted through undercooked pork meat. This infection has been linked to various extrahepatic manifestations, while chronic infections with a rapid development of liver failure have been described in heavily immunosuppressed patients undergoing solid organ transplantations (SOTs), in patients with hematological diseases or with immunodeficiency virus infection. Main body of abstract: The purpose of this review article is to describe rheumatic manifestations related to HEV infection and their implications for rheumatologists in the daily clinical practice. Despite recent accumulating literature in this field, little is known about the course of the infection in patients with rheumatic diseases (RDs) and about the impact of immunosuppressive drugs. Moreover, HEV infection can mimic RDs’ manifestations or drugs toxicity. Specific guidelines on management are lacking and the majority of data are referred to SOTs receivers. Conclusions: More studies are needed to better understand the real impact of HEV infection in patients with RDs, regarding both clinical outcomes and their management. Keywords: Hepatitis E virus, Rheumatic diseases, Immunosuppressive therapy, Chronic hepatitis, Rheumatic manifestations
Background Hepatitis E virus (HEV) is a non-enveloped, icosahedral, single-stranded positive RNA virus of 27–34 nm in diameter, that belongs to the Hepeviridae family [1, 2]. It was isolated for the first time in 1983 after an outbreak of fecal-oral transmitted non-A, non-B hepatitis among Soviet troops in Afghanistan [3], and in 1990 the virus genome was cloned [4]. It replicates in the cytoplasm of infected cells. Although HEV is a primary hepatotropic virus, infections of other tissues, including small intestine, colon, lymph nodes, neurons, kidney and placental tissue have been reported, partially explaining the pathogenesis of some extra-hepatic manifestations [5–7]. * Correspondence: [email protected] 1 Rheumatology Unit, Department of Biotechnological and Applied Clinical Science, School of Medicine, University of L’Aquila, L’Aquila, Italy 2 Department of Medicine, ASL1 Avezzano-Sulmona-L’Aquila, L’Aquila and Sulmona, Italy
HEV has a 7.2-kb genome which is organized in three open reading frames (ORFs). ORF1 encodes nonstructural proteins involved in the replication of viral genome (the so called “replicase”), including a methyl transferase, a putative protease, an RNA helicase and an RNA-dependent RNA polymerase. ORF2 encodes the viral capsid protein and ORF3 encodes a protein involved in release of
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