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Foodborne Pathogens and Nanoparticles as a Tool for Quality Assurance and Intervention of Foodborne Pathogens
Published in Moayad N. Khalaf, Michael Olegovich Smirnov, Porteen Kannan, A. K. Haghi, Environmental Technology and Engineering Techniques, 2020
Porteen Kannan, S. Wilfred Ruban, M. Nithya Quintoil
The hepatitis E virus (HEV) usually enters the body through water or food, especially raw shellfish that has been contaminated by sewage. Anti-HEV activity has been determined in the serum of a number of domestic animals in areas with a high endemicity of human infection, indicating that this may be an emerging zoonosis.
Production and characterization of a fusion form of hepatitis E virus tORF2 capsid protein in Escherichia coli
Published in Preparative Biochemistry & Biotechnology, 2021
Mohamed Boumaiza, Khaled Trabelsi, Zeineb Choucha, Ines Akrouti, Serena Leone, Delia Picone, Héla Kallel
Hepatitis E virus (HEV), a small, non-enveloped RNA virus of the family Hepeviridae, is associated with endemic and epidemic acute viral hepatitis in developing countries. HEV genome is a positive-sense, single-stranded, 7.2-kb RNA containing three open reading frames (ORFs). ORF1 encodes nonstructural polyprotein (nsP) with multiple domains.[1]ORF2 encodes the viral structural protein of 660 amino acids (aa) which is involved in virion assembly and immunogenicity[2] and ORF3 encodes a small protein associated with virion morphogenesis and release.[3] It has been reported that this protein, encoded by ORF3, generates transient antibodies that are unsuitable for serological diagnosis of HEV.[4] Clinical strains of HEV have been diagnosed by quantifying viral RNA in culture supernatants and cell lysates.[5] On the other hand, the ORF2 gene is highly conserved among HEV species and has been shown to induce long-lived immunity, therefore it has been selected for serological diagnosis of HEV and used as the main antigen for vaccine development against HEV infection.[4,6,7] Furthermore, it has been reported that HEV infection leads to the secretion of 3 forms of ORF2: infectious ORF2 (ORF2i), glycosylated ORF2 (ORF2g), and cleaved ORF2 (ORF2c).[8] Indeed, TORF2i, which correspond to the structural component of infectious particles, is not glycosylated. However, it has been demonstrated recently that ORFg/c protein is N-glycosylated on N1 and N3 sites but not on the N2 site and that N-glycosylation of ORF2 protein does not play any role in replication and assembly of infectious HEV particles.[9]