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    • Substantial epidemics and sporadic outbreaks of

    2018-11-09

    Substantial epidemics and sporadic outbreaks of hepatitis E occur in tropical and sub-tropical countries (e.g., in India, Uganda, Sudan, and Mexico), with up to tens of thousands affected (Dalton et al., 2013; Kamar et al., 2012). Approximately two billion people (one-third of the world population) live in areas endemic for HEV and are at risk (Perez-Gracia et al., 2013). HEV infections are less frequently documented in industrialized countries, as it is believed to be associated with travel to HEV-endemic countries. However, by the end of the millennium, the numbers of autochthone cases were rising exponentially. HEV infections in Western Europe have been reported (Dalton et al., 2013; Kamar et al., 2012; Pischke et al., 2014). Reasons for discrepancies of HEV presentation between developing and developed countries are diverse. The possible likelihood refers to the route of transmission and the different distribution of HEV genotypes (Pauli et al., 2015; Sayed et al., 2015). In developing countries, HEV infection is transmitted mainly as waterborne/fecal-oral due to poor hygiene conditions, whereas in developed countries HEV is transmitted mainly foodborne due to zoonotic transmission by consumption of undercooked meat and bowels (Mansuy et al., 2016). In this regard, HEV is unique, as the only hepatitis virus with an animal reservoir. HEV variants are viral factors that are known to be associated with transmission dynamics and pathogenicity (Kamar et al., 2012, 2014a; Lee et al., 2016; Meng, 2011). HEV mutations occur under selective pressure imposed by the host order Exendin-3 (9-39) amide and by antivirals. HEV heterogeneity shall contribute towards HEV physiology, pathogenesis and transmission patterns (Lhomme et al., 2014a). In this review, we aim to compile knowledge and discuss recent advances on the casual role of HEV heterogeneity and its variants on viral morphogenesis, pathogenesis, clinical relevance and antiviral resistance.
    Clinical Course and Pathogenesis of HEV Infection Although the majority of HEV infections are asymptomatic, the clinical course of symptomatic infections includes acute and chronic hepatitis E, fulminant liver failure and extrahepatic symptoms (Debing et al., 2016a; Hoan et al., 2015). Acute hepatitis E is usually defined as a self-limiting disease and lasts approximately 8weeks and the symptoms are typically unspecific and mostly indistinguishable from other types of acute viral hepatitis (Wedemeyer et al., 2012). HEV-RNA can be detected in both serum and stool before the onset of clinical symptoms and lasts less than a month after symptom onset in serum but may persist longer in the stool (Krain et al., 2014). A severe form of acute hepatitis (fulminant hepatic failure) has been observed in patients with pre-existing liver diseases and in pregnant women (Dalton et al., 2007; Navaneethan et al., 2008). The severity of HEV infection in pregnant women may be associated with the hormonal balance and immunologic complexity during pregnancy (Bose et al., 2011; Navaneethan et al., 2008). HEV replication occurring in the human placenta may lead to poor pregnant outcomes, including HEV transmission from mother to newborn and abortion (Bose et al., 2014; Navaneethan et al., 2008). Chronic hepatitis E is defined by the persistence of HEV-RNA and/or anti-HEV IgM for more than six months with elevated alanine aminotransferase (ALT) levels. Chronic HEV infection has been reported primarily in immunocompromised individuals, in organ transplant recipients, patients under chemotherapy, and HIV-infected patients (Dalton et al., 2009; Kamar et al., 2008). Chronic hepatitis E has been associated with the development of fibrosis and/or cirrhosis in patients with solid-organ-transplantation (Kamar et al., 2008). Chronic HEV infection largely depends on the host immune responses, and thus the suppressed immunity in those specific groups of patients enables the virus to persist and establish chronic infection. The impairment of HEV-specific T-cell responses is likely associated with the development of chronic hepatitis E (Suneetha et al., 2012). However, rare cases of chronic and/or persistent HEV infection have also been reported in healthy, immunocompetent individuals (Gonzalez Tallon et al., 2011).