Hemolysis and methemoglobinemia due to hepatitis E virus infection in patient with G6PD deficiency

Au, Wing Y.; Ngai, Chun-Wai; Chan, Wan Mui; Leung, Roland; Chan, See‐Ching

doi:10.1007/s00277-011-1167-6

Cited by 28 publications

(17 citation statements)

References 6 publications

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“…The clinical implications of how the G6PD status affects cellular susceptibility to viruses such as coronavirus [14], enterovirus [13], and dengue virus [15] remain to be determined. Certain clinical findings regarding individuals with G6PD-deficiency are compelling: They develop symptoms (e.g., hemolysis and pancreatitis) that are more severe after infection with the hepatitis E virus [60,61], they are more susceptible to dengue virus type 2 infection than normal subjects [15], and they develop severe pneumonia symptoms after microbial infection [62,63]. Redox imbalance may account for the impairment of antiviral immunity in patients with G6PD-deficiency.…”

Section: Discussionmentioning

confidence: 99%

Glucose-6-Phosphate Dehydrogenase Enhances Antiviral Response through Downregulation of NADPH Sensor HSCARG and Upregulation of NF-κB Signaling

Chiu

Lin

et al. 2015

Viruses

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Glucose-6-phosphate dehydrogenase (G6PD)-deficient cells are highly susceptible to viral infection. This study examined the mechanism underlying this phenomenon by measuring the expression of antiviral genes—tumor necrosis factor alpha (TNF-α) and GTPase myxovirus resistance 1 (MX1)—in G6PD-knockdown cells upon human coronavirus 229E (HCoV-229E) and enterovirus 71 (EV71) infection. Molecular analysis revealed that the promoter activities of TNF-α and MX1 were downregulated in G6PD-knockdown cells, and that the IκB degradation and DNA binding activity of NF-κB were decreased. The HSCARG protein, a nicotinamide adenine dinucleotide phosphate (NADPH) sensor and negative regulator of NF-κB, was upregulated in G6PD-knockdown cells with decreased NADPH/NADP+ ratio. Treatment of G6PD-knockdown cells with siRNA against HSCARG enhanced the DNA binding activity of NF-κB and the expression of TNF-α and MX1, but suppressed the expression of viral genes; however, the overexpression of HSCARG inhibited the antiviral response. Exogenous G6PD or IDH1 expression inhibited the expression of HSCARG, resulting in increased expression of TNF-α and MX1 and reduced viral gene expression upon virus infection. Our findings suggest that the increased susceptibility of the G6PD-knockdown cells to viral infection was due to impaired NF-κB signaling and antiviral response mediated by HSCARG.

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Section: Discussionmentioning

confidence: 99%

Glucose-6-Phosphate Dehydrogenase Enhances Antiviral Response through Downregulation of NADPH Sensor HSCARG and Upregulation of NF-κB Signaling

Chiu

Lin

et al. 2015

Viruses

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“…Patients presented with fever, chills, leucocytosis, hyperbilirubinemia and impaired renal function [64][65][66][67][68]. Sometimes the decreased renal function requires dialysis, and rarely this disease took a fatal course due to cerebral bleeding, sepsis or liver failure [69,70].…”

Section: Hemolytic Anemiamentioning

confidence: 99%

Hepatitis E virus: Infection beyond the liver?

Pischke

Hartl

Pas

et al. 2017

Journal of Hepatology

203

182

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“…Nevertheless, the number of published cases is rather small, and the causative relationship between HEV infection and anaemia is difficult to establish. Several cases of haemolytic anaemia, caused by glucose‐6‐phosphate dehydrogenase deficiency during HEV1 infection, have been published . A few cases of autoimmune haemolytic anaemia have been also reported in HEV‐infected patients .…”

Section: Hepatitis E Virus and Haematological Disordersmentioning

confidence: 99%

Extrahepatic manifestations of hepatitis E virus

Kamar

Marion

Abravanel

et al. 2016

Liver International

108

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Hepatitis E virus can cause acute, fulminant and chronic hepatitis and has been associated with a range of extrahepatic manifestations. Guillain-Barré syndrome, neuralgic amyotrophy and encephalitis are the main neurological manifestations associated with acute and chronic hepatitis E virus infection. Renal injuries have been also reported, including membranoproliferative glomerulonephritis with or without cryoglobulinemia and membranous glomerulonephritis. Acute pancreatitis, haematological disorders and other autoimmune extrahepatic manifestations of hepatitis E virus, such as myocarditis and thyroiditis, have been also reported. In this comprehensive article, we review all published reports describing hepatitis E virus-associated extrahepatic manifestations.

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Hemolysis and methemoglobinemia due to hepatitis E virus infection in patient with G6PD deficiency

Cited by 28 publications

References 6 publications

Glucose-6-Phosphate Dehydrogenase Enhances Antiviral Response through Downregulation of NADPH Sensor HSCARG and Upregulation of NF-κB Signaling

Glucose-6-Phosphate Dehydrogenase Enhances Antiviral Response through Downregulation of NADPH Sensor HSCARG and Upregulation of NF-κB Signaling

Hepatitis E virus: Infection beyond the liver?

Extrahepatic manifestations of hepatitis E virus

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