Transfusion-Transmitted Hepatitis E Virus Infection in France

Gallian, Pierre; Pouchol, Elodie; Djoudi, Rachid; Lhomme, Sébastien; Mouna, Lina; Gross, Sylvie; Bierling, Philippe; Assal, Azzedine; Kamar, Nassim; Mallet, Vincent; Roque–Afonso, Anne–Marie; Izopet, Jacques; Tiberghien, Pierre

doi:10.1016/j.tmrv.2019.06.001

Cited by 53 publications

(47 citation statements)

References 45 publications

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“…4 Using the INTER-CEPT process, PR is also considered robust for a wide variety of viruses and parasites 22 ; however, breakthrough cases of hepatitis E virus, a known PR-resistant virus, have occurred. 23,24 Our investigation demonstrated that the INTERCEPT process was successfully performed and that >5.9-log/mL in vitro inactivation occurred for both ACBC and SS isolates provided by the hospital microbiology laboratory. Independent evidence presented here also demonstrates that residual amotosalen and S-59 photoproducts were present in the CC, and that the ACBC/SS contamination did not arise from the patient, supported by negative pretransfusion cultures and plasma metagenomic sequencing, and negative TBF Y-chromosomal signal, likely ruling out retrograde bag contamination.…”

Section: Discussionmentioning

confidence: 73%

Sepsis from an apheresis platelet contaminated with Acinetobacter calcoaceticus/baumannii complex bacteria and Staphylococcus saprophyticus after pathogen reduction

et al. 2020

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Background Strategies to reduce platelet (PLT) bacterial contamination include donor screening, skin disinfection, sample diversion, bacterial culture, pathogen reduction (PR), and day‐of‐transfusion tests. We report bacterial sepsis following a pathogen‐reduced PLT transfusion. Case Report An adult male with relapsed acute lymphoblastic leukemia was successfully treated for central catheter–associated Staphylococcus aureus bacteremia. A peripherally inserted central catheter (PICC) was placed. Chills, rigors, and flushing developed immediately after PICC‐infused pathogen‐reduced PLTs, progressing to septic shock requiring intensive care management. Methods PICC and peripheral blood (PB), transfused bag saline flushes (TBFs), environmental samples, and the pathogen‐reduced untransfused co‐component (CC) were cultured. Plasma metagenomic and bacterial isolate whole‐genome sequencing; PLT mitochondrial DNA (mtDNA) testing of untransfused CC and TBF; CC testing for amotosalen (S‐59)/S‐59 photoproducts; isolate PR studies (INTERCEPT); and TBF polymerase chain reaction for recipient Y‐chromosome DNA were performed. Results PB and PICC cultures grew Acinetobacter calcoaceticus/baumannii complex (ACBC). TBF was gram‐positive; mass spectrometry identified ACBC and Staphylococcus saprophyticus (SS). CC Gram stain and cultures were negative. Environmental cultures, some done after decontamination, were ACBC/SS negative. Posttransfusion patient plasma and TBF ACBC sequences were genetically identical. No Y‐chromosome signal was detected in TBF. S‐59 photoproducts and evidence of mtDNA amplification inhibition were found in the CC. Spiking PR studies showed >5.9‐log inactivation for both isolates. Donor skin cultures for Acinetobacter were negative. Conclusion CC sterility, PR studies, residual S‐59 photoproducts, and mtDNA amplification inhibition suggest successful PR. Unidentified environmental sources and inherent or acquired bag defects may have contributed to postmanufacturing pathogen‐reduced PLT contamination.

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Section: Discussionmentioning

confidence: 73%

Sepsis from an apheresis platelet contaminated with Acinetobacter calcoaceticus/baumannii complex bacteria and Staphylococcus saprophyticus after pathogen reduction

et al. 2020

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“…Similarly, HCV infection can induce autoimmune hemolytic anemia, leukopenia, thrombocytopenia, and anemia of chronic disease, probably due to extrahepatic replication of HCV in bone marrow [ 22 , 37 ]. Moreover, transmission of HEV by whole blood and/or transfusion of blood products has been documented [ 7 , 38 , 39 ]. Blood products that were documented as sources of transfusion-transmitted (TT) HEV infection were plasma, red blood cells, apheresis platelets concentrate, cryoprecipitate, pooled granulocytes, and whole blood pooled platelet concentrates [ 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

Replication of Hepatitis E Virus (HEV) in Primary Human-Derived Monocytes and Macrophages In Vitro

et al. 2020

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HEV is the most causative agent of acute viral hepatitis globally. HEV causes acute, chronic, and extrahepatic manifestations. Chronic HEV infection develops in immunocompromised patients such as organ transplant patients, HIV-infected patients, and leukemic patients. The source of chronic HEV infection is not known. Also, the source of extrahepatic manifestations associated with HEV infection is still unclear. Hepatotropic viruses such as HCV and HBV replicate in peripheral blood mononuclear cells (PBMCs) and these cells become a source of chronic reactivation of the infections in allograft organ transplant patients. Herein, we reported that PBMCs and bone marrow-derived macrophages (BMDMs), isolated from healthy donors (n = 3), are susceptible to HEV in vitro. Human monocytes (HMOs), human macrophages (HMACs), and human BMDMs were challenged with HEV-1 and HEV-3 viruses. HEV RNA was measured by qPCR, the marker of the intermediate replicative form (ds-RNA) was assessed by immunofluorescence, and HEV capsid protein was assessed by flow cytometry and ELISA. HEV infection was successfully established in primary HMOs, HMACs, and human BMDMs, but not in the corresponding cells of murine origin. Intermediate replicative form (ds RNA) was detected in HMOs and HMACs challenged with HEV. The HEV load was increased over time, and the HEV capsid protein was detected intracellularly in the HEV-infected cells and accumulated extracellularly over time, confirming that HEV completes the life cycle inside these cells. The HEV particles produced from the infected BMDMs were infectious to naive HMOs in vitro. The HEV viral load was comparable in HEV-1- and HEV-3-infected cells, but HEV-1 induced more inflammatory responses. In conclusion, HMOs, HMACs, and human BMDMs are permissive to HEV infection and these cells could be the source of chronic and recurrent infection, especially in immunocompromised patients. Replication of HEV in human BMDMs could be related to hematological disorders associated with extrahepatic manifestations.

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“…In France, the prevalence of positive HEV viraemia in blood donors is estimated to be 1/800 . A French study reported 23 cases of transfusion‐transmitted infections between 2006 and 2016, including 14 with chronic hepatitis in immunosuppressed patients …”

Section: Epidemiologymentioning

confidence: 99%

“…9 A French study reported 23 cases of transfusion-transmitted infections between 2006 and 2016, including 14 with chronic hepatitis in immunosuppressed patients. 10 In the developed countries, acute hepatitis E usually affects middle aged and elderly men (sex ratio of 4/1, median age 55) often with excessive alcohol consumption. 2,7 Patients with chronic liver disease are at risk of decompensation and death, and maternal complications have not yet been described.…”

Section: Epidemi Ologymentioning

confidence: 99%

Hepatitis E, what’s the real issue?

Larrue

Abravanel

Péron

2020

Liver International

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Hepatitis E Virus (HEV) infection is a worldwide disease and the primary cause of acute viral hepatitis in the world with an estimated 20 million cases every year and 70 000 deaths. Hepatitis E is a waterborne infection in the developing countries. In these countries, HEV genotypes 1 and 2 cause large outbreaks and affect young subjects, resulting in significant mortality in pregnant women and patients with cirrhosis. In the developed countries, HEV genotypes 3 and 4 are responsible for autochthonous, sporadic hepatitis and transmission is zoonotic. Parenteral transmission by the transfusion of blood products has been identified as a potential new mode of transmission. The prevalence of positive HEV viraemia in blood donors in Europe ranges from 1/600 to 1/2500 in highly endemic European countries. HEV can cause neurological disorders and chronic infections in immunocompromised patients. The progression of acute hepatitis E is usually asymptomatic and resolves spontaneously. Diagnostic tools include anti‐HEV IgM antibodies in serum and/or viral RNA detection in the blood or the stools by PCR. Ribavirin is used to treat chronic infection. A vaccine has been developed in China.

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Transfusion-Transmitted Hepatitis E Virus Infection in France

Cited by 53 publications

References 45 publications

Sepsis from an apheresis platelet contaminated with Acinetobacter calcoaceticus/baumannii complex bacteria and Staphylococcus saprophyticus after pathogen reduction

Sepsis from an apheresis platelet contaminated with Acinetobacter calcoaceticus/baumannii complex bacteria and Staphylococcus saprophyticus after pathogen reduction

Replication of Hepatitis E Virus (HEV) in Primary Human-Derived Monocytes and Macrophages In Vitro

Hepatitis E, what’s the real issue?

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