Chronic Hepatitis E Virus Infection during Lymphoplasmacytic Lymphoma and Ibrutinib Treatment.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Schmidt, Hartmut H
MetadataShow full item record
AbstractHepatitis E virus (HEV) is an increasingly recognised pathogen, affecting several hundred thousand individuals in western countries each year. Importantly, the majority of immunocompromised individuals are not able to clear HEV but develop a chronic course of infection. In the case of lymphoma, which is an inherent immunosuppressive disease per se, chemotherapy can even further exacerbate the immunosuppressive status. As the mechanism of HEV chronification is barely understood, it is important to gain knowledge about the influence of chemotherapeutic drugs on the HEV replication cycle to guide rational clinical management of HEV infection in such patients. In this case report, a 70 year old man was diagnosed with lymphoplasmacytic lymphoma. As we observed the occurrence of chronic HEV after treatment with the Bruton's tyrosine kinase (BTK) inhibitor ibrutinib in vivo, we investigated the influence of BTK signaling and ibrutinib treatment in the HEV replication cycle in vitro. First, we detected an HEV-induced mobilisation of BTK in human liver cells during HEV replication. A moderate antiviral effect against HEV replicating isolates including genotypes 1 and 3 was observed, suggesting that ibrutinib did not support HEV replication in a direct manner. Combinatory treatments of ibrutinib with ribavirin indicated that ibrutinib did not influence the antiviral effect of ribavirin. Taken together, chemotherapy targeting cellular factors for the treatment of lymphomas may be a neglected risk factor for the chronification of HEV. For ibrutinib, despite the upregulation of its target BTK during HEV replication, we observed neither a proviral effect on HEV replication nor an influence on the antiviral effect of ribavirin, suggesting that the chronification of HEV may be favoured by its immunosuppressive effect.
CitationPathogens. 2019 Aug 22;8(3). pii: pathogens8030129. doi: 10.3390/pathogens8030129.
AffiliationTWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH,Feodor-Lynen Str. 7, 30625 Hannover, Germany.
The following license files are associated with this item:
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-ShareAlike 4.0 International
- ISG15 Modulates Type I Interferon Signaling and the Antiviral Response during Hepatitis E Virus Replication.
- Authors: Sooryanarain H, Rogers AJ, Cao D, Haac MER, Karpe YA, Meng XJ
- Issue date: 2017 Oct 1
- Zinc Salts Block Hepatitis E Virus Replication by Inhibiting the Activity of Viral RNA-Dependent RNA Polymerase.
- Authors: Kaushik N, Subramani C, Anang S, Muthumohan R, Shalimar, Nayak B, Ranjith-Kumar CT, Surjit M
- Issue date: 2017 Nov 1
- Positive Regulation of Hepatitis E Virus Replication by MicroRNA-122.
- Authors: Haldipur B, Bhukya PL, Arankalle V, Lole K
- Issue date: 2018 Jun 1
- The natural compound silvestrol inhibits hepatitis E virus (HEV) replication in vitro and in vivo.
- Authors: Todt D, Moeller N, Praditya D, Kinast V, Friesland M, Engelmann M, Verhoye L, Sayed IM, Behrendt P, Dao Thi VL, Meuleman P, Steinmann E
- Issue date: 2018 Sep
- Analysis of the Effects of the Bruton's tyrosine kinase (Btk) Inhibitor Ibrutinib on Monocyte Fcγ Receptor (FcγR) Function.
- Authors: Ren L, Campbell A, Fang H, Gautam S, Elavazhagan S, Fatehchand K, Mehta P, Stiff A, Reader BF, Mo X, Byrd JC, Carson WE 3rd, Butchar JP, Tridandapani S
- Issue date: 2016 Feb 5