No abstract

This study shows that chronic norovirus infection is not a rare phenomenon among SOT recipients in a tertiary-care hospital. Further research is needed to study the risk of norovirus transmission to other immunocompromised patients in the hospital and to the general population.

Background-Herpes simplex virus (HSV) hepatitis is a rare and potential life-threatening disease. The diagnosis of HSV hepatitis is hampered by its indifferent clinical presentation, which necessitates confirmatory laboratory data to identify HSV in the affected liver. However, liver biopsies are often contraindicated in the context of coagulopathy, are prone to sampling errors and have low sensitivity in mild HSV hepatitis cases. There is an unmet need for less-invasive diagnostic tools.

No abstract

IFN-α has been used for decades to treat chronic hepatitis B and C, and as an off-label treatment for some cases of hepatitis E virus (HEV) infection. TNF-α is another important cytokine involved inCytokines orchestrate cellular communication in an autocrine, juxtacrine, or paracrine fashion through binding to distinct families of receptors, triggering specific immune responses against invading pathogens. The interferon (IFN)-mediated innate immune response is probably the most prominent response and provides a robust first defense line. Among different types of interferons, IFN-α (a type I member) has been used for decades to treat chronic hepatitis B or C infection in the clinic 1 . When stimulated by its cognate ligand, interferon receptors respond by the activation of kinases of the Janus family (JAKs), which in turn phosphorylate tyrosine residues in the intracellular tail of the interferon receptors. These phosphotyrosines serve as docking sites for recruitment and phosphorylation of the Signal Transducers and Activators of Transcription (STAT) family, which provokes STAT1 and STAT2 dimerization and subsequent binding to interferon regulatory factor 9 (IRF9) to form the IFN-stimulated gene factor 3 (ISGF3) complex. The ISGF3 complex translocates into the nucleus, and binds to specific promotor elements denoted as interferon signaling response elements (ISREs) and thus mediate the