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Epstein-Barr virus infection and central nervous system involvement after orthoptic liver transplant.

ABSTRACT: Epstein-Barr virus (EBV) infection presenting as encephalitis in seronegative adults in the context of solid organ transplantation is rarely reported. EBV seroconversion illnesses in the adult population after organ transplantation are quite uncommon. This report describes a case of encephalitis due to EBV infection after liver transplantation in an adult patient. The patient was seronegative for EBV pretransplant. She showed persistent viral replication indicated by high levels of EBV DNA in the serum, which raised concerns for future development of post-transplant lymphoproliferative disorder. The report discusses the management of such patients, awareness of EBV infection and earlier diagnosis by use of EBV PCR in adult immunocompromised individuals where infection may cause particular problems.

SUBMITTER: Shafiq K

PROVIDER: S-EPMC5517235 | biostudies-other | 2011 Oct

REPOSITORIES: biostudies-other

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Project description:The overall goal of the study was to use in vivo data combined with functional genomics to define gene expression signatures representative of a spectrum of HSV CNS infections. Innate immune deficiencies result in a spectrum of severe clinical outcomes following infection. In particular, there is a strong association between loss of the signal transducer and activator of transcription (Stat) pathway, breach of the blood-brain barrier (BBB), and virus-induced neuropathology. The gene signatures that characterize resistance, disease, and mortality in the virus-infected nervous system have not been defined. Herpes simplex virus type 1 (HSV-1) is commonly associated with encephalitis in humans, and humans and mice lacking Stat1 display increased susceptibility to HSV central nervous system (CNS) infections. In this study, two HSV-1 strains were used, KOS (wild type [WT]), and Δvhs, an avirulent recombinant lacking the virion host shutoff (vhs) function. In addition, two mouse strains were used: strain 129 (control) and a Stat1-deficient (Stat1(-/-)) strain. Using combinations of these virus and mouse strains, we established a model of infection resulting in three different outcomes: viral clearance without neurological disease (Δvhs infection of control mice), neurological disease followed by viral clearance (Δvhs infection of Stat1(-/-) mice and WT infection of control mice), or neurological disease followed by death (WT infection of Stat1(-/-) mice). Through the use of functional genomics on the infected brain stem and liver, we determined gene signatures that were representative of the three infection outcomes. Gender matched, 6- to 8- week old immunocompetent, control 129S6 and 129S6 Stat1 knockout mice were infected corneally with 2x10^6 PFU of either wild type HSV-1, a vhs-null HSV virus, or mock-infected. Brain stems and liver of individual mice were isolated at days 1, 3, 5 and 7 post-inoculation for microarray analysis. For microarray analysis, samples were collected from n=2 animals (1 male, 1 female) per mouse strain and virus strain for each time point. Equal masses of tissue were pooled from two mock-infected mice per time point and run on microarray.

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Epstein-Barr virus infection and central nervous system involvement after orthoptic liver transplant.

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