eg5 EBV occasionally reactivates to switch its replication

EBV occasionally reactivates to switch its replication mode from latent to lytic, producing a large number of infectious virions with the lysis of host cells [7]. Although reactivation is dangerous for the virus, its triggering factors have not yet been identified. EBV reactivation is associated not only with several autoimmune or cardiovascular diseases, but also with prolonged stress events among immunocompetent patients [8]. The pathophysiology of EBV reactivation currently remains unclear. Recent findings suggest that EBV triggers inflammation through the modulation of interleukin-6 [9]. Other studies indicated that EBV promotes an immune deficiency in T-cell responses [10]. Under conditions of immune perturbation, this deficit may contribute to counteracting immune responses. EBV reactivation induces the production of immunoglobulins by host B cells. Although the exact triggers for lytic cycle reactivation have not yet been identified, the process is a dynamic interaction between the host\'s immune response to EBV and the infection state. Activation of the promoter for early lytic genes and, thus, the initiation of lytic replication are triggered by the differentiation of infected B-cells into plasma cells. Nagata et al. previously demonstrated that EBV rescues autoreactive eg5 to produce autoantibodies, which contribute to the development and exacerbation of autoimmune disease [7]. The systemic EBV reactivation of B-cells and epithelial cells may occur, leading to the various overlapping systemic manifestations observed in systemic autoimmune diseases. The reactivation of EBV and, thus, an increased number of EBV-infected cells presumably result in increased amounts of cellular waste, which is followed by the stimulation of autoreactive B-cells and production of autoantibodies, leading to disease flares. TTP has been associated with a deficiency in plasma ADAMTS13 activity, which is caused by genetic mutations in or acquired autoantibodies to this enzyme. In the idiopathic form, TTP is an autoimmune disease and, thus, may be triggered by immunological stimuli such as vaccination or viral infection. It has been hypothesized that a cross-reactive stimulation between vaccinal or virus antigens and ADAMTS13 protease or the bystander activation of a vaccination or virus with ADAMTS13-specific IgG causes a response. Furthermore, inflammatory responses caused by immunological factors represent another pathway linking endothelial injury and TTP [2]. EBV may rescue autoreactive B cells to produce autoantibodies that contribute to the development of TTP. The present case had a transient ADAMTS13 deficiency that was attributed to autoantibodies against ADAMTS13. The increased EBV load suggested active EBV lytic replication in the presence of TTP. Since the viral load was associated with ADAMTS13 activity, the reactivation of EBV may be associated with the development of TTP.
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Case description Fusariosis in patients with prolonged neutropenia have a dismal prognosis and survival is extremely low at 4% [2]. Fusarium species are plant pathogens found in air and soil, and enter the human body through inhalation, ingestion, and heel or toe fissures. Early detection of Fusarium infections is difficult due to lack of specific laboratory assays. Management is challenging due to variability of anti-fungal susceptibilities and lack of optimal treatment strategy [1]. We report the successful treatment of a patient with relapsed AML and invasive sino-pulmonary and cutaneous Fusarium solani infection during a course of salvage chemotherapy and subsequent allogeneic SCT. A 66-year-old Caucasian male with diabetes, hyperlipidemia and obstructive sleep apnea presented to the NIH Clinical Center with relapsed AML. At the time of presentation, he was noted to have firm, non-tender, erythematous subcutaneous nodules on his bilateral anterior lower limbs and painful edematous feet (Fig. 1A/B). A skin biopsy of one of these nodules was interpreted as septal panniculitis.