A modulation of the UPR pathway was reported not only during viral but also bacterial infections. On the other hand, an ERS-induced upregulation of UPR-related genes was linked with an enhanced production of pro-inflammatory cytokines in monocytes and B-cells. Moreover, facilitated replication of viruses and immune evasion represent key features following UPR activation by Mouse hepatitis virus (MHV) and Herpes simplex virus 1 (HSV-1).
Activation of the UPR via an induction of glucose-regulated protein 78 (GRP78) has previously been shown in cells infected with Human immunodeficiency virus (HIV), Dengue virus (DENV), West Nile virus (WNV) or Human cytomegalovirus (HCMV). cholera toxin, pore-forming toxins) or by the increased demand of newly synthesized proteins for the production of virions. Several bacteria and viruses have been described to modulate unfolded protein response (UPR) and endoplasmic reticulum stress (ERS), either by bacterial virulence factors such as toxins ( e. Considering these circumstances, the rising number of reported cases of AE especially in Europe and the lack of a curative drug treatment, emphasizes the necessity to further investigate the mechanisms underlying this threat and search for improved therapeutic options. Recent experiments using mice indicated a requirement of functional T cell immunity for efficient treatment of AE with ABZ. An inadequate adherence to chemotherapy, due to adverse side effects, and development of resistance can explain the relapsing spread of AE and a worsening general condition of patients with severe E. For example, several cases with hepatotoxic effects due to treatment with the benzimidazole albendazole (ABZ) were reported with various outcomes. If lesions cannot be completely removed by surgery, a lifelong medication is required, usually using benzimidazoles, which can cause adverse side effects. Treatment by radical surgical resection is limited by the diffuse infiltrations of AE lesions in liver and other tissues in advanced cases. The variable clinical outcomes of AE development depend on the immunological status, and the specific immunological profile with T cell exhaustion seems to play an important role in the established tolerance state in chronic AE. AE is characterized by a slow but progressive tumor-like growth of metacestodes (larval stage) mainly in the liver, with a tendency to spread to various organs like spleen, brain, heart and other tissues such as bile ducts and blood vessels.
After an incubation period of 5 up to 15 years without perceivable symptoms, AE has a fatal outcome in up to 90% of cases when left untreated. Alveolar echinococcosis (AE) is a severe helminth disease caused by accidental ingestion of eggs from the fox tapeworm Echinococcus multilocularis.
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