Introduction
The varicella zoster virus (VZV) infection causes chickenpox and herpes zoster. Primary infection occurs more frequently in the pediatric age as chickenpox. Virus can be latent in cranial nerve or dorsal root ganglia and reactivate several decades later as the form of herpes zoster generally in immunosuppressed patients. Varicella zoster virus is associated with severe neurological complications, including post herpetic neuralgia, aseptic meningitis, polyneuropathy, cranial nerve palsy, meningoencephalitis, vasculopathy, encephalitis, and transverse myelitis. The transverse myelitis caused by VZV is reported rarely.
Case Report
A 77-year-old immunocompetent patient presented with muscle weakness and sensation loss due to the demyelinating lesion caused by VZV on C5 dermatome. Proprioception and vibratory sensation loss were also marked. Cervical spinal magnetic resonance imaging showed expansive intramedullary high-signal intensity lesion on C5 with focal swelling on T2-weighted images and gadalinium enhancement on T1-weighted images. cerebrospinal fluid viral antibody test was positive for immunoglobulin G of VZV but negative for VZV DNA. The patient was treated with oral valacyclovir (1 g) 3 times daily for 7 days and with methylprednisolone (1.0 g) every day for 5 days. After treatment, his muscle strength increased but sensorial loss and neuropathic pain did not recover.
Conclusions
About 40% of transverse myelitis cases are caused by viral infections, some of them are herpes viruses and poliovirus. Varicella zoster infection is a common disease but not a common cause of transverse myelitis particularly in immuncompetent patients. The clinicians must be aware of this rare complication of VZV.
Aim of the Study: Interferon-beta (IFNβ), multiple sclerosis (MS) drug for years, does not have therapeutic effects on each patient. Yet, a considerable portion has experienced no therapeutic response to IFNβ. Therefore, it is necessary to determine disease-specific biomarkers that affect drug response. Here, we aimed to determine the effects of interleukin 10 (IL10) and 23 (IL23A), as well as forkhead box P3 (FOXP3) genes on MS after IFNβ therapy.Materials and Methods: Peripheral blood mononuclear cells (PBMCs) of 42 MS patients were isolated to obtain CD4+ and CD25+ T cells. Both cell types were characterised by flow cytometry. To determine optimum drug concentration of IFNβ, cytotoxicity assays were assessed on each cell type for 4, 16, 24 and 48 hours respectively. Then, cells were cultured in the presence of 500 IU/mL of IFNβ. cDNA synthesis was performed after mRNA extraction. RT-PCR was performed to measure gene expressions of IL10, IL23A and FOXP3. Results were evaluated statistically.Results: It was found that the cytotoxic effect of IFNβ was more efficient as the exposure time was expanded regardless of drug concentration. Moreover, CD25+ T lymphocytes were more resistant to IFNβ. IL23A was down-regulated, whereas FOXP3 was up-regulated at 48 hours in CD4+ T cells. For CD25+ T cells, the graded increase in FOXP3 was obtained while IL10 expression was gradually decreased throughout the drug intake.
Conclusion:Although a considerable change in expression was obtained, the longterm IFNβ effect on both genes and cells should be determined by follow-up at least a year.
What's knownIFNβ reduces the number of episodes and slows down the progression of disability in MS patients. However, the expected therapeutic response has not been experienced in the majority How to cite this article:
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.