چاپ صفحه |  صفحه نخست سامانه |  نویسندگان |  اطلاعات تفضیلی |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| نویسنده ثبت کننده مقاله | مهین آهنگر اسکوئی |
| مرحله جاری مقاله | تایید نهایی |
| دانشکده/مرکز مربوطه | دانشکده پزشکی |
| کد مقاله | 80973 |
| عنوان فارسی مقاله | تعامل رتروویروس اندوژن انسانی با پیشروی بیماری مولتیپل اسکلروزیس |
| عنوان لاتین مقاله | Human endogenous retrovirus interaction with multiple sclerosis disease progression |
| نوع ارائه | پوستر |
| عنوان کنگره / همایش | چهاردهمین کنگره بین المللی آزمایشگاه و بالین |
| نوع کنگره / همایش | بین المللی |
| کشور محل برگزاری کنگره/ همایش | Iran (Islamic Republic) |
| شهر محل برگزاری کنگره/ همایش | تهران |
| سال انتشار/ ارائه شمسی | 1401 |
| سال انتشار/ارائه میلادی | 2023 |
| تاریخ شمسی شروع و خاتمه کنگره/همایش | 1401/11/13 الی 1401/11/15 |
| آدرس لینک مقاله/ همایش در شبکه اینترنت | https://b2n.ir/y25058 |
| آدرس علمی (Affiliation) نویسنده متقاضی | Department of Microbiology and Virology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran |
| نویسنده | نفر چندم مقاله |
|---|---|
| سینا مهدوی | اول |
| مهدی اصغری عظمی | دوم |
| ندا مهدوی | سوم |
| مهین آهنگر اسکوئی | چهارم |
| عنوان | متن |
|---|---|
| کلمات کلیدی | Multiple Sclerosis, Human Endogenous Retrovirus, Central Nervous System |
| خلاصه مقاله | Human endogenous retrovirus interaction with multiple sclerosis disease progression Sina Mahdavi1,2, Mahdi Asghari Ozma1,3 , Neda Mahdavi3 , Mahin Ahangar Oskouee1,* 1. Department of Microbiology and Virology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran 2. Infectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran 3. Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran *Corresponding Author: Mahin Ahangar Oskouee, Department of Microbiology and Virology, School of Medicine, Tabriz University of Medical Sciences, Tel +98 41 33364661, Fax +98 41 3336 4661, Email: ahangarm@tbzmed.ac.ir Background: Multiple sclerosis (MS) is an inflammatory autoimmune disease of the central nervous system that interferes with the myelination process. Autoimmunity and disease progression may be triggered by complex interactions between various 'environmental or infectious' factors. The link between viral infections, particularly human endogenous retrovirus (HERV), and MS is a potential cause that is not fully understood. This study aims to review the existing data on HERV infection and the progression of multiple sclerosis. Materials and Methods: For this study, the keywords 'Multiple sclerosis', 'Human endogenous retrovirus', and 'central nervous system' in the databases PubMed, Google Scholar, Sid, and MagIran between 2016 and 2022 were searched and 14 articles chosen, studied, and analyzed. Results: Multiple sclerosis-associated retroviruses (MSRV) have been identified in the leptomeningeal cells of MS patients as a retrovirus-like element associated with reverse transcriptase (RT) activity. Even though there are mechanisms to suppress their expression, HERVs are expressed in the human CNS. HERV gene expression can be activated by environmental stimuli, including viral infections like influenza virus, Epstein-Barr virus, and herpes simplex virus type 1. Toll-like receptor 4 (TLR4) is activated at the brain's surface by the MSRV coat protein, specifically in oligodendroglial progenitor cells and macrophages, triggering immune cascades and ultimately leading to the downregulation of myelin protein expression. MS patients have inflammatory reactions in response to the HERV-K18 envelope gene (env), which acts as a superantigen. Conclusion: There is a significant expression of human endogenous retroviruses during the course of MS, indicating a link between HERV and MS and that this virus can play a role in the development of MS by causing inflammation. Therefore, strategies for reducing inflammatory processes in MS patients' demyelinated areas may be achieved through efforts to modulate the expression of human endogenous retroviruses. |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| congress.pdf | 1401/11/25 | 407826 | دانلود |
| presentation.pdf | 1401/11/25 | 626176 | دانلود |
