{"title":"Correlation Between TWEAK Serum Level and HTLV-1 Proviral Load in HAM/TSP.","authors":"Nafiseh Taheri, Mona Fani, Hashem Khanbabaei, Zohreh Vahidi, Fariba Zemorshidi, Reza Boostani, Houshang Rafatpanah, Saeedeh Ebrahimi","doi":"10.1089/vim.2024.0070","DOIUrl":null,"url":null,"abstract":"<p><p>Human T-cell lymphotropic virus type-I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP), the main neurological manifestation of HTLV-I, is a chronic inflammatory disease. Viral-host interaction and host genetics are two important contributors to the development of the HAM/TSP. This study was conducted to measure the serum level of tumor necrosis factor-alpha-like weak inducer of apoptosis (TWEAK) by ELISA method in three groups of participants including 34 HAM/TSP patients (HAM/TSP), 35 asymptomatic HTLV-1 carriers (ACs), and 20 healthy controls (HCs). Also, the titer of the proviral load in two groups of HAM/TSP and ACs was assessed by the real-time polymerase chain reaction (PCR). The statistical results showed that, there is no significant difference between the three groups in TWEAK cytokine level (<i>p</i> = 0.667). Also, there was no significant difference in proviral load titer between groups of HAM/TSP and ACs (<i>p</i> = 0.08). Furthermore, no significant difference was observed between proviral load and TWEAK cytokine concentration between groups of HAM/TSP and ACs. Our findings showed that despite the inflammatory nature of HAM/TSP disease, the expression level of TWEAK in HAM/TSP patients is not significantly different from the groups of ACs and HCs. Therefore, the involvement of other factors in causing HAM/TSP is not unexpected.</p>","PeriodicalId":23665,"journal":{"name":"Viral immunology","volume":" ","pages":""},"PeriodicalIF":1.5000,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Viral immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1089/vim.2024.0070","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Human T-cell lymphotropic virus type-I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP), the main neurological manifestation of HTLV-I, is a chronic inflammatory disease. Viral-host interaction and host genetics are two important contributors to the development of the HAM/TSP. This study was conducted to measure the serum level of tumor necrosis factor-alpha-like weak inducer of apoptosis (TWEAK) by ELISA method in three groups of participants including 34 HAM/TSP patients (HAM/TSP), 35 asymptomatic HTLV-1 carriers (ACs), and 20 healthy controls (HCs). Also, the titer of the proviral load in two groups of HAM/TSP and ACs was assessed by the real-time polymerase chain reaction (PCR). The statistical results showed that, there is no significant difference between the three groups in TWEAK cytokine level (p = 0.667). Also, there was no significant difference in proviral load titer between groups of HAM/TSP and ACs (p = 0.08). Furthermore, no significant difference was observed between proviral load and TWEAK cytokine concentration between groups of HAM/TSP and ACs. Our findings showed that despite the inflammatory nature of HAM/TSP disease, the expression level of TWEAK in HAM/TSP patients is not significantly different from the groups of ACs and HCs. Therefore, the involvement of other factors in causing HAM/TSP is not unexpected.
期刊介绍:
Viral Immunology delivers cutting-edge peer-reviewed research on rare, emerging, and under-studied viruses, with special focus on analyzing mutual relationships between external viruses and internal immunity. Original research, reviews, and commentaries on relevant viruses are presented in clinical, translational, and basic science articles for researchers in multiple disciplines.
Viral Immunology coverage includes:
Human and animal viral immunology
Research and development of viral vaccines, including field trials
Immunological characterization of viral components
Virus-based immunological diseases, including autoimmune syndromes
Pathogenic mechanisms
Viral diagnostics
Tumor and cancer immunology with virus as the primary factor
Viral immunology methods.