Abstract
Human T-lymphotropic virus type 1 (HTLV-1) deregulates the immune system and cell cycle, resulting in loss of immune tolerance and disease, including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Three prime repair exonuclease 1 (TREX1) maintains innate immune tolerance of the host and host-cell permissiveness to retroviral infections. TREX1 polymorphisms may influence the course of infection and autoimmune manifestations. The influence of TREX1 531C/T polymorphism was investigated in HTLV-1 infection and development of symptoms among 151 persons infected with HTLV-1 (32 HAM/TSP, 19 rheumatologic manifestations, two dermatitis, five more than one diagnosis, two probable HAM/TSP, and 91 asymptomatic individuals) and 100 uninfected persons in the control group. Polymorphism genotyping and proviral load quantification were performed by real-time polymerase chain reaction (PCR) and antinuclear antibodies (ANAs) were screened by an indirect immunofluorescence assay. No statistically significant difference was found in polymorphism genotype and allele frequencies between the infected and control groups. HAM/TSP patients showed higher frequency of TT genotype than asymptomatic persons (p = 0.0339). Proviral load was significantly higher among individuals with CT/TT genotypes and CC genotype carriers had lower proviral load and higher levels of proinflammatory cytokines. ANAs were present only in the HAM/TSP group. TREX1 531C>T polymorphism seems to be associated with TREX-1 regulation and HTLV-1 infection.
Highlights
Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus responsible for the development of different types of diseases, including adult T-cell leukemia/lymphoma and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), in addition to other inflammatory syndromes [1,2,3,4].Virus infection is endemic in certain regions such as Japan, Australia, Melanesia, the Caribbean, the Middle East, and South America, and it is estimated that 5 to 10 million people are infected worldwide [5].The pathogenesis of HAM/TSP is a result of the interaction between the virus and the host immune system, including innate and adaptive immunity mechanisms [6]
The present study investigated the association of the Three prime repair exonuclease 1 (TREX1) 531C>T polymorphism with the susceptibility to HTLV-1 infection, the development of infection-related symptoms, and the presence of antinuclear antibodies (ANAs)
The present study included blood samples from 151 individuals infected with HTLV-1 (32 clinically diagnosed with HAM/TSP, 19 with rheumatologic manifestations, two with dermatitis, five with more than one diagnosis, two with probable HAM/TSP, and 91 asymptomatic), who were treated at the outpatient clinic of the Tropical Medicine Center of the Federal University of Pará
Summary
Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus responsible for the development of different types of diseases, including adult T-cell leukemia/lymphoma and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), in addition to other inflammatory syndromes [1,2,3,4]. Restriction factors inhibit replication, inducing the activation of type I interferon (IFN). TREX-1 is able to recognize and degrade dsDNA and ssDNA molecules present in cytosol, contributing to innate immune tolerance of the host and inhibiting activation of autoimmune mechanisms [10,11]. TREX-1 renders cells permissive to retroviral infections inhibiting the activation of the innate immune response, mainly related to type I IFN synthesis [9]. The present study investigated the association of the TREX1 531C>T polymorphism with the susceptibility to HTLV-1 infection, the development of infection-related symptoms, and the presence of ANAs
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