Human T-cell leukemia virus type 1 may invalidate T-SPOT.TB assay results in rheumatoid arthritis patients: A retrospective case-control observational study

Abstract

Background CD4-positive T cells are the main target of human T-cell leukemia virus type 1 (HTLV-1). Interferon-γ release assays rely on the fact that T-lymphocytes release this cytokine when exposed to tuberculosis-specific antigens and are useful in testing for latent tuberculosis infection before initiating biologic therapy, such as anti-tumor necrosis factor agents. However, the reliability of interferon-γ release assays in detecting tuberculosis infection among HTLV-1-positive patients with rheumatoid arthritis (RA) remains unclear. The present study aimed to evaluate the use of the T-SPOT.TB assay in HTLV-1-positive RA patients. Methods Overall, 29 HTLV-1-positive RA patients and 87 age-and sex-matched HTLV-1-negative RA patients (controls) were included from the HTLV-1 RA Miyazaki Cohort Study. Results of the T-SPOT.TB assay for latent tuberculosis infection screening were collected from medical records of patients. Results Approximately 55% of the HTLV-1-positive RA patients showed invalid T-SPOT.TB assay results (odds ratio: 108, 95% confidence interval: 13.1-890, p < 0.0001) owing to a spot count of >10 in the negative controls. HTLV-1 proviral load values were significantly higher in patients with invalid results compared with those without invalid results (p = 0.003).

Factors Influencing the Indeterminate Results in a T-SPOT.<i>TB</i> test: A Matched Case-control Study

“…The only factor found to influence high nil-control was HTLV-1 positivity (p＜0.01). Previously reported factors influencing high nil-control included male gender, Behçet's syndrome, use of corticosteroids, hypoalbuminemia, and HTLV-1 positivity ( 6 , 17 ). Age, gender, corticosteroid use, hypoalbuminemia, and HTLV-1 positivity were chosen as explanatory variables.…”

Strongyloides stercoralis colitis in a patient positive for human T-cell leukaemia virus with rheumatoid arthritis during an anti-rheumatic therapy: a case report

“…Therefore, IFN-c produced by HTLV-1-infected T cells may play crucial role in decreasing the Th2 response in the setting of a Strongyloides infection. Spontaneous production of IFN-c has been reported in carriers of HTLV-1 with high PVLs [34]. Interestingly, the HTLV-1 PVLs associated with strongyloidiasis/HTLV-1 co-infection were reported to be higher than those in HTLV-1 asymptomatic carriers [29,30,35].…”

Effect of HTLV-1 Infection on the Clinical Course of Patients with Rheumatoid Arthritis

“…diseases. Actually, PBMCs obtained from HTLV-1-positive RA patients have been shown to be autonomously involved in IFN-γ production ex vivo [65]. In one study, the SFs obtained from RA patients co-cultured with an HTLV-1-infected cell line were found to secrete inflammatory cytokines [27].…”

“…If a process similar to that of HAM/TSP occurs in HTLV-1-positive RA patients, HTLV-1 infection can be an environmental factor responsible for initiation and/or maintenance of chronic inflammation in rheumatic diseases. Actually, PBMCs obtained from HTLV-1-positive RA patients have been shown to be autonomously involved in IFN-γ production ex vivo [ 65 ]. In one study, the SFs obtained from RA patients co-cultured with an HTLV-1-infected cell line were found to secrete inflammatory cytokines [ 27 ].…”

“…A recent study demonstrated that approximately 55% of the HTLV-1-positive RA patients showed invalid T-SPOT.TB (Oxford Immunotec Ltd., Abingdon, UK) assay results owing to a spot count of >10 in the negative controls. HTLV-1 PVL values seemed to be significantly higher in patients with invalid results than in those without invalid results [ 65 ]. HTLV-1-infected T cells often behave in a manner similar to T helper (Th) 1-like cells, which autonomously produce IFN-γ [ 52 , 66 ].…”