Abstract
Severe fever with thrombocytopenia syndrome (SFTS) is caused by SFTS virus (SFTSV). We investigated the detailed kinetics of serologic response in patients with SFTS. Twenty-eight patients aged ≥18 years were enrolled between July 2015 and October 2018. SFTS was confirmed by detecting SFTSV RNA in their plasma using reverse transcription polymerase chain reaction. SFTSV-specific IgG and IgM were measured using immunofluorescence assay (IFA) and enzyme-linked immunosorbent assay (ELISA). We found that SFTSV-specific IgG was detected at days 5–9 after symptom onset, and its titer was rising during the course of disease. SFTSV-specific IgM titer peaked at around week 2–3 from symptom onset. The SFTSV-specific seropositive rates for days 5–9, 10–14, 15–19, and 20–24 from symptom onset using IFA and ELISA were 63%, 76%, 90%, and 100%, and 58%, 86%, 100%, and 100%, respectively, for IgG, whereas they were 32%, 62%, 80%, and 100%, and 53%, 62%, 70%, and 100%, respectively, for IgM. The delayed IgM response could be attributed to the low sensitivity of SFTSV-specific IgM IFA or ELISA and/or impaired immune responses. The IgM test using IFA or ELISA that we used in this study is, therefore, insufficient for the early diagnosis of SFTS.
Highlights
Severe fever with thrombocytopenia syndrome (SFTS), which is caused by SFTS virus in the genus Bandavirus, family Phenuiviridae, and order Bunyavirales [1], is an emerging endemic zoonosis usually transmitted by ticks, such as Haemaphysalis longicornis [2]
A prior study [18] suggested that anti-SFTS virus (SFTSV) immunoglobulin M (IgM) levels could be detected at a medium of 9 days, peaking at week 4, and persisted until six months after disease onset; anti-SFTSV immunoglobulin G (IgG) could still be detected at a medium of six weeks and peaked at six months
Another study [13] reported that SFTSV NP-specific IgM was detected at an early phase after symptom onset, persisting throughout hospitalization in all recovered patients, with SFTSV NP-specific IgG detected from week 2 after symptom onset
Summary
Severe fever with thrombocytopenia syndrome (SFTS), which is caused by SFTS virus (renamed as Dabie bandavirus) in the genus Bandavirus, family Phenuiviridae, and order Bunyavirales [1], is an emerging endemic zoonosis usually transmitted by ticks, such as Haemaphysalis longicornis [2]. SFTS has become a significant threat to public health in East Asian countries with a high fatality rate of 16.2–32.6% [5,6], and effective antiviral therapy for SFTS virus (SFTSV) has not been available [7,8,9]. Previous studies [10,11] have reported that one of the major pathophysiological characteristics that causes high mortality in SFTS is related to cytokine storm. Other studies [12,13] revealed that the impairment of both innate and adaptive immune responses was associated with disease progression and mortality in SFTS. Song et al [13] described a defect in serological responses to SFTSV that plays an important role in disease mortality rate, and impairment of both B and T cells could contribute to low anti-viral immunity. We investigated the detailed kinetics of anti-SFTSV antibody response in patients with SFTS
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