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Kinetics of Serological Response in Patients with Severe Fever with Thrombocytopenia Syndrome
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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.
Title: Kinetics of Serological Response in Patients with Severe Fever with Thrombocytopenia Syndrome
Description:
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.
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