Search

Introduction: Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2. We investigated the antibody response against SARS-CoV-2 until 1 year after symptom onset. Methods: We collected 314 serum samples from 97 patients with COVID-19. Antibody responses were tested using an indirect immunofluorescence assay (IFA), enzyme-linked immunosorbent assay (ELISA), and plaque reduction neutralization test (PRNT) to detect specific neutralizing antibodies. Results: The positivity rates for neutralizing antibodies at a 1:10 titer cutoff were 58.1% at 1 week, 97.8% at 4 weeks, and 78% at 1 year after symptom onset (53.8% in asymptomatic patients and 89.3% in symptomatic patients). The IFA and anti-S1 ELISA IgG results significantly correlated with neutralizing antibody titers. Critical/fatal cases showed significantly higher antibody titers than the asymptomatic or mild-to-moderate illness groups. Nonetheless, the median number of days to the seroconversion of neutralizing antibodies was 10 and 15 in asymptomatic and symptomatic patients, respectively. The asymptomatic group had a significantly higher neutralizing potency index than the mild-to-severe illness groups. Conclusions: Neutralizing antibodies corresponded to earlier seroconversion but had a shorter presence in the asymptomatic group than in the symptomatic group and were still present 1 year after symptom onset in critical/fatal cases. [ABSTRACT FROM AUTHOR]

IntroductionCoronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2. We investigated the antibody response against SARS-CoV-2 until 1 year after symptom onset.MethodsWe collected 314 serum samples from 97 patients with COVID-19. Antibody responses were tested using an indirect immunofluorescence assay (IFA), enzyme-linked immunosorbent assay (ELISA), and plaque reduction neutralization test (PRNT) to detect specific neutralizing antibodies.ResultsThe positivity rates for neutralizing antibodies at a 1:10 titer cutoff were 58.1% at 1 week, 97.8% at 4 weeks, and 78% at 1 year after symptom onset (53.8% in asymptomatic patients and 89.3% in symptomatic patients). The IFA and anti-S1 ELISA IgG results significantly correlated with neutralizing antibody titers. Critical/fatal cases showed significantly higher antibody titers than the asymptomatic or mild-to-moderate illness groups. Nonetheless, the median number of days to the seroconversion of neutralizing antibodies was 10 and 15 in asymptomatic and symptomatic patients, respectively. The asymptomatic group had a significantly higher neutralizing potency index than the mild-to-severe illness groups.ConclusionsNeutralizing antibodies corresponded to earlier seroconversion but had a shorter presence in the asymptomatic group than in the symptomatic group and were still present 1 year after symptom onset in critical/fatal cases.

Vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic (VEXAS) syndrome is an autoinflammatory disease caused by somatic variants in the UBA1 gene that lead to severe systemic inflammation and myelodysplastic syndrome. Although no standard therapy has been established yet, azacitidine and bone marrow transplantation have been reported to be promising possibilities; however, the indications for these treatments are problematic and not necessarily applicable to all patients. We previously reported the results of short-term treatment with tocilizumab (TCZ) and glucocorticoids in three patients with VEXAS syndrome. In this paper, we report that the combination of TCZ and glucocorticoids allowed the patients to continue treatment for at least one year without significant disease progression. Glucocorticoids were able to be reduced from the start of TCZ. Adverse events were herpes zoster, skin ulceration after cellulitis, and decreased blood counts. The results suggest the significance of this treatment as a bridge therapy for the development of future therapies. [ABSTRACT FROM AUTHOR]

Vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic (VEXAS) syndrome is an autoinflammatory disease caused by somatic variants in the UBA1 gene that lead to severe systemic inflammation and myelodysplastic syndrome. Although no standard therapy has been established yet, azacitidine and bone marrow transplantation have been reported to be promising possibilities; however, the indications for these treatments are problematic and not necessarily applicable to all patients. We previously reported the results of short-term treatment with tocilizumab (TCZ) and glucocorticoids in three patients with VEXAS syndrome. In this paper, we report that the combination of TCZ and glucocorticoids allowed the patients to continue treatment for at least one year without significant disease progression. Glucocorticoids were able to be reduced from the start of TCZ. Adverse events were herpes zoster, skin ulceration after cellulitis, and decreased blood counts. The results suggest the significance of this treatment as a bridge therapy for the development of future therapies.

This paper reports the 1-year follow-up results from a randomized controlled trial (RCT), which examined the efficacy of metacognitive therapy (MCT) for unipolar depression compared to a waiting condition. Thirty-nine patients with major depression were offered MCT and were divided into two conditions; immediate MCT with 10 weekly sessions or a waiting period that had a 10-week delayed MCT start. Two participants dropped out during the waiting condition. Thirty-four patients participated in the follow-up assessment. Based on the intent-to-treat sample and all patients, 67% were classified as recovered, 13% improved, and 20% were unchanged at 1-year follow-up. For the completers sample 73% recovered, 12% improved, and 15% were unchanged. Five of the 31 patients (13%) that were in remission at post-treatment experienced relapse at 1-year follow-up. Within-group effect sizes were large for reductions in symptoms of depression (d = 2.09) and anxiety (d = 1.16) at 1-year. Treatment response was associated with reductions in rumination, worry, and metacognitive beliefs as predicted by the metacognitive model, but reductions in metacognitions independently predicted reductions in depression scores from pre-treatment to 1-year follow-up. The results suggest that treatment gains are stable at 1-year follow-up. The study sets the stage for future research, which should evaluate MCT over a longer term and compare it with active treatments using suitably powered RCTs.

This paper reports the 1-year follow-up results from a randomized controlled trial (RCT), which examined the efficacy of metacognitive therapy (MCT) for unipolar depression compared to a waiting condition. Thirty-nine patients with major depression were offered MCT and were divided into two conditions; immediate MCT with 10 weekly sessions or a waiting period that had a 10-week delayed MCT start. Two participants dropped out during the waiting condition. Thirty-four patients participated in the follow-up assessment. Based on the intent-to-treat sample and all patients, 67% were classified as recovered, 13% improved, and 20% were unchanged at 1-year follow-up. For the completers sample 73% recovered, 12% improved, and 15% were unchanged. Five of the 31 patients (13%) that were in remission at post-treatment experienced relapse at 1-year follow-up. Within-group effect sizes were large for reductions in symptoms of depression (d = 2.09) and anxiety (d = 1.16) at 1-year. Treatment response was associated with reductions in rumination, worry, and metacognitive beliefs as predicted by the metacognitive model, but reductions in metacognitions independently predicted reductions in depression scores from pre-treatment to 1-year follow-up. The results suggest that treatment gains are stable at 1-year follow-up. The study sets the stage for future research, which should evaluate MCT over a longer term and compare it with active treatments using suitably powered RCTs. [ABSTRACT FROM AUTHOR]