The fate of protective immunity following mild severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection remains ill defined. Here, we characterize antibody responses in a cohort of participants recovered from mild SARS-CoV-2 infection with follow-up to 6 months. We measure immunoglobulin A (IgA), IgM, and IgG binding and avidity to viral antigens and assess neutralizing antibody responses over time. Furthermore, we correlate the effect of fever, gender, age, and time since symptom onset with antibody responses. We observe that total anti-S trimer, anti-receptor-binding domain (RBD), and anti-nucleocapsid protein (NP) IgG are relatively stable over 6 months of follow-up, that anti-S and anti-RBD avidity increases over time, and that fever is associated with higher levels of antibodies. However, neutralizing antibody responses rapidly decay and are strongly associated with declines in IgM levels. Thus, while total antibody against SARS-CoV-2 may persist, functional antibody, particularly IgM, is rapidly lost. These observations have implications for the duration of protective immunity following mild SARS-CoV-2 infection.

During the past decade, the medical community has expressed a growing concern over the high prevalence of postpartum depression and the tragic repercussions of untreated illness. However, many questions persist about the pathogenesis of postpartum depression, the natural course of the illness, and the safety and effectiveness of available treatments. To summarize the data on pharmacologic treatments for postpartum depression, we performed a systematic review of four major databases to identify original research published from 1960-September 2009 that featured pharmacologic treatments for depression detected in women during the 12 months after delivery. Pharmacologic treatments included prescription drugs (antidepressants and hormones), herbal remedies, and dietary supplements. Case reports, studies examining the prevention of postpartum depression, and those including diagnosed episodes of depression preceding the postpartum period (i.e., antepartum onset) were excluded. Treatment randomization or the presence of a control group was not required for inclusion in this review. Fourteen investigations met inclusion criteria. Nine studies examined the effects of prescription antidepressants, two investigated hormones, and three featured omega-3 fatty acid supplementation. Significant heterogeneity was evident in study design and prevented a pooled quantitative analysis of treatment effects. The power of most investigations was limited, and numerous confounding biases were evident. Therapeutic effects were documented for prescription antidepressants and hormone supplementation (estrogen derivatives). Tolerability of the interventions in depressed mothers and breastfed infants was not well described. The effectiveness of omega-3 fatty acids was not evident in postpartum depression trials, although significant limitations in study methodology were apparent. Postpartum depression is a common and serious medical problem, but most cases go undetected and untreated. The need to identify safe, effective, and convenient treatments for postpartum depression is urgent, but the current state of the medical literature describing pharmacologic interventions is not impressive. Preliminary evidence documenting the effectiveness of serotonergic antidepressants and hormone supplementation should serve as an impetus for rigorous controlled investigations in the future.

This pilot showed that trainee collaboratives can work together to deliver an audit using an encrypted data capture tool cost-effectively, whilst maintaining the highest levels of data quality.

We compared the phenotype, diversity, and antigen specificity of T cells in the breastmilk and peripheral blood of lactating individuals who received SARS-CoV-2 mRNA vaccination. Relative to blood, breastmilk contained higher frequencies of T effector and central memory populations that expressed mucosal-homing markers. T cell receptor (TCR) sequence overlap was limited between blood and breastmilk. Overabundant breastmilk clones were observed in all individuals, were structurally diverse, and contained CDR3 sequences with known epitope specificity including to SARS-CoV-2 Spike. Spike-specific TCRs were more frequent in breastmilk compared to blood and expanded in breastmilk following a third mRNA vaccine dose. Our observations indicate that the lactating breast contains a distinct T cell population that can be modulated by maternal vaccination with potential implications for infant passive protection.SummaryThe breastmilk T cell repertoire is distinct and enriched for SARS-CoV-2 Spike-specificity after maternal mRNA vaccination.

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Background Coronavirus disease 2019 (COVID-19) is associated with endothelial activation and coagulopathy, which may be related to pre-existing or infection-induced pro-thrombotic autoantibodies such as those targeting angiotensin II type I receptor (AT1R-Ab). Methods We compared prevalence and levels of AT1R-Ab in COVID-19 cases with mild or severe disease to age and sex matched negative controls utilizing multivariate logistic and quantile regression adjusted for comorbidities including hypertension, diabetes, and heart disease. Results There were trends toward increased prevalence (50% vs. 33%, p = 0.1) and level of AT1R-Ab (median 9.8 vs. 6.1 U/mL, p = 0.06) in all cases versus controls. When considered by COVID-19 disease severity, there was a trend toward increased prevalence of AT1R-Ab (55% vs. 31%, p = 0.07), as well as significantly higher AT1R-Ab levels (median 10.7 vs. 5.9 U/mL, p = 0.03) amongst individuals with mild COVID-19 versus matched controls. In contrast, the prevalence (42% vs. 37%, p = 0.9) and level (both medians 6.7 U/mL, p = 0.9) of AT1R-Ab amongst those with severe COVID-19 did not differ from matched controls. Conclusions These findings support an association between COVID-19 and AT1R-Ab, emphasizing that vascular pathology may be present in individuals with mild COVID-19 as well as those with severe disease.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is associated with endothelial activation and coagulopathy, which may be related to pre-existing or infection-induced pro-thrombotic autoantibodies such as those targeting angiotensin II type I receptor (AT1R-Ab). METHODS: We compared prevalence and levels of AT1R-Ab in COVID-19 cases with mild or severe disease to age and sex matched negative controls. RESULTS: There were no significant differences between cases and controls. However, there were trends toward a higher proportion with AT1R-Ab positivity among severe cases versus controls (32% vs. 11%, p=0.1) and higher levels in those with mild COVID-19 compared to controls (median 9.5U/mL vs. 5.9U/mL, p=0.06). CONCLUSIONS: These findings suggest that AT1R-Ab are not consistently associated with COVID-19 but do not exclude a contribution to endothelial pathology in a subset of people.