and sterilisation of milk pumps and tubes). However, whether New born 2 was infected by breastfeeding or other modes of transmission remains unclear. Fur ther studies of milk samples from lactating women and possible virus transmission via breastfeeding are needed to develop recommendations on whether mothers with COVID19 should breastfeed.We declare no competing interests. RG, CC, and JAM contributed equally.

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Purpose To compare neuromuscular electrical stimulation (NMES) versus sham on leg strength at hospital discharge in mechanically ventilated patients. Materials and Methods We conducted a randomized pilot study of NMES versus sham applied to 3 bilateral lower extremity muscle groups for 60 minutes daily in ICU. Between 6/2008 and 3/2013, we enrolled adults who were receiving mechanical ventilation within the first week of ICU stay, and who could transfer independently from bed to chair before hospital admission. The primary outcome was lower extremity muscle strength at hospital discharge using Medical Research Council score (maximum = 30). Secondary outcomes at hospital discharge included walking distance and change in lower extremity strength from ICU awakening. Clinicaltrials.gov:NCT00709124. Results We stopped enrollment early after 36 patients due to slow patient accrual and the end of research funding. For NMES versus sham, mean (SD) lower extremity strength was 28(2) versus 27(3), p=0.072. Among secondary outcomes, NMES versus sham patients had a greater mean (SD) walking distance (514(389) vs. 251(210) feet, p=0.050) and increase in muscle strength (5.7(5.1) vs. 1.8(2.7), p=0.019). Conclusions In this pilot randomized trial, NMES did not significantly improve leg strength at hospital discharge. Significant improvements in secondary outcomes require investigation in future research.

Background Recent data suggests an association between blood hyperviscosity and both propensity for thrombosis and disease severity in patients with COVID‐19. This raises the possibility that increased viscosity may contribute to endothelial damage and multiorgan failure in COVID‐19, and that therapeutic plasma exchange (TPE) to decrease viscosity may improve patient outcomes. Here we sought to share our experience using TPE in the first 6 patients treated for COVID‐19‐associated hyperviscosity. Study Design and Methods Six critically ill COVID‐19 patients with plasma viscosity levels ranging from 2.6 to 4.2 centipoise (cP; normal range, 1.4‐1.8 cP) underwent daily TPE for 2‐3 treatments. Results TPE decreased plasma viscosity in all six patients (Pre‐TPE median 3.75 cP, range 2.6‐4.2 cP; Post‐TPE median 1.6 cP, range 1.5‐1.9 cP). TPE also decreased fibrinogen levels in all five patients for whom results were available (Pre‐TPE median 739 mg/dL, range 601‐1188 mg/dL; Post‐TPE median 359 mg/dL, range 235‐461 mg/dL); D‐dimer levels in all six patients (Pre‐TPE median 5921 ng/mL, range 1134‐60 000 ng/mL; Post‐TPE median 4893 ng/mL, range 620‐7518 ng/mL); and CRP levels in five of six patients (Pre‐TPE median 292 mg/L, range 136‐329 mg/L; Post‐TPE median 84 mg/L, range 31‐211 mg/L). While the two sickest patients died, significant improvement in clinical status was observed in four of six patients shortly after TPE. Conclusions This series demonstrates the utility of TPE to rapidly correct increased blood viscosity in patients with COVID‐19‐associated hyperviscosity. Large randomized trials are needed to determine whether TPE may improve clinical outcomes for patients with COVID‐19.

Severe SARS-CoV-2 infection1 has been associated with highly inflammatory immune activation since the earliest days of the COVID-19 pandemic2–5. More recently, these responses have been associated with the emergence of self-reactive antibodies with pathologic potential6–10, although their origins and resolution have remained unclear11. Previously, we and others have identified extrafollicular B cell activation, a pathway associated with the formation of new autoreactive antibodies in chronic autoimmunity12,13, as a dominant feature of severe and critical COVID-19 (refs. 14–18). Here, using single-cell B cell repertoire analysis of patients with mild and severe disease, we identify the expansion of a naive-derived, low-mutation IgG1 population of antibody-secreting cells (ASCs) reflecting features of low selective pressure. These features correlate with progressive, broad, clinically relevant autoreactivity, particularly directed against nuclear antigens and carbamylated proteins, emerging 10–15 days after the onset of symptoms. Detailed analysis of the low-selection compartment shows a high frequency of clonotypes specific for both SARS-CoV-2 and autoantigens, including pathogenic autoantibodies against the glomerular basement membrane. We further identify the contraction of this pathway on recovery, re-establishment of tolerance standards and concomitant loss of acute-derived ASCs irrespective of antigen specificity. However, serological autoreactivity persists in a subset of patients with postacute sequelae, raising important questions as to the contribution of emerging autoreactivity to continuing symptomology on recovery. In summary, this study demonstrates the origins, breadth and resolution of autoreactivity in severe COVID-19, with implications for early intervention and the treatment of patients with post-COVID sequelae.