The gut of healthy human neonates is usually devoid of viruses at birth, but quickly becomes colonized, in some cases leading to gastrointestinal disorders 1 – 4 . Here we report that viral community assembly in neonates takes place in distinct steps. Fluorescent staining of virus-like particles purified from infant meconium/early stool samples show few or no particles, but by one month of life particle numbers achieve 10 9 per gram, and these numbers appear to persist through life 5 – 7 . We investigated the origin of these viral populations using shotgun metagenomic sequencing of viral-enriched preparations and whole microbial communities, and followed up with targeted microbiological analyses. Results indicate that, early after birth, pioneer bacteria colonize the infant gut, and by one month prophage induced from these bacteria provide the predominant population of virus-like particles. By four months of life, identifiable viruses that replicate in human cells become more prominent. Multiple human viruses were more abundant in stool samples from babies exclusively fed formula versus those fed partially or fully on breast milk, paralleling reports that breast milk can be protective against viral infections 8 – 10 . Phage populations also differed associated with breastfeeding. Evidently colonization of the infant gut is stepwise, first mainly by temperate bacteriophages induced from pioneer bacteria, and later by viruses that replicate in human cells, with the second phase modulated by breastfeeding.

SARS-CoV-2 infection has been shown to trigger a wide spectrum of immune responses and clinical manifestations in human hosts. Here, we sought to elucidate novel aspects of the host response to SARS-CoV-2 infection through RNA sequencing of peripheral blood samples from 46 subjects with COVID-19 and directly comparing them to subjects with seasonal coronavirus, influenza, bacterial pneumonia, and healthy controls. Early SARS-CoV-2 infection triggers a powerful transcriptomic response in peripheral blood with conserved components that are heavily interferon-driven but also marked by indicators of early B-cell activation and antibody production. Interferon responses during SARS-CoV-2 infection demonstrate unique patterns of dysregulated expression compared to other infectious and healthy states. Heterogeneous activation of coagulation and fibrinolytic pathways are present in early COVID-19, as are IL1 and JAK/STAT signaling pathways, which persist into late disease. Classifiers based on differentially expressed genes accurately distinguished SARS-CoV-2 infection from other acute illnesses (auROC 0.95 [95% CI 0.92–0.98]). The transcriptome in peripheral blood reveals both diverse and conserved components of the immune response in COVID-19 and provides for potential biomarker-based approaches to diagnosis.

Invasive candidiasis is a leading infectious cause of morbidity and mortality in premature infants. Improved recognition of modifiable risk factors and antifungal prophylaxis have contributed to the recent decline in the incidence of this infection among infants. Invasive candidiasis typically occurs in the first six weeks of life and presents with non-specific signs of sepsis. Definitive diagnosis relies on growth of Candida in blood culture or cultures from other normally sterile sites, but this may identify fewer than half of cases. Improved diagnostics are needed to guide initiation of antifungal therapy in premature infants.

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