Pregnant women and neonates are at risk for adverse SARS CoV-2 infection outcomes, but few studies have evaluated this population for adaptive immunity. Here, we utilized samples collected from pregnant women 18 years or older reporting two or more respiratory symptoms. Information about trimester of COVID positive test or history of vaccination was also collected. Maternal blood (MB) samples were collected at prenatal clinic visits, or at delivery together with the fetal cord blood (CB)(n=70 dyads). Groups were selected based on trimester of infection, vaccination only, or no history of vaccination or infection (n=9–24) and compared with banked samples from a non-pregnant, age-matched woman from the same time period (n=7–12). Data shows IgG transfer to baby irrespective of trimester of infection (n=9–24 per group). Highest levels of antibodies were observed with vaccinated, uninfected women. Functional antibodies are transferred from mother to fetus following infection and vaccination. CD4 and CD8 T-cell activation and cytokine secretion were detected in maternal PBMCs, with highly variable expression between subjects. In at least one dyad with a PCR-confirmed infection during second trimester, both maternal and cord blood samples had low level expression of anti-S, N, RBD antibodies at delivery and the cord blood mononuclear cells showed CD4 T cell activation (CD134+) and cytokine secretion (IL-2, IL-6, TNFalpha) to spike antigens. These results indicate the unusual immunity to SARS CoV-2 infection during pregnancy and suggest at least one case of a neonate with anti-viral cellular immunity. Ongoing analyses and surveillance for perinatal outcomes may reveal how these immune responses impact infant respiratory outcomes.

SARS CoV-2 in children or special populations post-infection has not been well studied. Asthma is a heterogenous disease marked by chronic airway inflammation; triggers include cockroaches (CRA), and other inhaled irritants. Asthma also has links to viral infections like respiratory syncytial virus (RSV). Additionally, some with moderate to severe asthma are more likely to be hospitalized with COVID. T cells play key roles in asthma and control of viruses such; however, there is limited information connecting T cell responses in people with asthma to viral infections. We aimed to evaluate T cells and antibodies in an asthma confirmed cohort. Thirty-five children aged 5–17 years were included. We measured SARS CoV-2 spike (S) and Nucleoprotein (N) plasma antibody responses or effector functions and CD4, CD8 T cells specific to CRA or peptide pools made from RSV, S and N antigen using an activation induced markers (AIM) assay. Surprisingly, in this population many CD4 and CD8 T-cell AIM responses to S, N, CRA, and RSV were significantly associated, particularly for CD8 T-cells (Spearmans r = 0.57–0.76) and the restimulation antigens CRA and RSV. N-specific CD4 AIM was the only immune measure to correlate to a recent asthma attack within a month of the blood collection visit, though anti-N antibodies, CD4 AIM to CRA, RSV or CD8 AIM to CRA, RSV, or N antigens also correlated with asthmatic outcomes (e.g., ER visits, night waking from symptoms, etc.) whereas allergen specific IgE or anti-S IgG did not. Taken together these results indicate an immunological association between viral infection and asthma, broadly allowing for the conjecture that viral infections, in particular RSV and SARS-CoV-2 could act together as possible triggers of asthma.