A 1-year longitudinal study on COVID-19 convalescents reveals persistence of anti-SARS-CoV-2 humoral and cellular immunity.

The immune memory of over 400 million COVID-19 convalescents is not completely understood. In this integrated study, we recorded the post-acute sequelae symptoms and tested the immune memories, including circulating antibodies, memory B cell, and memory CD4 or CD8 T cell responses of a cohort of 65 COVID-19 patients over 1-year after infection. Our data show that 48% of them still have one or more sequelae symptoms and all of them maintain at least one of the immune components. The chances of having sequelae symptoms or having better immune memory are associated with peak disease severity. We did four-time points sampling per subject to precisely understand the kinetics of durability of SARS-CoV-2 circulating antibodies. We found that the RBD IgG levels likely reach a stable plateau at around 6 months, albeit it is waning at the first 6 months after infection. At 1-year after infection, more than 90% of the convalescents generated memory CD4 or CD8 T memory responses, preferably against the SARS-CoV-2 M peptide pool. The convalescents also have polyfunctional and central memory T cells that could provide rapid and efficient response to SARS-CoV-2 re-infection. Based on this information, we assessed the immune protection against the Omicron variant and concluded that convalescents should still induce effective T cell immunity against the Omicron. By studying the circulating antibodies and memory B or T cell responses to SARS-CoV-2 in an integrated manner, our study provides insight into the understanding of protective immunity against diseases caused by secondary SARS-CoV-2 infection.

Expression of Lung Surfactant Proteins SP-B and SP-C and Their Regulatory Factors in Fetal Lung of GDM Rats.

This study investigated the expression of lung surfactant proteins (SP-B and SP-C), and regulatory factors [forkhead box A2 (FOXA2) and nitrolyogenic FOXA2 (N-FOXA2)] in the fetal lung of rats with gestational diabetes mellitus (GDM) in order to study the mechanism of pulmonary dysplasia. The rat GDM model was established by using streptozotocin intraperitoneally in the first stage of pregnancy. There were 10 rats in the GDM group, and 10 healthy rats in normal control group without any treatment. Fetal lungs of two groups were taken at day 21 of pregnancy. Blood glucose levels of maternal rats and fetal rats were measured by Roche blood glucose meter. The histological changes in the fetal lung were observed under the light microscope in both groups. The SP-B, SP-C and FOXA2 were determined in the fetal lung of two groups immunohistochemically. The expression levels of SP-B, SP-C, total FOXA2, FOXA2 in nucleus (n-FOXA2), N-FOXA2 proteins were detected by Western blotting, and the relative expression levels of SP-B, SP-C, FOXA2 mRNA in the fetal lung of two groups were detected by RTPCR. The results showed that blood glucose levels of maternal rats and fetal rats in GDM group were higher than those in control group. The light microscope revealed fetal lung development retardation in GDM group. The expression of SP-B and SP-C in GDM group was significantly reduced as compared with control group (P<0.05). As compared with control group, the n-FOXA2 expression was significantly decreased in the fetal lung tissue, and N-FOXA2 was significantly increased in control group (P<0.05), but there was no significant changes in the total FOXA2 (P>0.05). It was concluded that GDM can cause fetal lung development and maturation disorders, and FOXA2 in fetal lung tissue decreases while nitrocellulose FOXA2 increases.