Clinical and Epidemiological Assessment of Children and Adolescents Hospitalized with SARS-CoV-2 in the Pre-Amazon Region.

INTRODUCTION: SARS-CoV-2 infection usually presents similarly to other respiratory viral pathogens. Children and adolescents do not present as a group that is highly affected by the disease, having low infection rates. However, limited publications are associated with the findings of pneumonia in pediatric patients with COVID-19. OBJECTIVE: To analyze the clinical and epidemiological aspects of children and adolescents hospitalized with SARS-CoV-2 in a pre-Amazon region. METHODS: A retrospective study, carried out in four public hospitals in São Luís, Brazil where medical records of children and adolescents aged from 0 to 13 years, of both sexes, with clinical diagnosis of community-acquired pneumonia were evaluated from March 2020 to March 2021. RESULTS: Almost 40.0% of children were aged between 1 year and 5 years. Of the 128 children who had SARS-CoV-2, 3 are of indigenous ethnicity. Additionally, 78.6% of the children had fever and there was no significant difference between COVID-19 patients and those of other respiratory viruses. Eighteen patients had chronic neurological disease, which is the most common comorbidity observed in patients with coronavirus infection. Ground glass opacity attenuation was observed in 24.8% of children and adolescents with COVID-19. Anemia and increased inflammatory response markers were related to SARS-CoV-2 infection. More than 90.0% of patients admitted to hospital, regardless of etiology, were treated with antibiotics. Eighteen patients died. Pediatric multisystem inflammatory syndrome (PMIS) was diagnosed in 17 patients. CONCLUSIONS: SARS-CoV-2 in children and adolescents is mild, but the condition of patients with PMIS is more serious, with an increase in inflammatory biomarkers which can lead to death. Therefore, rapid diagnosis and differentiation of agents causing respiratory diseases are necessary for better therapeutic decision making, since the results of this study make us question the excessive use of antibiotics without meeting well-defined clinical-epidemiological criteria.

Genetically modified pigs lacking CD163 PSTII-domain-coding exon 13 are completely resistant to PRRSV infection.

CD163 expressed on cell surface of porcine alveolar macrophages (PAMs) serves as a cellular entry receptor for porcine reproductive and respiratory syndrome virus (PRRSV). The extracellular portion of CD163 contains nine scavenger receptor cysteine-rich (SRCR) and two proline-serine-threonine (PST) domains. Genomic editing of pigs to remove the entire CD163 or just the SRCR5 domain confers resistance to infection with both PRRSV-1 and PRRSV-2 viruses. By performing a mutational analysis of CD163, previous in vitro infection experiments showed resistance to PRRSV infection following deletion of exon 13 which encodes the first 12 amino acids of the 16 amino acid PSTII domain. These findings predicted that removal of exon 13 can be used as a strategy to produce gene-edited pigs fully resistant to PRRSV infection. In this study, to determine whether the deletion of exon 13 is sufficient to confer resistance of pigs to PRRSV infection, we produced pigs possessing a defined CD163 exon 13 deletion (ΔExon13 pigs) and evaluated their susceptibility to viral infection. Wild type (WT) and CD163 modified pigs, placed in the same room, were infected with PRRSV-2. The modified pigs remained PCR and serologically negative for PRRSV throughout the study; whereas the WT pigs supported PRRSV infection and showed PRRSV related pathology. Importantly, our data also suggested that removal of exon 13 did not affect the main physiological function associated with CD163 in vivo. These results demonstrate that a modification of CD163 through a precise deletion of exon 13 provides a strategy for protection against PRRSV infection.

Cryptosporidium: Host-Parasite Interactions and Pathogenesis.

PURPOSE OF REVIEW: Cryptosporidium spp. (C. hominis and C. parvum) are a major cause of diarrhea-associated morbidity and mortality in young children globally. While C. hominis only infects humans, C. parvum is a zoonotic parasite that can be transmitted from infected animals to humans. There are no treatment or control measures to fully treat cryptosporidiosis or prevent the infection in humans and animals. Our knowledge on the molecular mechanisms of Cryptosporidium-host interactions and the underlying factors that govern infectivity and disease pathogenesis is very limited. RECENT FINDINGS: Recent development of genetics and new animal models of infection, along with progress in cell culture platforms to complete the parasite lifecycle in vitro, is greatly advancing the Cryptosporidium field. SUMMARY: In this review, we will discuss our current knowledge of host-parasite interactions and how genetic manipulation of Cryptosporidium and promising infection models are opening the doors towards an improved understanding of parasite biology and disease pathogenesis.