ABSTRACT
An outbreak of a potentially fatal form of pneumonia in 1976 and in the annual convention of the American Legion was the first time that Legionella spp. was identified. Thereafter, the term Legionnaires' disease (LD) was established. The infection in humans is transmitted by the inhalation of aerosols that contain the microorganisms that belong to the Legionellaceae family and the genus Legionella. The genus Legionella contains genetically heterogeneous species and serogroups. The Legionella pneumophila serogroup 1 (Lp1) is the most often detected strain in outbreaks of LD. The pathogenesis of LD infection initiates with the attachment of the bacterial cells to the host cells, and subsequent intracellular replication. Following invasion, Legionella spp. activates its virulence mechanisms: generation of specific compartments of Legionella-containing vacuole (LCV), and expression of genes that encode a type IV secretion system (T4SS) for the translocation of proteins. The ability of L. pneumophila to transmigrate across the lung's epithelium barrier leads to bacteremia, spread, and invasion of many organs with subsequent manifestations, complications, and septic shock. The clinical manifestations of LD depend on the bacterial load in the aerosol, the virulence factors, and the immune status of the patient. The infection has two distinct forms: the non- pneumatic form or Pontiac fever, which is a milder febrile flu-like illness, and LD, a more severe form, which includes pneumonia. In addition, the extrapulmonary involvement of LD can include heart, brain, abdomen, and joints.
ABSTRACT
The newly identified human coronavirus was named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), based on a detailed analysis of clinical manifestation. It was reported that blood type O individuals were less likely to become infected by SARS-CoV, while blood type A individuals have an increased risk of severe illness. The Forssman antigen, or Forssman glycolipid synthase (FS), was first described in 1911 by John Frederick Forssman. Blood type A/B glycosyltransferases (AT/BTs) and Forssman glycolipid synthase (FS) are encoded by the evolutionarily related ABO (A/B alleles) and GBGT1 genes. In this article, based on published studies about the pathogenesis of the COVID-19, we hypothesize the possible relationship between the COVID-19 infection and rare blood type systems, such as the Forssman antigen system.
ABSTRACT
The aim of this study was to estimate the immunogenic effect of mRNA vaccine against SARS-CoV-2. This study included 510 participants who received mRNA vaccine. The measurement of anti-COVID-19 antibodies was performed using the Abbott SARS-CoV-2 IgG quantitative assay (Abbott). Overall, mean titer of anti-Spike antibodies was 19,319.2 ± 1787.5 AU/mL. Vaccination induced a robust immunogenic response in those previously infected with SARS-CoV-2 compared with non-infected subjects. Additionally, individuals that were asymptomatic after vaccination produced lower levels of antibodies compared to feverish individuals. In conclusion, remarkably high levels of anti-Spike COVID-19 antibodies were observed after vaccination.
ABSTRACT
Previous studies have shown that COVID-19 leads to thrombotic complications, which have been associated with high morbidity and mortality rates. Neutrophils are the largest population of white blood cells and play a pivotal role in innate immunity. During an infection, neutrophils migrate from circulation to the infection site, contributing to killing pathogens. This mechanism is regulated by chemokines such as IL-8. Moreover, it was shown that neutrophils play an important role in thromboinflammation. Through a diverse repertoire of mechanisms, neutrophils, apart from directly killing pathogens, are able to activate the formation of thrombi. In COVID-19 patients, neutrophil activation promotes neutrophil extracellular trap (NET) formation, platelet aggregation, and cell damage. Furthermore, neutrophils participate in the pathogenesis of endothelitis. Overall, this review summarizes recent progress in research on the pathogenesis of COVID-19, highlighting the role of the prothrombotic action of neutrophils in NET formation.