AI Article Synopsis
- - Increased sepsis cases during COVID-19, even without typical bacterial infections, suggest that viruses may also cause sepsis.
- - A study investigated 45 viral sepsis patients and compared them with 186 non-sepsis COVID-19 patients to uncover molecular mechanisms behind viral sepsis.
- - Findings revealed distinct changes in coagulation and immune response pathways, with increased fibrinogen and decreased complement proteins, contributing to the risk of secondary infections and severe disease.
Article Abstract
Increased cases of sepsis during COVID-19 in the absence of known bacterial pathogens highlighted role of viruses as causative agents of sepsis. In this study, we investigated clinical, laboratory, proteomic, and metabolomic characteristics of viral sepsis patients ( = 45) and compared them to non-sepsis patients with COVID-19 ( = 186) to identify molecular mechanisms underlying the pathology of viral sepsis in COVID-19. We identified unique metabolomic and proteomic signatures that suggest a substantial perturbation in the coagulation, complement, and platelet activation pathways in viral sepsis. Our proteomic data indicated elevated coagulation pathway protein (fibrinogen), whereas a decrease in many of the complement proteins was observed. These alterations were associated with the functional consequences such as susceptibility to secondary bacterial infections and potentially contributing to both local and systemic disease phenotypes. Our data provide novel aspect of COVID-19 pathology that is centered around presence of sepsis phenotype in COVID-19.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11225851 | PMC |
| http://dx.doi.org/10.1016/j.isci.2024.110110 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!