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Life

Scientists identify marker of dangerous form of COVID-19 infection

The Italian and Australian scientists have discovered a marker of a dangerous form of COVID-19 infection that can lead to the death of a patient.

According to a study published in the International Journal of Infectious Diseases, the level of serum amyloid protein in critically ill patients becomes abnormally high during an acute reaction of the body to the SARS-CoV-2 coronavirus.

Health Europe reported that scientists conducted a meta-analysis of studies from the PubMed, Web of Science, and Scopus databases, which examined the link between the severity of COVID-19 symptoms, serum amyloid A (SAA) protein concentrations in patients with coronavirus, and patient survival. A total of 19 studies were included in the meta-analysis, which involved a total of 5617 patients with COVID-19. At the same time, in 3723 people (49%) the disease was mild or moderate.

Analysis of the results showed that SAA concentrations were significantly high in those patients who did not survive or who had a very severe form of COVID-19. The standardized mean difference (SMD) between the mild and severe patient groups was 1.20 with a 95% confidence interval of 0.91-1.49, indicating a strong relationship between high SAA values ​​and severe COVID-19. Scientists have also found a link between amyloid A levels and gender, which may explain why men are more vulnerable to the virus.

Tracking SAA, which serves as a sign of severe complications of the disease, could be useful in identifying risk groups and monitoring the condition of patients with coronavirus infection, scientists said.

SAA is significantly activated during the acute phase response - a general body response that develops in response to the release of cytokines during infection. The normal concentration of amyloid A is 20-50 milligrams per liter, but it can increase up to 1000 times during the first 24-48 hours of the acute phase response. This is due to increased protein production in the liver, which is triggered in response to stimuli such as interferon-gamma, interleukin-1β and -6, and tumor necrosis factor (TNF). In turn, SAA enhances inflammation by increasing the synthesis of these stimuli and activating other pro-inflammatory cytokines that can cause cytokine storms and other complications in COVID-19.