Cytokines, chemokines, and cells growth factors in patients with mild to moderate SARS‐CoV‐2 infection: A case‐control study

Abstract

Several biomarkers have been evaluated as predictors of severity or in directing the treatment of COVID‐19, however there are no conclusive results. In this study, we evaluated serum levels of cytokines, chemokines, and cell growth factors in association with the pathobiology of mild to moderate SARS‐CoV‐2 infection. Serum levels of SARS‐CoV‐2 infected patients (n = 113) and flu symptoms individuals negative for SARS‐CoV‐2 (n = 58), tested by the RT‐qPCR test—nasal swab were compared to healthy controls (n = 53). Results showed that the proinflammatory cytokines IL‐1β, MCP‐3, TNF‐α, and G‐CSF were increased in symptomatic patients and the cytokines IL‐6 and IL‐10 were associated with patients positive for SARS‐CoV‐2 when compared to healthy controls. Symptoms associated with COVID‐19 were fever, anosmia, ageusia, and myalgia. For patients without SARS‐CoV‐2 infection, their major symptom was sore throat. The pathobiology of mild to moderate SARS‐CoV‐2 infection was associated with increasing proinflammatory cytokines and a pleiotropic IL‐6 and anti‐inflammatory IL‐10 cytokines compared to healthy controls. Thus, knowledge about the pathophysiology and the involvement of biomarkers in the mild to moderate profile of the disease should be evaluated. Monitoring these biomarkers in patients with mild to moderate disease can help establish adequate treatment and prevention strategies for long‐term COVID‐19.

Current clinical findings of acute neurological syndromes after SARS‐CoV‐2 infection

“…Interestingly, Neuro‐COVID patients exhibited generally lower CSF cytokine levels compared with those with VE, and levels were similar to the control group. The lower level of TNF‐α in the RNA CSF ‐positive group compared with the negative group hints at a less intense immune response in the CNS of Neuro‐COVID patients than expected 71–73 . In scientific and medical terms, these results contribute to our understanding of the complex interplay between SARS‐CoV‐2 and the nervous system.…”