Association between inflammatory cytokines and anti-SARS-CoV-2 antibodies in hospitalized patients with COVID-19

Abstract

Background COVID-19 patients may experience “cytokine storm” when human immune system produces excessive cytokines/chemokines. However, it remains unclear whether early responses of inflammatory cytokines would lead to high or low titers of anti-SARS-CoV-2 antibodies. Methods This retrospective study enrolled a cohort of 272 hospitalized patients with laboratory-confirmed SARS-CoV-2. Laboratory assessments of serum cytokines (IL-2R, IL-6, IL-8, IL-10, TNF-α), anti-SARS-CoV-2 IgG/IgM antibodies, and peripheral blood biomarkers were conducted during hospitalization. Results At hospital admission, 36.4% patients were severely ill, 51.5% patients were ≥ 65 years, and 60.3% patients had comorbidities. Higher levels of IL-2R and IL-6 were observed in older patients (≥65 years). Significant differences of IL-2R (week 2 to week ≥5 from symptom onset), IL-6 (week 1 to week ≥5), IL-8 (week 2 to week ≥5), and IL-10 (week 1 to week 3) were observed between moderately-ill and severely ill patients. Anti-SARS-CoV-2 IgG titers were significantly higher in severely ill patients than in moderately ill patients, but such difference was not observed for IgM. High titers of early-stage IL-6, IL-8, and TNF-α (≤2 weeks after symptom onset) were positively correlated with high titers of late-stage IgG (≥5 weeks after symptom onset). Deaths were mostly observed in severely ill older patients (45.9%). Survival analyses revealed risk factors of patient age, baseline COVID-19 severity, and baseline IL-6 that affected survival time, especially in severely ill older patients. Conclusion Early responses of elevated cytokines such as IL-6 reflect the active immune responses, leading to high titers of IgG antibodies against COVID-19.

Trends in the disease burden of HBV and HCV infection in China from 1990-2019

“…Our results indicate that male patients are at higher risk for HBV-associated liver cancer, which should be the focus of future prevention and control. Moreover, the COVID-19 pandemic that causes severe morbidity and mortality ( Jing et al, 2022, Jiang et al, 2020Li and De Clercq, 2020 ;Miao et al, 2021 ;Zhou et al, 2020b ) exerts an impact on the HBV/HCV screening and management ( Mandel et al, 2022 ). Future studies need to estimate HBV/HCV disease burden with detailed data of other social, economic, and pandemic factors.…”

The Variable Nature of Vitamin C—Does It Help When Dealing with Coronavirus?

“…Interleukin-1β plays a pivotal role in the induction of cytokine storms due to uncontrolled immune responses in COVID-19 infections [ 21 ]. At the same time, IL-6 may even serve as an early biomarker for monitoring inflammatory and immune responses in COVID-19 [ 10 ]. In turn, the level of TNF-α is associated directly with the probability of hospitalization and severe COVID-19 [ 22 ].…”

“…The uncontrolled and unregulated secretion of inflammatory and pro-inflammatory cytokines is positively associated with the severity of viral infection and mortality [ 6 ]. The secretion of various pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 leads to a hyperinflammatory response by recruiting macrophages, as well as T and B lymphocytes, in alveolar cells [ 7 , 8 , 9 , 10 ]. This process results in multi-organ failure, which can lead to death.…”

“…People with reduced immunity are the most vulnerable to severe infection. These patients have low levels of inflammatory cytokines or chemokines such as IL-6 and TNF [ 10 ]. Currently, substances are being sought that would limit the effects of infection by modulating the immune system to reduce the inflammatory response or activate the antiviral response.…”

Immune Profiles to Distinguish Hospitalized Versus Ambulatory Covid-19 Cases in Older Patients

“…In addition to Abs, cytokine responses in severe vs. mild COVID-19 cases have been evaluated. An association was shown between SARS-CoV-2 infection and marked elevation of several plasma cytokines including interferon gamma-induced protein 10 (IP-10), chemokine (C-X-C motif) ligand 16 (CXCL16), interleukin (IL)-1β, IL-2R, IL-4, IL-6, IL-8, IL-10 and IL-17 (10,(14)(15)(16)(17)(18)(19)(20)(21). Several other studies provided evidence that type I interferon deficiency may lead to severe COVID-19, implying that disease severity may be due to impaired viral clearance and uncontrolled viral replication due to poor induction of early innate immunity (15,(22)(23)(24)(25)(26).…”