Frank A. Boksa, University of Iowa College of Dentistry, Iowa City, IA, presented "Salivary Immune Signature of SARS-nCoV2 Infection" at the hybrid 51st Annual Meeting & Exhibition of the AADOCR, held in conjunction with the 46th Annual Meeting of the Canadian Association for Dental Research (CADR), online and onsite in Atlanta, GA, on March 26, 2022.
With more than 219 million confirmed cases of SARS-nCoV2 infection and 4.55 million deaths, the COVID-19 pandemic has led to a dramatic loss of human life worldwide. Besides saliva being a reservoir for the virus, emerging evidence correlates the salivary virus levels to severity of infection, hospitalization, and death. Saliva is a complex secretory fluid with several bacterial and host breakdown products that perform numerous housekeeping functions. The inflammatory complications of COVID-19 are well-established at this time, however, the levels of these inflammatory mediators in saliva are not quantified. The researchers quantified the salivary inflammatory mediators in COVID-19 using a cross-sectional study design.
The researchers collected saliva from 87 patients that were frequency matched for gender, age, BMI, and smoking status were divided into three groups: Symptomatic COVID-19 positive (symptomatic), Symptomatic COVID-19 negative (presenting with a flu-like illness, FLI), Asymptomatic (Negative) based on their titers from RT-PCR in nasopharyngeal swabs and saliva. Levels of proinflammatory cytokines and other immune mediators were quantified using a TH-17 cytokine assay kit and read using the Bio-Plex 200 fluorescent microplate reader. Steel-Dwass test protecting the overall error rate was used to determine statistical significance.
The researchers concluded that identification of inflammatory markers in COVID-19 patients that is different than the other flu-like illnesses indicate a unique immune signature associated with the disease. Salivary levels of several of these immune mediators mirror the systemic levels, indicating a potential role of saliva in COVID pathogenesis.