The Expression Level of miR-199a and miR-93 after Hematopoietic Stem Cell Transplantation and Its Relation with Acute Graft-versus-Host Disease, Cytomegalovirus, and COVID-19 Infection

Abstract

Background: The The possible role of different microRNAs (miRNAs) as indicators of acute graft-versus-host disease (GVHD) following allogeneic hematopoietic stem cell transplantation (HSCT) has recently come to light. Human cytomegalovirus (CMV) is another common problem that can arise after HSCT. Given human CMV's capacity to remain dormant in human cells indefinitely, the virus has likely refined sophisticated survival mechanisms. miRNAs facilitate one such approach. Coronavirus disease 2019 (COVID-19) is also associated with dysregulation of miRNA expression

Objective:  This study aimed to the expression level of miR-199a and miR-93 after HSCT and its relation with cytomegalovirus and COVID-19 Infection on transplant outcomes.

Methods: One hundred and twenty consecutive patients who received an allogeneic stem cell transplant were enrolled from Namazi Hospital's Transplant Center in Shiraz Iran (2017-2019). In this project, patients are bone marrow transplant recipients. We assessed the expression levels of miR 199a and miR-93 in the peripheral blood of HSCT patients by SYBR Green Real-Time PCR. Cytomegalovirus load was determined via CMV antigenemia assay and COVID-19 load was also determined via Real-time PCR using the COVID-19 kit.

Results: The results showed that miR-93 expression was considerably higher in patients following HSCT (-5.4 1.5 vs. -0.26 0.86; P=0.008). Furthermore, the miR-199a expression level was significantly increased in HSCT CMV+ patients (P=0.005). This study also indicated that the expression of miR-199a was remarkably higher in HSCT patients with COVID-19 (P=0.010).

Conclusion: miR-93 could be a possible prognostic biomarker in patients who had HSCT due to its higher expression in HSCT patients who got aGVHD. Moreover, the level of miR-199a expression in HSCT patients might be related to the pathophysiology of CMV and COVID-19 infection.