Effect of N-terminal region of human parvovirus B19-VP1 unique region on cardiac injury in naive mice

A unique region of human parvovirus B19 virus-VP1 (B19V-VP1u) has been linked to a variety of cardiac disorders. However, the precise role of B19V-VP1u in inducing cardiac injury remains unknown. The present study investigated the effects of B19V-VP1u and different regions of B19V-VP1u, including B19V-VP1uA (residues 1-60), B19V-VP1uB (residues 61-129), B19V-VP1uC (residues 130-195) and B19V-VP1uD (residues 196-227), on inducing cardiac injury in naive mice by zymography, immunoblotting, H&E staining and cytokine immunoassay. A significantly higher MMP-9/MMP-2 ratio and increased levels of inflammatory cytokines, including IL-6 and IL-1 beta, were detected in the left ventricles of the mice injected with B19V-non-structural protein 1 (B19V-NS1) and B19V-VP1u, accompanied by increased expression levels of phosphorylated (p-)ERK and p-P38. Significantly upregulated expression levels of atrial natriuretic peptide (ANP), heart-type fatty acid-binding protein (H-FABP) and creatine kinase isoenzyme-MB (CK-MB), which are well-known cardiac injury markers, as well as increased infiltration of lymphocytes, were detected in the left ventricles of the mice injected with B19V-VP1, B19V-NS1 and B19V-VP1u. Moreover, a significantly higher MMP-9/MMP-2 ratio and increased levels of IL-6 and IL-1 beta were observed in the left ventricles of the mice injected with B19V-VP1u, B19V-VP1u-A, B19V-VP1u-B and B19V-VP1u-C, accompanied by upregulated p-ERK and p-P38 expression. Notably, significantly lower levels of IL-6 and IL-1 beta were observed in the left ventricles of the mice injected with B19V-VP1uD. Furthermore, significantly increased ANP, H-FABP and CK-MB expression levels were detected in the left ventricles of the mice injected with B19V-VP1u, B19V-VP1u-A and B19V-VP1u-B, along with enhanced infiltration of lymphocytes. Significantly higher serum IL-1 beta, IL-6, TNF-alpha and IFN-gamma levels were also detected in the mice injected with B19V-VP1u, B19V-VP1u-A and B19V-VP1u-B. To the best of our knowledge, the findings of the present study were the first to demonstrate that the N-terminal region (residues 1-129) of B19V-VP1u induces an increase in the levels of cardiac injury markers, thus providing evidence for understanding the possible functional regions within B19V-VP1u.

Automated summary

The study demonstrated that the N-terminal region (residues 1-129) of B19V-VP1u induces an increase in cardiac injury markers, providing insights into the potential functional regions within B19V-VP1u.