A synthetic and soluble form of CAR <unk>  has been created to prevent viral infection with CVB3. Attaching<unk>  domain of immunoglobulin IgG1 to<unk> <unk>  enhances solubility and extends its half-life. Furthermore, once<unk>  binds the virus, macrophages and other phagocytic immune cells with<unk>  receptor recognition bind to the<unk> -viral complex to eliminate the virus. Essentially,<unk>  mimics CAR receptors on cardiac cells, competitively inhibiting viral attachment and entry into myocytes. Decreased lesions in cardiac tissues, reduced cell necrosis, and diminished inflammatory responses are observed in<unk>  treated cells (CITE). This suggests protective effects against myocardial damage by CVB3. Conformational changes in a viral particle (A-particle) with<unk> -virus binding causing the loss of the virus’ internal capsid protein, VP4. This irreversible reaction prevents the virus from interacting with cellular receptors (CAR) on cardiac cells, decreasing infectivity of CVB3.
SCAR-Fc
TA-CD
MPI-CDG
Metab-L
Ze339
ScotSTAR
LAE-32
IPrEx