CMV is a common virus that affects people of all ages. The virus is comprised of double-stranded DNA and is a member of the herpesviridea family (e.g., HSV1, HSV2, varicella-zoster, Epstein-Barr). The Centers for Disease Control estimate that between 50% and 80% are infected with CMV by the age of 40. While the virus is typically asymptomatic in healthy individuals, it can cause severe and life-threatening disease in those with weakened or uneducated immune systems. Patients undergoing allogeneic stem cell and solid organ transplantation are at particularly high risk of acquiring CMV through a primary infection, or reactivating an existing and latent CMV infection while in an immune-suppressed state following transplant. Similarly, a growing fetus (having an uneducated immune system) is at high risk of acquiring a primary CMV infection via transmission of the virus in utero. In fact, CMV is the most common congenital infection occurring in between 0.5% and 2% of all pregnancies. Development of vaccines to prevent and treat CMV has been deemed a priority by both the US Food and Drug Administration and the Institute of Medicine. CMV is transmitted via infected saliva, urine and other bodily fluids (and in utero). Most healthy individuals who have CMV are unaware of their infection and exhibit no symptoms of the virus. In those with weakened or uneducated immune systems, CMV infection or reactivation manifests itself through viral syndrome, causing fever malaise, myalgia, as well leukopenia and thrombocytopenia. CMV may further invade tissue, causing end-organ disease including hepatitis, pneumonitis, colitis, nephritis, pancreatitis, retinitis and encephalitis. While antivirals are approved for controlling CMV in the post-transplant setting, such agents are often associated with nephrotoxicity and myelotoxicity, as well as delayed immune reconstitution (and late CMV). Studies have established that a humoral (e.g., neutralizing antibody) response may prevent or attenuate a primary infection of CMV. Moreover, it is believed that cell-mediated immunity (e.g., induction of cytotoxic, virus-specific T-cells) is needed to control CMV once an infection has been established. Helocyte is currently advancing two immunotherapeutic programs for both preventing primary CMV infection as well as controlling reactivation of existing (latent) infections in the post-transplant setting.