In addition, the low number of cases of overt CMV disease in our cohort precluded the appreciation of potential associations between severe viral disease and genetic variation in PTX3. Functional studies are ultimately required to understand how PTX3 is regulated in response and during CMV infection after HSCT, and what is the relative involvement of genetic variation in defining the levels of PTX3 and contributing to infection. This evidence concerns the gene PTX3 and viral infectious disease.