Galectins are a family of lectin binding proteins, characterised by the presence of a carbohydrate recognition domain. Members of this widely expressed protein family have been demonstrated to exert profound effects on innate and adaptive immune responses. Gal-1, a prototype galectin, in particular has been implicated in a number of immune regulatory processes, both normal and disease associated, including cancer and autoimmune disease. Human cytomegalovirus (HCMV) is a large double stranded DNA virus of the herpesvirus family. While HCMV infection is generally asymptomatic in the immunocompetent, HCMV can have devastating consequences in immunocompromised individuals, in particular those with impaired or under-developed cell mediated immunity, including transplant recipients and neonates. Although a massive proportion (~10%) of peripheral T-cells are directed against HCMV in healthy seropositive individuals, HCMV is never cleared, indicating the virus has developed a range of mechanisms to evade and modulate host cell immunity. A role for Gal-1 in viral host-pathogen interactions has recently emerged. Indeed studies with another herpesvirus, Epstein Barr virus (EBV), identified Gal-1 as a virally regulated immunomodulatory molecule controlling anti-EBV T-cell immunity. Gal-1 expression has not previously been studied in the context of HCMV infection and so we examined the expression, localisation and secretion of Gal-1 during productive HCMV infection of primary human fibroblasts. Whilst HCMV infection did not alter total cellular Gal-1 protein levels, expression of cell-surface Gal-1 was significantly up-regulated during infection. Additionally, HCMV infection increased secretion of Gal-1 from infected cells, raising the intriguing possibility that bystander cells may also be impacted. Thus, the functional impacts of Gal-1 on HCMV-specific CD8+ T-cells were assessed. Initial analyses indicated that Gal-1 profoundly impairs HCMV peptide-specific CD8+ T-cell proliferation. This study provides the first evidence that HCMV up-regulates cell-surface and secreted Gal-1 and identifies an immunomodulatory role for this protein in the anti-HCMV T-cell response.