Human lactoferrin (hLF) as well as bovine lactoferrin (bLF) inhibited infection of tissue culture cells with human cytomegalovirus (HCMV) and human herpes simplex virus-1(HSV-1). The addition of lactoferrin (LF) inhibited both in vitro infection and replication of HCMV and HSV-1 in human embryo lung host cells. The maximum inhibition by more than six exponentials of TCID50 for HCMV and four exponentials for HSV-1 was obtained at a concentration in a range from 0.5 to 1 mg of LF per ml of medium. The antiviral activity of LF was associated with its protein moiety, but not with its iron molecule or sialic acid. None of other transferrin gene family members bound to ferrous ions or sialic acid possessed significant antiviral activity. Additionally, we found that LF prevented virus adsorption and/or penetration into host cells, indicating an effect on the early events of virus infection. Preincubation of host cells with LF for 5 to 10 min was sufficient to prevent HCMV infection, even when LF was removed after addition of virus. These results suggest that LF possesses a potent antiviral activity and may be useful in preventing HCMV and HSV-1 infection in humans. J. (1988): Comparative study of the primary structures of sero-, lacto-, ovotransferrin glycans from different species. Biochimie, 70, 1459-1469. 2. Kawakata, N. (1984): The isolation and characterization of human milk lactoferrin and the fluctuations of its concentration at different stages of lactation. J

The administration of bovine lactoferrin (LF) with 1 mg/g body weight before the murine cytomegalovirus (MCMV) infection completely protected the BALB/c mice from death due to the infection. In these LF-treated mice, a significant increase in the activity was found in the NK cells but not in the cytolytic T lymphocytes which recognized an MCMV-derived peptide. Moreover, the elimination of the NK cell activity by an injection with anti-asialo GM1 antibody abrogated such augmented resistance, thus supporting the hypothesis that the LF-mediated antiviral effect in vivo is performed through the augmentation of NK cell activity. No such LF-mediated antiviral effect in vivo with the increased NK cell activity was found in athymic nude mice, whereas it was restored completely by the transfer of splenic T cells from LF-treated donors. These findings therefore suggest that T lymphocytes induce both the augmentation of NK cell activity and the resultant antiviral effect in the LF-treated hosts.

No abstract

No abstract

No abstract