Nanocrystal quantum dots (QDs) have been applied to molecular biology because of their greater and longer fluorescence. Here we report the potential cytotoxicity of our characterized QDs modified with various molecules. Surface modification of QDs changed their physicochemical properties. In addition, the cytotoxicity of QDs was dependent on their surface molecules. These results suggested that the properties of QDs are not related to those of QD-core materials but to molecules covering the surface of QDs.

Filoviruses, represented by the genera Ebolavirus and Marburgvirus, cause a lethal hemorrhagic fever in humans and in nonhuman primates. Although filovirus can replicate in various tissues or cell types in these animals, the molecular mechanisms of its broad tropism remain poorly understood. Here we show the involvement of members of the Tyro3 receptor tyrosine kinase family-Axl, Dtk, and Mer-in cell entry of filoviruses. Ectopic expression of these family members in lymphoid cells, which otherwise are highly resistant to filovirus infection, enhanced infection by pseudotype viruses carrying filovirus glycoproteins on their envelopes. This enhancement was reduced by antibodies to Tyro3 family members, Gas6 ligand, or soluble ectodomains of the members. Live Ebola viruses infected both Axl-and Dtk-expressing cells more efficiently than control cells. Antibody to Axl inhibited infection of pseudotype viruses in a number of Axl-positive cell lines. These results implicate each Tyro3 family member as a cell entry factor in filovirus infection.

Filoviruses cause lethal hemorrhagic disease in humans and nonhuman primates. An initial target of filovirus infection is the mononuclear phagocytic cell. Calcium-dependent (C-type) lectins such as dendritic cell-or liver/lymph node-specific ICAM-3 grabbing nonintegrin (DC-SIGN or L-SIGN, respectively), as well as the hepatic asialoglycoprotein receptor, bind to Ebola or Marburg virus glycoprotein (GP) and enhance the infectivity of these viruses in vitro. Here, we demonstrate that a recently identified human macrophage galactose-and N-acetylgalactosamine-specific C-type lectin (hMGL), whose ligand specificity differs from DC-SIGN and L-SIGN, also enhances the infectivity of filoviruses. This enhancement was substantially weaker for the Reston and Marburg viruses than for the highly pathogenic Zaire virus. We also show that the heavily glycosylated, mucin-like domain on the filovirus GP is required for efficient interaction with this lectin. Furthermore, hMGL, like DC-SIGN and L-SIGN, is present on cells known to be major targets of filoviruses (i.e., macrophages and dendritic cells), suggesting a role for these C-type lectins in viral replication in vivo. We propose that filoviruses use different C-type lectins to gain cellular entry, depending on the cell type, and promote efficient viral replication.

This Article describes research on chemical reactions on molecules attached to the surface of silicon quantum dots that have been performed to produce quantum dots with reactive surface functionalities such as diols and epoxides. Characterization of the surface reactions includes NMR and FT-IR studies, and the quantum dots were characterized by transmission electron microscopy (TEM) and energy dispersive spectroscopy (EDS). Cytotoxicity and cell viability assay conducted on silicon dots capped with polar molecules indicated low toxicity with quantum dots with more reactive functionalities found to be more toxic. The silicon quantum dots photoluminesce and have been used as a blue chromophore for the biological imaging of cells.