Crystal structure of the human astrovirus capsid spike.

Astroviruses are single-stranded, plus-sense RNA viruses that infect both mammals and birds, causing gastroenteritis and other extraintestinal diseases. Clinical studies have established astroviruses as the second leading cause of viral diarrhea in young children. Here we report the crystal structure of the human astrovirus dimeric surface spike determined to 1.8-Å resolution. The overall structure of each spike/projection domain has a unique three-layered ß-sandwiches fold, with a core, six-stranded ß-barrel structure that is also found in the hepatitis E virus capsid protrusions, suggesting a closer phylogenetic relationship between these two viruses than previously acknowledged. Based on a hepatitis E virus capsid model, we performed homology modeling and produced a complete, T = 3 astrovirus capsid model with features remarkably similar to those observed in a cryoelectron microscopy reconstruction image of a human astrovirus. Mapping conserved residues onto the astrovirus projection domain revealed a putative receptor binding site with amino acid compositions characteristic for polysaccharide recognition. Our results will have an important impact on future characterization of astrovirus structure and function, and will likely have practical applications in the development of vaccines and antivirals.

Photocatalytic inactivation of diarrheal viruses by visible-light-catalytic titanium dioxide.

Titanium dioxide (TiO2) that had been irradiated with visible light (VL) was demonstrated to inactivate rotavirus, astrovirus, and feline calicivirus (FCV). The virus titers were dramatically reduced after exposure for 24 hrs to the VL-catalytic TiO2. The addition of bovine serum albumin could protect the virus against inactivation by VL-catalytic TiO2 in a dose-dependent manner. This finding implied that the VL-catalytic TiO2 products might somehow interact initially with the viral proteins in the process of virus inactivation. Moreover, we showed partial degradation of the rotaviral dsRNA genome. This was more prominent when the virus was exposed to the VL-catalytic TiO2 treatment for at least 2 days. An attempt was made to elucidate the mechanism underlying the inactivation of the viruses. It was found that upon activation of TiO2 with VL by using a white fluorescent lamp, the reactive oxygen species such as superoxide anions (O2-) and hydroxyl radicals (*OH) were generated in a significant amount after stimulation for 8, 16, and 24 hrs. We therefore assume that virus inactivation by VL-catalytic TiO2 might occur through the generation of O2- and *OH followed by damage to the viral protein and genome. This is the first report, to the best of our knowledge, demonstrating the inactivation of rotavirus, astrovirus and FCV by the presence of TiO2 film under VL as well as describing its mechanism.