Amorphous TiO2: An unexpected antiviral shield for surfaces.

HYPOTHESIS: Amorphous oxides are often considered catalytically inert, yet their disordered interfaces may influence interactions with biological systems. We hypothesized that amorphous TiO2 could exhibit antiviral activity through surface-mediated interactions under ambient, light-free conditions rather than through conventional photocatalytic pathways.

EXPERIMENTS: Amorphous TiO2 films were prepared by low-temperature sol-gel processing and annealed at 200 °C and 350 °C. Their antiviral activity against lentivirus was evaluated using infectivity and real-time polymerase chain reaction (PCR) assays under ambient, light-free conditions. Additional control experiments using inert surfaces were performed to distinguish material-specific antiviral activity from desiccation-induced viral inactivation. Complementary transmission electron microscopy, cryo-TEM, zeta-potential, and X-ray photoelectron spectroscopy analyses were conducted to investigate possible virus-surface interactions.

FINDINGS: The amorphous TiO2 films achieved rapid lentivirus inhibition within 20 min under ambient, light-free conditions, with inhibition rates of 82.3% and 87.8% for the 200 °C and 350 °C films, respectively, in infectivity assays and viral genome reductions of 92.1% and 94.2% in PCR assays. The films also outperformed commercial antimicrobial reference coatings, while inert-surface controls demonstrated that the observed antiviral activity could not be attributed to desiccation alone. TEM and cryo-TEM observations revealed viral adhesion and structural disruption following contact with the TiO2 surface. Zeta-potential measurements indicated changes in the surface-charge characteristics of viral particles after TiO2 exposure, while XPS analysis revealed shifts in phosphate- and nitrogen-containing species associated with the viral material, consistent with surface-induced alterations following virus-surface interaction. Collectively, these findings support a plausible non-photocatalytic, interface-driven antiviral pathway involving surface-mediated interactions.