Transport and Attenuation of Human Viruses in Groundwater: Assessment of Adsorption-Induced Interfacial Inactivation and Evidence of Aggregation

Virus transport in groundwater is a key pathway contributing to waterborne disease outbreaks and poses significant risks to public health. However, the mechanisms governing virus transport and attenuation remain poorly understood. Here, using the human enteric virus Coxsackievirus (CV-A16), we coupled experiments with a dual-marker approach (TCID50 and RT-qPCR) and a stepwise modeling strategy to quantify virus inactivation, interfacial inactivation, and adsorption during virus transport and attenuation in heterogeneous sediments. Static batch experiments revealed markedly slower CV-A16 inactivation in the aqueous phase, requiring 106-191 days to achieve a 90% loss of infectivity, compared with about 12 days in saturated sediments. Column experiments indicated that kinetic adsorption-desorption was the dominant attenuation mechanism, while surface-associated interfacial inactivation represented an additional important pathway that increased with virus adsorption, reflecting a coupled adsorption-inactivation process. Further analysis showed that inactivation rate constants ranged from 0.002 to 0.004 min-1 from coarse sand to silt, suggesting enhanced virus-solid interface reactivity in finer sediments. Furthermore, bimodal particle-size distributions from laser particle sizing and TEM observations of virus clusters indicate the formation of aggregates during transport, while zeta potential variations suggest that this process most likely occurs during the early to intermediate stages of transport. By evaluating the interplay between physical retention and biological inactivation, this study provides a mechanistic framework to improve the prediction of virus transport and the accuracy of pathogen-related health risk assessments in subsurface environments.