Virus Inactivation Mechanisms: Impact of Disinfectants on Virus Function and Structural Integrity

TLDR

Oxidative processes are widely used for pathogen disinfection, yet virus inactivation mechanisms remain contradictory compared to the well‑understood bacterial pathways. The study quantitatively analyzes the total damage to bacteriophage MS2 caused by five common virucidal agents—heat, UV, hypochlorous acid, singlet oxygen, and chlorine dioxide. The authors examined how each agent disrupts virus functions—UV, singlet oxygen, and hypochlorous acid render the genome nonreplicable, while chlorine dioxide and heat block host‑cell recognition—and mapped distinct molecular modifications in capsid proteins or genome that cause inactivation. UV and chlorine treatments cause site‑specific capsid protein backbone cleavage that blocks genome injection, and the overall findings provide insights for improving waterborne and foodborne virus control and understanding viral adaptation to stressors.

Abstract

Oxidative processes are often harnessed as tools for pathogen disinfection. Although the pathways responsible for bacterial inactivation with various biocides are fairly well understood, virus inactivation mechanisms are often contradictory or equivocal. In this study, we provide a quantitative analysis of the total damage incurred by a model virus (bacteriophage MS2) upon inactivation induced by five common virucidal agents (heat, UV, hypochlorous acid, singlet oxygen, and chlorine dioxide). Each treatment targets one or more virus functions to achieve inactivation: UV, singlet oxygen, and hypochlorous acid treatments generally render the genome nonreplicable, whereas chlorine dioxide and heat inhibit host-cell recognition/binding. Using a combination of quantitative analytical tools, we identified unique patterns of molecular level modifications in the virus proteins or genome that lead to the inhibition of these functions and eventually inactivation. UV and chlorine treatments, for example, cause site-specific capsid protein backbone cleavage that inhibits viral genome injection into the host cell. Combined, these results will aid in developing better methods for combating waterborne and foodborne viral pathogens and further our understanding of the adaptive changes viruses undergo in response to natural and anthropogenic stressors.