Distinct kinetics and mechanisms of microbial inactivation of enteric virus revealed by capsid and genome integrity
- 1Ecole Polytechnique Federale de Lausanne (EPFL)
Abstract
Enteric viruses are important contaminants of surface waters and a significant burden on public health. In aquatic ecosystems, the stability of these pathogens is differentially impacted by abiotic and biotic stressors, which can exert inactivating effects. Here, we investigated the fate of two enteroviruses, echovirus 11 (E11) and coxsackievirus B5 (CVB5), and one adenovirus, human adenovirus 2 (HAdV2), in lakewater and explored the mechanisms underlying their microbial inactivation. By combining infectivity assays, genome quantification, and capsid integrity analysis, we characterized virus-specific inactivation kinetics and mechanisms and examined the relationship between infectivity loss and capsid structural integrity. We observed rapid, intermediate, and negligible decay for HAdV2, E11, and CVB5, respectively, and confirmed that microbial proteases contribute to their inactivation. In addition, we revealed that loss of capsid structural integrity drives E11 inactivation, but not HAdV2 inactivation. Genome decay did not consistently correlate with loss of infectivity, highlighting the limitations of genome-based detection for assessing the presence of infectious viruses. These findings provide new insights into the mechanisms governing virus inactivation in aquatic environments and emphasize the importance of understanding viral fate when interpreting molecular detection data to assess virus-associated microbial risks.
Related
- Comparative viral inactivation kinetics of electron beam and gamma irradiation and functional characterization of electron beam inactivated viruses
- STAG2-truncating variants reveal a mosaic STAG2 inactivation pattern and compensatory mechanisms involving cohesin complex remodeling
- Phase Separation Potential of Marsupial RSX RNA Reveals Convergent Evolution of X-Chromosome Inactivation Mechanisms
- Invasive Chinese tallow is associated with distinct rhizosphere microbial communities, core microbiomes, and functional potential relative to native Loblolly pine
- Distinct epitope-specific memory kinetics within influenza B nucleoprotein shape long-term CD8+ T cell differentiation in the lung
BibTeX
@misc{meibom2026distinct,
title = {{Distinct kinetics and mechanisms of microbial inactivation of enteric virus revealed by capsid and genome integrity}},
author = {J. Meibom and L. D. Morales and H. K. Wynn and S. Shin and T. Kohn},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.23.753694},
url = {https://www.biorxiv.org/content/10.64898/2026.09.23.753694v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Distinct kinetics and mechanisms of microbial inactivation of enteric virus revealed by capsid and genome integrity
AU - J. Meibom
AU - L. D. Morales
AU - H. K. Wynn
AU - S. Shin
AU - T. Kohn
PY - 2026
DA - 2026/09/23
PB - bioRxiv
DO - 10.64898/2026.09.23.753694
UR - https://www.biorxiv.org/content/10.64898/2026.09.23.753694v1
AB - Enteric viruses are important contaminants of surface waters and a significant burden on public health. In aquatic ecosystems, the stability of these pathogens is differentially impacted by abiotic and biotic stressors, which can exert inactivating effects. Here, we investigated the fate of two enteroviruses, echovirus 11 (E11) and coxsackievirus B5 (CVB5), and one adenovirus, human adenovirus 2 (HAdV2), in lakewater and explored the mechanisms underlying their microbial inactivation. By combining infectivity assays, genome quantification, and capsid integrity analysis, we characterized virus-specific inactivation kinetics and mechanisms and examined the relationship between infectivity loss and capsid structural integrity. We observed rapid, intermediate, and negligible decay for HAdV2, E11, and CVB5, respectively, and confirmed that microbial proteases contribute to their inactivation. In addition, we revealed that loss of capsid structural integrity drives E11 inactivation, but not HAdV2 inactivation. Genome decay did not consistently correlate with loss of infectivity, highlighting the limitations of genome-based detection for assessing the presence of infectious viruses. These findings provide new insights into the mechanisms governing virus inactivation in aquatic environments and emphasize the importance of understanding viral fate when interpreting molecular detection data to assess virus-associated microbial risks.
ER -