Mechanistic Insights Into the Decay of Viruses on Surfaces

KE ZHANG, University of Michigan

     Abstract Number: 617
     Working Group: Bioaerosols

Abstract
Influenza and other respiratory viruses continue to pose a significant threat to public health worldwide. Fomite-mediated transmission (e.g., via contact with contaminated surfaces or objects) is one of the major ways that respiratory viruses are transmitted in indoor environments. Consequently, understanding viral persistence on surfaces is critical for effective transmission control. Currently, two major challenges hinder this research area: (1) the mechanisms underlying virus decay on surfaces remain poorly understood; and (2) surface contamination is usually assessed via detection of viral genomic RNA rather than direct quantification of viral infectivity, despite limited understanding of the relationship between RNA persistence and infectious virus survival on surfaces. To address these challenges, we investigated the decay dynamics of influenza A virus and two commonly used surrogates (e.g., bacteriophages MS2 and phi6) under representative indoor relative humidity (RH) conditions. Under constant RH levels, we observed that viral infectivity declined much more rapidly than viral genomic RNA, which remained relatively stable for up to two months. Notably, under fluctuating humidity conditions, we observed accelerated degradation of both viral infectivity and RNA. These findings support a mechanistic hypothesis in which fluctuating humidity promotes decay by damaging both structural and non-structural viral proteins, whereas constant RH conditions primarily affect non-structural viral proteins. This work advances our understanding of virus persistence in indoor environments and informs the development of more accurate transmission models and environmental surveillance strategies for respiratory viruses.