The Dynamic Role of Aerosol and Exudate Transport in the Diffusion of Lung Infection in Respiratory Infectious Diseases (taking SARS-CoV-2 as an example): A Hypothesis Model

TL;DR

This paper introduces a hypothesis model highlighting the dual role of aerosols and exudates in the progression of SARS-CoV-2 lung infection, emphasizing the dynamic shift in transmission mechanisms within the host.

Contribution

It presents a novel conceptual framework for understanding the intra-host transmission dynamics of respiratory viruses, integrating aerosol and exudate roles in disease progression.

Findings

Aerosols are crucial in initial infection seeding.

Exudates facilitate large-scale intra-lung spread.

A dynamic shift occurs from aerosol to exudate dominance.

Abstract

This paper proposes a hypothetical model for the dual role of respiratory aerosols and inflammatory exudates in the dynamics and progression of SARS-CoV-2 lung infection. Starting from a new paradigm in infectious disease transmission, we reflect on the often-overlooked role of physical transmission media within the host individual. The hypothesis posits that tiny aerosols (including those inhaled externally and those self-generated and re-inhaled by the host) play a crucial role in the initial seeding and early expansion of the infection in the lungs, explaining the multifocal characteristics observed in early CT imaging. As the infection progresses, inflammatory exudates, formed due to lung inflammation, become a new efficient vehicle, driving the large-scale spread of the virus within the lungs and accounting for the development of diffuse lesions. This model reveals a "dynamic equilibrium point" where the dominant mechanism shifts from aerosol-mediated to exudate-mediated spread. Although direct validation of this hypothesis faces ethical and technical challenges, existing clinical imaging, viral kinetics, and epidemiological patterns provide indirect support. The paper also conceptualizes ideal experimental designs and retrospective analyses to validate the hypothesis. Finally, we discuss the implications of this hypothesis for public health practice, emphasizing the importance of improving ventilation in the microenvironment of infected individuals to achieve a "for all, by all" (literally "everyone for me, I for everyone") bidirectional protection. This research aims to provide a new framework for understanding the pathophysiology of respiratory infectious diseases and to offer theoretical basis for developing more cost-effective and broadly applicable intervention strategies.