Journal
VIRUSES-BASEL
Volume 13, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/v13050850
Keywords
influenza viral dynamics; cell-surface mucin MUC1; immune response; mathematical models
Categories
Funding
- Melbourne Research Scholarship
- Australian Research Council (ARC) [DP170103076]
- National Health and Medical Research Council (NHMRC) [1078068]
- National Health and Medical Research Council of Australia [1078068] Funding Source: NHMRC
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This study analyzed the impact of MUC1 on influenza virus dynamics and host immune response using mathematical models, revealing that MUC1 can reduce viral replication rate and macrophage numbers, but has minimal effect on viral load. The research suggests that the viral replication rate in the early stages of infection plays a crucial role in the dynamics of the host immune response and infection severity.
MUC1 belongs to the family of cell surface (cs-) mucins. Experimental evidence indicates that its presence reduces in vivo influenza viral infection severity. However, the mechanisms by which MUC1 influences viral dynamics and the host immune response are not yet well understood, limiting our ability to predict the efficacy of potential treatments that target MUC1. To address this limitation, we use available in vivo kinetic data for both virus and macrophage populations in wildtype and MUC1 knockout mice. We apply two mathematical models of within-host influenza dynamics to this data. The models differ in how they categorise the mechanisms of viral control. Both models provide evidence that MUC1 reduces the susceptibility of epithelial cells to influenza virus and regulates macrophage recruitment. Furthermore, we predict and compare some key infection-related quantities between the two mice groups. We find that MUC1 significantly reduces the basic reproduction number of viral replication as well as the number of cumulative macrophages but has little impact on the cumulative viral load. Our analyses suggest that the viral replication rate in the early stages of infection influences the kinetics of the host immune response, with consequences for infection outcomes, such as severity. We also show that MUC1 plays a strong anti-inflammatory role in the regulation of the host immune response. This study improves our understanding of the dynamic role of MUC1 against influenza infection and may support the development of novel antiviral treatments and immunomodulators that target MUC1.
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