Abstract
OPINION article Front. Cell. Infect. Microbiol., 23 October 2020Sec. Virus and Host Volume 10 - 2020 | https://doi.org/10.3389/fcimb.2020.559209
Highlights
The new SARS-CoV-2 reminds us about the potential of infectious pathogens to fiercely spread worldwide and puts our well-being in danger
Tissue damage of various severity is observed but the host survives. How can this qualitative description of virus-induced pathogenicity be transformed into a more quantitative characterization of host protection and its limits? A systems biology-based analysis combining experimental data of murine coronavirus infection and mathematical modeling has Determinants of Coronavirus Pathogenicity shown that the robustness of innate immune response-mediated protection from severe disease is rather limited when putative CoV variants exhibiting enhanced tropism and replication in peripheral organ cells like hepatocytes rather than lymphoid tissue cells were considered (Bocharov et al, 2010, 2018)
The remarkable similarity of the values and the preferential tropism of the SARS-CoV viruses to cells of the upper respiratory tract and lungs would suggest that the robustness of protection against SARS-CoV spreading in this peripheral organ by the innate IFN response is limited
Summary
The new SARS-CoV-2 reminds us about the potential of infectious pathogens to fiercely spread worldwide and puts our well-being in danger. A systems biology-based analysis combining experimental data of murine coronavirus infection and mathematical modeling has Determinants of Coronavirus Pathogenicity shown that the robustness of innate immune response-mediated protection from severe disease is rather limited (summarized in Figure 1C) when putative CoV variants exhibiting enhanced tropism and replication in peripheral organ cells like hepatocytes rather than lymphoid tissue cells were considered (Bocharov et al, 2010, 2018).
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