tetano
Editor, Senior Moderator
Math Biosci
. 2020 Aug 6;108438.
doi: 10.1016/j.mbs.2020.108438. Online ahead of print.
Modeling the viral dynamics of SARS-CoV-2 infection
Sunpeng Wang[SUP] 1 [/SUP], Yang Pan[SUP] 2 [/SUP], Quanyi Wang[SUP] 3 [/SUP], Hongyu Miao[SUP] 4 [/SUP], Ashley N Brown[SUP] 5 [/SUP], Libin Rong[SUP] 6 [/SUP]
Affiliations
Abstract
Coronavirus disease 2019 (COVID-19), an infectious disease caused by the infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is spreading and causing the global coronavirus pandemic. The viral dynamics of SARS-CoV-2 infection have not been quantitatively investigated. In this paper, we use mathematical models to study the pathogenic features of SARS-CoV-2 infection by examining the interaction between the virus, cells and immune responses. Models are fit to the data of SARS-CoV-2 infection in patients and non-human primates. Data fitting and numerical simulation show that viral dynamics of SARS-CoV-2 infection have a few distinct stages. In the initial stage, viral load increases rapidly and reaches the peak, followed by a plateau phase possibly generated by lymphocytes as a secondary target of infection. In the last stage, viral load declines due to the emergence of adaptive immune responses. When the initiation of seroconversion is late or slow, the model predicts viral rebound and prolonged viral persistence, consistent with the observation in non-human primates. Using the model we also evaluate the effect of several potential therapeutic interventions for SARS-CoV-2 infection. Model simulation shows that anti-inflammatory treatments or antiviral drugs combined with interferon are effective in reducing the duration of the viral plateau phase and diminishing the time to recovery. These results provide insights for understanding the infection dynamics and might help develop treatment strategies against COVID-19.
. 2020 Aug 6;108438.
doi: 10.1016/j.mbs.2020.108438. Online ahead of print.
Modeling the viral dynamics of SARS-CoV-2 infection
Sunpeng Wang[SUP] 1 [/SUP], Yang Pan[SUP] 2 [/SUP], Quanyi Wang[SUP] 3 [/SUP], Hongyu Miao[SUP] 4 [/SUP], Ashley N Brown[SUP] 5 [/SUP], Libin Rong[SUP] 6 [/SUP]
Affiliations
- PMID: 32771304
- DOI: 10.1016/j.mbs.2020.108438
Abstract
Coronavirus disease 2019 (COVID-19), an infectious disease caused by the infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is spreading and causing the global coronavirus pandemic. The viral dynamics of SARS-CoV-2 infection have not been quantitatively investigated. In this paper, we use mathematical models to study the pathogenic features of SARS-CoV-2 infection by examining the interaction between the virus, cells and immune responses. Models are fit to the data of SARS-CoV-2 infection in patients and non-human primates. Data fitting and numerical simulation show that viral dynamics of SARS-CoV-2 infection have a few distinct stages. In the initial stage, viral load increases rapidly and reaches the peak, followed by a plateau phase possibly generated by lymphocytes as a secondary target of infection. In the last stage, viral load declines due to the emergence of adaptive immune responses. When the initiation of seroconversion is late or slow, the model predicts viral rebound and prolonged viral persistence, consistent with the observation in non-human primates. Using the model we also evaluate the effect of several potential therapeutic interventions for SARS-CoV-2 infection. Model simulation shows that anti-inflammatory treatments or antiviral drugs combined with interferon are effective in reducing the duration of the viral plateau phase and diminishing the time to recovery. These results provide insights for understanding the infection dynamics and might help develop treatment strategies against COVID-19.