Abstract
The duration of viral shedding is determined by a balance between de novo infection and removal of infected cells. That is, if infection is completely blocked with antiviral drugs (100% inhibition), the duration of viral shedding is minimal and is determined by the length of virus production. However, some mathematical models predict that if infected individuals are treated with antiviral drugs with efficacy below 100%, viral shedding may last longer than without treatment because further de novo infections are driven by entry of the virus into partially protected, uninfected cells at a slower rate. Using a simple mathematical model, we quantified SARS-CoV-2 infection dynamics in non-human primates and characterized the kinetics of viral shedding. We counterintuitively found that treatments initiated early, such as 0.5 d after virus inoculation, with intermediate to relatively high efficacy (30-70% inhibition of virus replication) yield a prolonged duration of viral shedding (by about 6.0 d) compared with no treatment.
Highlights
Two main processes are involved in the pathogenesis of coronavirus disease 2019 (COVID-19): the disease primarily develops through replication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is driven by exaggerated host immune/inflammatory responses to the virus, leading to various tissue damage
It is well known that entry of SARS-CoV-2 into cells requires interaction of the virus spike protein with host angiotensin-converting enzyme 2 (ACE2) receptor, and cleavage and activation of spike by a serine protease, TMPRSS2 [31]
Analyses of single-cell sequencing datasets have demonstrated that ACE2 receptor is abundantly expressed in multiple organs, such as nose, lung, eye, and intestine [27], which suggests that the target organ of SARS-CoV-2 is not limited to respiratory tracts
Summary
Two main processes are involved in the pathogenesis of coronavirus disease 2019 (COVID-19): the disease primarily develops through replication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is driven by exaggerated host immune/inflammatory responses to the virus, leading to various tissue damage. Remdesivir (RDV) is currently the only antiviral drug approved by the Food and Drug Administration for the treatment of COVID-19 and is recommended for hospitalized patients who require supplemental oxygen. It is not routinely recommended for patients at advanced stages of the disease, such as for patients maintained on artificial respiration by means of mechanical ventilators, owing to the lack of data showing benefit [2, 3, 4, 5]. Reporting viral load has an important role in infection prevention practices, given that viral load correlates with levels of infectiousness [17, 18, 19], even though detection of viral RNA by PCR does not necessarily indicate the infectivity of SARSCoV-2 in the late phase of disease
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