Abstract
In the absence of a vaccine and other effective prophylactic or therapeutic countermeasures the severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) remains a significant public health threat. Attachment and entry of coronaviruses including SARS-CoV-2 is mainly mediated by the spike glycoprotein. Here, we show that iota-carrageenan can inhibit the cell entry of the SARS-CoV-2 spike pseudotyped lentivirus in a dose dependent manner. SARS-CoV-2 spike pseudotyped lentivirus particles were efficiently neutralized with an IC50 value of 2.6 μg/ml iota-carrageenan. Experiments with patient isolated wild type SARS-CoV-2 virus showed an inhibition of replication in a similar range. In vitro data on iota-carrageenan against various Rhino- and endemic Coronaviruses showed similar IC50 values and translated readily into clinical effectiveness when a nasal spray containing iota-carrageenan demonstrated a reduction of severity and duration of symptoms of common cold caused by various respiratory viruses. Accordingly, our in vitro data on SARS-CoV-2 spike pseudotyped lentivirus and replication competent SARS-CoV-2 suggest that administration of iota-carrageenan may be an effective and safe prophylaxis or treatment for SARS-CoV-2 infections.
Highlights
The spread of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2) around the world has created a pandemic situation regarded as a significant public health threat [1,2,3,4]
The sequence of the spike glycoprotein (SGP) of SARS-CoV-2 is significantly different compared to the SGP of SARS-CoV-1, both bind to the same receptor, human angiotensin converting enzyme 2
To determine whether iota-carrageenan can block the infection of cells with Spike Pseudotyped Lentivirus (SSPL) we incubated the viral particles with 10 μg/ml iota-carrageenan dissolved in 0.5% NaCl solution for 30 minutes prior infection
Summary
The spread of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2) around the world has created a pandemic situation regarded as a significant public health threat [1,2,3,4]. SARS-CoV-2 is a betacoronavirus closely related to SARS-CoV-1. The sequence of the spike glycoprotein (SGP) of SARS-CoV-2 is significantly different compared to the SGP of SARS-CoV-1, both bind to the same receptor, human angiotensin converting enzyme 2 (hACE2). Upon binding to hACE2 the protease TMPRSS2 modifies SGP, allowing envelope fusion and viral entry [5] In addition to this rather specific mechanism, many viruses (including some betacoronaviruses) use cellular polysaccharides as cellular attachment coreceptors, allowing the virus to adhere to the surface of the cell. This unspecific interaction increases the local concentration of viral particles leading to higher infection rates
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