Dean Tatlow
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) undergoes blood type specific glycosylation which has implications for infection susceptibility and replication without detection from the immune system. SARS-CoV-2 hijacks the host cell glycotransferase resulting in spike protein glycosylation resembling blood type antigens. Infection risk correlates to blood types that do not have anti-A and/or anti-B antibodies similar to that seen for ABO blood type recipients. The universal recipient AB is highly susceptible to infection lacking both anti-A and B antibodies, whereas blood type O has both antibodies resulting in less risk of infection. Once infected, SARS-CoV-2 obtains the blood type specific glycosylation of the host resulting in an effective camouflage against immune system recognition. Decoding the link between blood type and coronavirus disease 2019 (COVID-19) susceptibility exposes a role for miglustat a glycosyltransferase inhibitor in treatment. Use of the FDA-approved glycosyltransferase inhibitor miglustat can inhibit spike protein glycosylation revealing the SARS-CoV-2 virus for immune system recognition.
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