Abstract
Since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), many vaccine trials have been initiated. An important goal of vaccination is the development of neutralizing antibody (Ab) against SARS-CoV-2. However, the possible induction of antibody-dependent enhancement (ADE) of infection, which is known for other coronaviruses and dengue virus infections, is a particular concern in vaccine development. Here, we demonstrated that human iPS cell-derived, immortalized, and ACE2- and TMPRSS2-expressing myeloid cell lines are useful as host cells for SARS-CoV-2 infection. The established cell lines were cloned and screened based on their function in terms of susceptibility to SARS-CoV-2-infection or IL-6 productivity. Using the resulting K-ML2 (AT) clone 35 for SARS-CoV-2-infection or its subclone 35–40 for IL-6 productivity, it was possible to evaluate the potential of sera from severe COVID-19 patients to cause ADE and to stimulate IL-6 production upon infection with SARS-CoV-2.
Highlights
Since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), many vaccine trials have been initiated
We demonstrated that human iPS cell-derived, immortalized, and Angiotensin-converting enzyme 2 (ACE2)- and transmembrane protease serine 2 (TMPRSS2)-expressing myeloid cell lines are useful as host cells for SARSCoV-2 infection
Antibody-dependent enhancement (ADE) of infection has been reported for several virus infections such as dengue[1,2] and Zika viruses[3]; severe acute respiratory syndrome (SARS)[4] and Middle East respiratory syndrome (MERS) coronaviruses[5]; human immunodeficiency virus (HIV)[6]; and Ebola virus[7]
Summary
Since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), many vaccine trials have been initiated. We show that using Mylc lines, it is possible to detect the potential of sera from COVID-19 patients to enhance infection of SARS-CoV-2 and to augment IL-6 production. The differentiation of clone 35 cells into DCs resulted in the down-expression of CD14 (Supplemental Fig. S3b) and higher levels of virus production in SNs (Fig. 2b).
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