The potential of COVID-19 patients’ sera to cause antibody-dependent enhancement of infection and IL-6 production

• Published in: Scientific reports 2021-12, Vol.11 (1), p.23713-23713, Article 23713
• Main Authors: Shimizu, Jun, Sasaki, Tadahiro, Yamanaka, Atsushi, Ichihara, Yoko, Koketsu, Ritsuko, Samune, Yoshihiro, Cruz, Pedro, Sato, Kei, Tanga, Naomi, Yoshimura, Yuka, Murakami, Ami, Yamada, Misuzu, Itoi, Kiyoe, Nakayama, Emi E., Miyazaki, Kazuo, Shioda, Tatsuo
• Format: Article
• Language: English
• Subjects: 631/250/254; 631/326/596/4130; ACE2; Angiotensin-converting enzyme 2; Angiotensin-Converting Enzyme 2 - metabolism; Antibodies; Antibodies, Neutralizing - immunology; Antibodies, Viral - immunology; Antibody-Dependent Enhancement; Cell Line; Cell lines; Clinical trials; Coronaviruses; COVID-19; COVID-19 - immunology; COVID-19 - metabolism; COVID-19 vaccines; Dengue fever; Humanities and Social Sciences; Humans; Infections; Interleukin 6; Interleukin-6 - metabolism; multidisciplinary; Myeloid Cells - immunology; Myeloid Cells - metabolism; Patients; SARS-CoV-2 - immunology; Science; Science (multidisciplinary); Serine Endopeptidases - metabolism; Severe acute respiratory syndrome coronavirus 2; Vaccination; Vaccine development; Vaccines; Vector-borne diseases
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-021-03273-0

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.