S1 Data - B Cell Receptor’s function in virus entry: Anti-SARS-CoV-2 B cell receptors can mediate viral entry in an ACE2-independent mechanism

Fig 1B: Percentage of transduction of Ramos cells with or without ectopic expression of control or anti-ZIKV BCR following infection with replication-competent ZIKV. Fig 1C: Percentage of transduction of CD79 Sp2/0 cells with or without ectopic expression of control or anti-ZIKV BCR following infection with replication-competent ZIKV. Fig 1D: Percentage of infection in Vero E6 cells using supernatants from ZIKV-infected cells. Fig 1F: Percentage of infection of primary human B cells with or without ectopic expression of control or anti-ZIKV BCR following exposure to a ZIKV replicon. Fig 2A: Percentage of splenic B cells expressing control or anti-ZIKV BCR during in vivo ZIKV infection across replicate experiments. Fig 2B: Percentage of ZIKV-infected splenic B cells expressing control or anti-ZIKV BCR following exposure to a ZIKV replicon. Fig 3C: Percentage of infection by heat-inactivated or infectious HIV-1 NL4-3 in CD79 293T or CD79 CXCR4 cells with or without ectopic expression of CD4. Fig 3D: Mean fluorescence intensity (MFI) values from virus-binding assays of Scalet-labeled HIV-1 to CD79 CXCR4 cells with or without ectopic expression of CD4, DC-SIGN, control BCR (REGN), or anti-HIV-1 BCRs derived from 3BNC117, VRC07, and eCD4-Ig. Fig 3E: Percentage of infection by heat-inactivated (HI) or infectious (I) HIV-1 NL4-3 in CD79 CXCR4 cells with or without ectopic expression of CD4, DC-SIGN, control BCR, or anti-HIV-1 BCRs derived from 3BNC117, VRC07, and eCD4-Ig. Fig 4A: Percentage of binding of Scalet-labeled lentiviral vectors pseudotyped with SARS-CoV-2 S protein to 293T cells with or without ectopic expression of TIM-1 or ACE2, and to CD79 293T cells expressing control (anti-HIV-1 3BNC117) or anti-SARS-CoV-2 BCRs (REGN10933 and CB6), across multiple MOIs (µg p24/ml). (XLSX)