Supplemental Information
Document S1. Author contributions
Table S1
Statistics and Gene Lists Related to Figure 1 (Non-Human Primate Lung) A. Cluster defining genes for cell types presented in Figure 1. B. ACE2 and TMPRSS2 statistics by cell type. C. Differentially expressed genes between ACE2+ and ACE2- Type II Pneumocytes.
Table S2
Statistics and Gene Lists Related to Figure 2 (Human Lung) A. Cluster defining genes for cell types presented in Figure 2. B. ACE2 and TMPRSS2 statistics by cell type. C. Differentially expressed genes between ACE2+TMPRSS2+ versus rest Type II Pneumocytes.
Table S3
Statistics and Gene Lists Related to STAR Methods and Figure S1 (NHP Tuberculosis Infected Lung and Granuloma) A. Cluster defining genes for cell types presented in Figure S1 B. ACE2 and TMPRSS2 statistics by cell type C. Abundances of ACE2+TMPRSS2+ cells by cell type and tissue of origin D. Differentially expressed genes between ACE2+TMPRSS2+ versus rest Type II Pneumocytes
Table S4
Statistics and Gene Lists Related to Figure 3 (Non-Human Primate Ileum) A. Cluster defining genes for cell types presented in Figure 3B B. ACE2 and TMPRSS2 statistics by cell type. C. Differentially expressed genes between ACE2+TMPRSS2+ versus rest Absorptive Enterocytes
Table S5
Statistics and Gene Lists Related to Figure 3 (Human Ileum) A. Cluster defining genes for cell types presented in Figure 3D B. ACE2 and TMPRSS2 statistics by cell type. C. Differentially expressed genes between ACE2+TMPRSS2+ Absorptive Enterocytes versus rest Enterocytes D. Differentially expressed genes between ACE2+TMPRSS2+ Absorptive Enterocytes versus rest Absorptive Enterocytes
Table S6
Statistics and Gene Lists Related to Figure 4 and 5 (Human Nasal Mucosa and Human Influenza) A. ACE2 and TMPRSS2 statistics by cell type presented in Figure 4B. B. Cluster defining genes for cell types presented in Figure 4C and 4D. C. Cluster defining genes for cell types presented in Figure 4C and 4F. D. ACE2 and TMPRSS2 statistics by cell type presented in Figure 4C. E. ACE2 and TMPRSS2 statistics by cell type presented in Figure 4D. F. Differentially expressed genes between ACE2+TMPRSS2+ epithelial cells versus rest epithelial cells in Figure 4E G. Differentially expressed genes between ACE2+TMPRSS2+ epithelial cells versus rest secretory epithelial cells in Figure 4E H. Raw data for cell type abundances by tissue and disease, Figure 4H I. Differentially expressed genes between ACE2+TMPRSS2+ versus Goblet Cells from Human Influenza dataset (Figure 6E-G).
Table S7
Differentially Expressed Genes in Human and Mouse Basal Epithelial Cells Treated with Various Cytokines and Interferons, Related to Figure 5 A. Mouse Untreated versus IFNβ B. Mouse Untreated versus IFNα2 C. Mouse Untreated versus IFNγ D. BEAS-2B Untreated versus IL4 E. BEAS-2B Untreated versus IL17A F. BEAS-2B Untreated versus IFNγ G. BEAS-2B Untreated versus IFNα2 H. Human Donor 1 Untreated versus IL4 I. Human Donor 1 Untreated versus IL17A J. Human Donor 1 Untreated versus IFNγ K. Human Donor 1 Untreated versus IFNα2 L. Human Donor 2 Untreated versus IL4 M. Human Donor 2 Untreated versus IL17A N. Human Donor 2 Untreated versus IFNγ O. Human Donor 2 Untreated versus IFNα2
Table S8
Statistics and Gene Lists Related to Figure 6 and Figure S5 (Mouse Nasal Epithelium) A. Cluster defining genes for cell types presented in Figure 6A B. Ace2 and Tmprss2 statistics by cell type C. Differentially expressed genes among Basal Epithelial Cells treated with Saline versus Intranasal IFNα
Table S9
Summary of Datasets Analyzed in this Study with Links to Data, Related to STAR Methods

Acknowledgments
We are grateful to the study participants who made this work possible. We would like to thank Bruce Horwitz, Ivan Zanoni, Matt Sampson, Michael Retchin, Peter Winter, Andrew Navia, Jamie Cohen, and Audrey Sporrij for discussions. Mengyang (Vicky) Li Horst, Timothy Tickle, Jonathan Bistline, Jean Chang, Eric Weitz, Eno-Abasi Augustine-Akpan, and Devon Bush for development and support of the Broad Institute Single Cell Portal. This work was supported in part by the Searle Scholars Program, the Beckman Young Investigator Program, the Pew-Stewart Scholars Program for Cancer Research, a Sloan Fellowship in Chemistry, the MIT Stem Cell Initiative through Fondation MIT, the 10.13039/100000002NIH (5U24AI118672 and BAA-NIAID-NIHAI201700104), and the 10.13039/100000865Bill and Melinda Gates Foundation to A.K.S., as well as NIH R56 AI139053 to J.L.F and P.L.L., and the Aeras Foundation to J.L.F. B.B. and S.K.N. are partially supported by NIH 5R01GM081871. We acknowledge support from the 10.13039/100001021Damon Runyon Cancer Research Foundation (DRG-2274-16) and 10.13039/100001341Richard and Susan Smith Family Foundation to J.O.-M; from a National Science Foundation Graduate Research Fellowship (1122374) to S.K.N., S.J.A., and C.N.T.; from a Fannie and John Hertz Foundation Fellowship to C.N.T.; by T32GM007753 from the 10.13039/100000057National Institute of General Medical Sciences to C.G.K.Z. This work was further supported by the UMass Center for Clinical and Translational Science Project Pilot Program; and the Office of the Assistant Secretary of Defense for Health Affairs, through the Peer Reviewed Medical Research Program (W81XWH-15-1-0317) to R.W.F. We also acknowledge support from 10.13039/100000002NIH grants AI078908, HL111113, HL117945, R37AI052353, R01AI136041, R01HL136209, and U19AI095219 to J.A.B.; by grants from the 10.13039/100000002NIH and National Heart, Lung, and Blood Institute (U19 HL129902) to H.P.K and L.S.K; from National Institute of Allergy and Infectious Diseases (UM1 AI126623) to H.P.K.; and to P.B. from the 10.13039/501100002915Fondation pour la Recherche Médicale (DEQ20180339158), and the 10.13039/501100001665Agence Nationale pour la Recherche (ANR-19-CE14-0027); and by the following grants to L.S.K: NIH/NIAID U19 AI051731, NIH/NHLBI R01 HL095791 NIH/NIAID R33-AI116184, NIH/NIAID U19 AI117945, and DHHS/NIH 1UM1AI126617. B.E.M. was supported by the Massachusetts Institute of Technology - GlaxoSmithKline (MIT-GSK) Gertrude B. Elion Postdoctoral Fellowship; T.M.L. by the NIH/NHLBI 1R01HL128241-01, K.M.B. by NIH/NIAID K23AI139352; and D.L. by NIH R01AI137057, DP2DA042422, and R01AI124378. This publication is part of the Human Cell Atlas (www.humancellatlas.org/publications).

Author Contributions
Document S1 details contributions of all authors.

Declaration of Interests
A.R. is an SAB member of ThermoFisher Scientific, Neogene Therapeutics, Asimov, and Syros Pharmaceuticals; a co-founder of and equity holder in Celsius Therapeutics; and an equity holder in Immunitas Therapeutics. A.K.S. reports compensation for consulting and/or SAB membership from Merck, Honeycomb Biotechnologies, Cellarity, Cogen Therapeutics, Orche Bio, and Dahlia Biosciences. L.S.K. is on the SAB for HiFiBio; she reports research funding from Kymab Limited, Bristol Meyers Squibb, Magenta Therapeutics, BlueBird Bio, and Regeneron Pharmaceuticals and consulting fees from Equillium, FortySeven, Inc, Novartis, Inc, EMD Serono, Gilead Sciences, and Takeda Pharmaceuticals. A.S. is an employee of Johnson and Johnson. N.K. is an inventor on a patent using thyroid hormone mimetics in acute lung injury that is now being considered for intervention in COVID-19 patients. J.L. is a scientific consultant for 10X Genomics, Inc. O.R.R, is a co-inventor on patent applications filed by the Broad Institute to inventions relating to single-cell genomics applications, such as in PCT/US2018/060860 and US Provisional Application No. 62/745,259. S.T. in the last three years was a consultant at Genentech, Biogen, and Roche and is a member of the SAB of Foresite Labs. M.H.W. is now an employee of Pfizer. F.J.T. reports receiving consulting fees from Roche Diagnostics GmbH and ownership interest in Cellarity, Inc. P.H. is a co-inventor on a patent using artificial intelligence and high-resolution microscopy for COVID-19 infection testing based on serology. Supplemental Information can be found online at https://doi.org/10.1016/j.cell.2020.04.035.