antibody levels against nucleocapsid (N) and the receptor binding domain (RBD) and the S2 48 region of spike protein. Unlike disease severity, age and sex played lesser roles in serological 49 responses. All cases, including asymptomatic individuals, seroconverted by 2 weeks post-PCR 50 confirmation. RBD-and S2-specific and neutralizing antibody titers remained elevated and 51 stable for at least 2-3 months post-onset, whereas those against N were more variable with 52 rapid declines in many samples. Testing of 5882 self-recruited members of the local community 53 demonstrated that 1.24% of individuals showed antibody reactivity to RBD. However, 18% 54 (13/73) of these putative seropositive samples failed to neutralize authentic SARS-CoV-2 virus. 55
Each of the neutralizing, but only 1 of the non-neutralizing samples, also displayed potent 56 reactivity to S2. Thus, inclusion of multiple independent assays markedly improved the 57 accuracy of antibody tests in low seroprevalence communities and revealed differences in 58 antibody kinetics depending on the viral antigen. In contrast to other reports, we conclude that 59 immunity is durable for at least several months after SARS-CoV-2 infection. 60 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020 . . https://doi.org/10.1101 relatively robust spread of the virus (Rosenberg et al., 2020; Stadlbauer et al., 2020) , prevalence in most of the world has been low. For example, studies in Spain and Switzerland 67 revealed overall seroprevalences of ~5%, with some communities at just 1% antibody positivity 68 (Pollán et al., 2020; Stringhini et al., 2020) . The challenges of accurate antibody testing for 69 SARS-CoV-2 in low seroprevalence communities have led to several unexpected conclusions. 70
As an example, a seroprevalence study in Santa Clara county, California suggested higher 71 infection rates than had been anticipated, thereby leading to the interpretation that SARS-CoV-2 72 was much less deadly than originally thought (Bendavid et al., 2020) . Yet this conclusion was 73 problematic given that the false positive rates of the administered test approached the true 74 seroprevalence of the community (Bennett and Steyvers, 2020). Thus, it is likely that many 75 positive results were inaccurate, and the overall infection fatality rate was substantially higher 76 than estimated in this study (Bennett and Steyvers, 2020) . Reducing this false positive rate is 77 critical for accurate seroprevalence studies. Moreover, serological testing has an additional 78 imperative to guard against false positive results that could entice the subject to falsely assume 79 immunity where none may exist. Indeed, the assumption of immunity associated with a positive 80 test result may be amongst the primary motivations for participation in these serological 81 surveys. Virus neutralization assays are functional correlates of immunity but require Biosafety 82
Level 3 facilities and are difficult to scale and deploy as clinical assays. Yet tests that fail to 83 provide confidence in functional immune status undermine this important epidemiological tool. 84 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020 . . https://doi.org/10.1101 Finally, poor positive predictive values are especially problematic in the context of convalescent 85 plasma donations, where most samples would be ineffective in passive transfer therapies. 86
Serological studies have also been used to estimate the durability of antibody production 87 and immunity after SARS-CoV-2 infections. Here again, several surprising conclusions have 88 been reached regarding the short duration of immunity, with several studies suggesting that in a 89 substantial number of subjects, antibody levels wane to below the limit of detection within a 90 matter of weeks to months (Ibarrondo et al., 2020; Long et al., 2020a; Pollán et al., 2020; Seow 91 et al., 2020) . Yet all T-dependent humoral responses, even ones that are exceptionally durable, 92 begin with an initial wave of short-lived plasma cells which decline quickly and are progressively 93 replaced by a smaller number of longer-lived antibody-secreting plasma cells (Amanna, 2007; 94 Manz et al., 1997; Slifka et al., 1998; Sze et al., 2000) . Thus, the decay in antibody production 95 after infection or vaccination is not linear and cannot be extrapolated from early timepoints, 96 demonstrating the need for longer-term follow-up studies. Indeed, such short-term antibody 97 production would be without precedent following acute coronavirus infections, which typically 98 induce immunity for at least a year and for SARS-CoV-1, often for much longer (Callow et al., 99 1990; Guo et al., 2020; Reed, 1984; Tan et al., 2020) . Keys to the accurate interpretation of 100 such studies are sensitive assays, PCR confirmation of test cases, and longitudinal tests of 101 seropositive individuals. Authentic virus neutralization assays are also useful as true correlates 102 of immunity (Zinkernagel and Hengartner, 2006) . Absent these components, conclusions about 103 the duration of immunity are premature. 104
Here, we successfully employed a strategy using RBD and S2 as antigenically distinct 105 tests to accurately identify seropositive individuals in the community. In doing so, this assay 106 greatly reduced the existing limitations to testing accuracy in low seroprevalence communities 107 and identified individuals for subsequent analysis of the immune response. We found that 108 disease severity, but not age or sex, were correlates of the magnitude of the response. Further, 109 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. (which was not certified by peer review)
The copyright holder for this preprint this version posted August 16, 2020 . . https://doi.org/10.1101 use of these two antigens, nucleocapsid protein, and neutralizing antibody titers revealed 110 discordance in the durability of antibody responses depending on the viral protein. Premkumar et al., 2020) . To begin validation of a serological assay for antibodies to RBD, 120 we tested 43 serum samples from PCR-confirmed COVID-19 patients in the hospital at various 121 stages of disease, 48 convalescent samples, and 23 samples from healthy donors. Serum 122 dilution ELISAs were performed to quantify RBD-reactive antibodies in these samples. 123
Mammalian RBD antigen preparations were selected as targets, as they demonstrated superior 124 signal:noise ratios relative to bacterially-produced protein ( Figure S1A ). Antibody titers were 125 quantified as area under the curve (AUC) and correlated with neutralization of the live USA-126 WA1/2020 strain of SARS-CoV-2, rather than S-protein pseudotyped virus (Giroglou et al., 127 2004) , due to the poor agreement between these functional assays ( Figure S1B) , and because 128 of the modest sensitivity of some pseudovirus neutralization tests relative to those of authentic 129 virus (Schmidt et al., 2020) . The correlation was strong between RBD-reactive IgG and plaque 130 reduction neutralization test (PRNT) titers, which we quantified as the final dilution at which 90% 131 viral neutralization occurred (PRNT 90) ( Figure 1A) . RBD-reactive IgM antibodies also correlated 132 with PRNT90 titers ( Figure S1C ). Because (i) IgM and IgG ratios are not indicative of the timing 133 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020. . https://doi.org/10.1101/2020.08.14.20174490 doi: medRxiv preprint of disease onset (Hou et al., 2020; Long et al., 2020b; Qu et al., 2020) , (ii) IgA is induced by 134 -CoV-2 (Isho et al., 2020; Iyer et al., 2020; Sterlin et al., 2020) , and (iii) both IgG and IgM 135 isotypes correlated with neutralizing titers, we chose to quantify total (all isotypes) antigen-136 specific antibodies for seroprevalence studies. 137
To determine if RBD was capable of distinguishing between SARS-CoV-2 exposed and 138 uninfected individuals and to set preliminary thresholds for positive calls, we initially tested 1:40 139 serum dilutions of samples from 30 PCR+ SARS-CoV-2 infected individuals and 32 samples 140 collected prior to September, 2019, well before the onset of the current pandemic ( Figure S1D) . 141
Using this test data set, we established a preliminary positive cutoff OD450 value of 0.12, equal 142 to 3 standard deviations above the mean values of the negative controls. We next used this 143 preliminary threshold to test an expanded cohort of 320 negative control samples collected prior 144 to 2020. ( Figure 1B ). Reactivity to RBD was clearly distinguishable for the majority of positive 145 samples from negative controls ( Figure 1B) . However, 6.5% of the expanded negative control 146 group displayed RBD reactivity that overlapped with PCR+ individuals (Figure 1B, blue shade) , 147 some of whom may have been early into disease and had not yet generated high levels of 148 antibodies. To quantify the sensitivity of the assay relative to time of diagnosis, we measured 149 antibody levels to RBD and plotted these values against time following SARS-CoV-2 PCR+ 150 confirmation. Whereas the sensitivity was modest within the first two weeks, after 2 weeks, 42 of 151 43 samples showed high ELISA signal ( Figure 1C ). Based on these data, samples were 152 considered seropositive at OD450 numbers above 0.39, a value slightly above the highest OD 153 obtained from the 352 subjects in the negative control group ( Figure 1B) . Sera were considered 154 negative at OD450 values below 0.12. Finally, we created an indeterminate call at OD450 values 155 between 0.12-0.39, as we observed some overlap between negative controls and PCR-156 confirmed samples in this range ( Figure 1B, blue shade) . 157 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020. . https://doi.org/10.1101/2020.08.14.20174490 doi: medRxiv preprint We next applied this assay to community testing and obtained serum samples from 5882 158 self-recruited volunteers from Pima County. Donors included healthcare workers (~26%), first 159 responders (~27%), University of Arizona students (~5%), and other members of the general 160 public (~42%). Currently febrile or otherwise symptomatic patients were excluded. Sera from 73 161 individuals preliminarily scored as seropositive ( Figure 1D ). These samples, along with another 162 171 samples with OD450 values in the indeterminate range were tested for virus neutralization at 163 a serum dilution of 1:20 ( Figure 1E ). Nine samples with RBD OD450 values below 0.39 were 164 observed to neutralize SARS-CoV-2 ( Figure 1E ). More problematically, we found that 13 of the 165 73 samples (17.8%) called positive by RBD-reactivity failed to neutralize authentic SARS-CoV-2 166 ( Figure 1E ). If virus neutralization is considered as a measure of 'true' seropositivity, RBD 167
ELISAs alone provided a relatively modest positive predictive value of 82%. These observations 168 indicated a clear need for a secondary screen to accurately quantify seropositivity in a 169 community with low infection rates. 170
To improve the positive predictive value, we considered the use of an orthogonal 171 antigenically distinct test. We first tested nucleocapsid (N) protein, as several other commercial 172 serological tests quantify antibodies to this antigen (Bryan et al., 2020; Burbelo et al., 2020) . IgG 173 antibody titers to N protein in our collected sample cohort showed a strong correlation to 174 PRNT90 titers (Figure 2A) . A weaker correlation was observed between N-reactive IgM levels 175 and PRNT90 titers ( Figure S2A ). We next assayed reactivity to N antigen using a subset of the 176 pre-2019 validation samples employed for RBD. N protein seroreactivity overlapped 177 substantially between negative and positive controls ( Figure 2B) . Moreover, 5 confirmed 178 COVID-19 samples showed very weak reactivity to N ( Figure 2B) . Because of the relatively 179 poor performance of N protein as an antigen in our hands, we next tested the S2 domain of S 180 protein as another candidate to determine seropositivity. RBD is located on the S1 domain, 181 rendering S2 antigenically distinct (Bosch et al., 2003; Li, 2016; Wrapp et al., 2020) . IgG 182 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020. . https://doi.org/10.1101/2020.08.14.20174490 doi: medRxiv preprint antibody titers to S2 correlated well with PRNT90 titers ( Figure 2C ). Assessment of S2 serum 183 reactivity in the pre-2019 cohort revealed that approximately 3.3% of these samples overlapped 184 with signals in PCR-confirmed COVID-19 samples ( Figure 2D) . We thereafter employed a 185 threshold of OD450>0.35, as our cutoff for S2 positivity, which was 5 standard deviations above 186 the average seroreactivity from the original 32-samples from the negative control cohort. 187
Specificity control testing using 272 negative control sera showed that reactivities of negative 188 samples against RBD and S2 were largely independent of one another, as samples with high 189 signal for one antigen rarely showed similar background for the other ( Figure 2E ). Based on 190 these data, we chose to rely on combined RBD and S2-reactivities as accurate indicators of 191 prior SARS-CoV-2 exposure. 192
With this improved combinatorial RBD and S2 assay to exclude false positives, we re- the assay, we tested 993 samples at random for neutralizing antibodies. Of these, none of the 207 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020. . https://doi.org/10.1101/2020.08.14.20174490 doi: medRxiv preprint samples called as negative possessed neutralizing activity (data not shown). These data 208 demonstrate that inclusion of S2 as a requisite confirmatory screen markedly improves the 209 positive predictive value of SARS-CoV-2 serological assays, especially in areas with low SARS-210
CoV-2 seroprevalence. 211
Several recent reports have suggested more robust immune responses in those with 212 severe disease relative to mild cases (Choe et al.; Ko et al., 2020; Long et al., 2020a; Qu et al., 213 2020) . Moreover, the ratios of S and N antibody specificities correlate with disease outcome 214 (Atyeo et al., 2020). We therefore examined our data for these trends. First, in our PCR-215 confirmed cohort, we plotted IgG titers relative to the time of disease onset, stratified by disease 216 severity. Severe disease (hospital admission) correlated with significantly higher antibody titers 217 against RBD, S2, and N than those with mild disease, who were symptomatic but did not require 218 hospital admission (Figure 3A-C) . Neutralizing titers were also higher in those with severe 219 disease relative to mild cases ( Figure 3D ). Through campus screening efforts, we also 220 identified 6 PCR+ individuals who either never developed symptoms or had only a brief and mild 221 headache or anosmia. Although previous reports suggested that such individuals may 222 infrequently seroconvert or frequently serorevert (Long et al., 2020a; Sekine et al., 2020) , all 223 such individuals in our cohort showed seroreactivity to RBD, S2, and all but one to N (Figures 224 S3A-C), consistent with other recent studies (Choe et al.; Ko et al., 2020) . Given that older 225 adults, as well as those of male sex, exhibit disproportional morbidity and mortality from COVID-226 19, we also sought to test whether humoral immunity in these subjects may be quantitatively 227 reduced (Liu et al., 2020) . Contrary to this expectation, we did not observe any adverse impact 228 of advanced age on humoral immunity (Figure 3E-H) . Similarly, within our cohort, females and 229 males had similar anti-RBD, N, S2, and neutralizing responses (Figure S3D-G) . 230
Individuals with mild disease have been reported to lose SARS-CoV-2-specific 231 antibodies quickly into convalescence (Ibarrondo et al., 2020; Long et al., 2020a; Seow et al., 232 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020. . https://doi.org/10.1101/2020.08.14.20174490 doi: medRxiv preprint community cohort of 5882 individuals. Twenty-nine of the seropositive subjects had reported 234 mild symptoms consistent with COVID-19. These positive samples were thus plotted alongside 235 PCR-confirmed mild disease cases against time post-disease onset to determine if any trends 236 could be observed in declining antibody levels. Across subjects, IgG specific for RBD ( Figure  237 4A) and S2 ( Figure 4B ) appeared to peak near 30 days post-onset and then partially decline 238 before settling to a more stable nadir at later timepoints, as would be expected for all acute viral 239 infections. We considered the possibility that we may have missed subjects that had 240 seroreverted prior to their antibody test, thereby incorrectly raising our estimates of the durability 241 of antibody production. Therefore, to examine the duration of IgG production in more depth, a 242 subset of seropositive individuals with relatively low titers was tested longitudinally up to 122 243 days post-onset. These data again revealed stable RBD and S2 IgG levels at later stages of 244 convalescence (Figures 4A-B) . However, N-reactive IgG levels were quite variable and 245 approached the lower limit of detection in several subjects at later timepoints ( Figure 4C) . A 246 direct comparison in matched subjects of the changes in RBD, S2, and N IgG titers over time 247 confirmed the variability in N responses and rapid decline in a subset of individuals ( Figure 4D) . 248
Most importantly, neutralizing antibody levels remained high with very little decay as a function 249 of time ( Figure 4E) . These data suggest stable neutralizing, RBD, and S2-specific antibodies, 250 but variable and often declining N-reactive titers during convalescence. Together, these data 251 are consistent with the maintenance of functionally important antibody production for at least 252 several months after infection, and caution against the use of α-N antibodies to estimate 253 immunity or seroprevalence. 254 255 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
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Here, we demonstrated that using two antigenically distinct serological tests can greatly 257 remedy specificity problems that are exacerbated in low SARS-CoV-2 seroprevalence 258 communities. RBD and S2 seroreactivity behaved independently for SARS-CoV-2-unexposed 259 individuals, thereby suggesting that the theoretical false positive rate of the overall assay is the 260 product of the two tests. Using neutralization assays to confirm these results, we found our 261 empirically determined false positive rate to be <0.02% (1/5882), consistent with the 262 independence of the RBD and S2 tests. The tight co-incidence between RBD/S2 positivity and 263 the presence of neutralizing antibodies, even in low seroprevalence populations, is especially 264 valuable for identifying individuals who likely have some degree of immunity and could 265 potentially serve as convalescent plasma donors. Surprisingly, nucleocapsid (N), which is used 266 by several commercial serological tests as an antigen, did not perform as well in our assays, 267 with high false positive and negative rates. 268
Though we are uncertain why N protein reactivity proved less discriminatory in our 269 hands relative to published work (Bryan et al., 2020; Steensels et al., 2020) , as one possible 270 explanation, we observed that in several subjects, N-specific antibodies declined more rapidly 271 than those against RBD or S2. This unexpected finding may in part help explain some 272 discrepancies in the literature. In some reports, SARS-CoV-2-specific N antibodies fell to 273 undetectable levels within 2-3 months in up to 40% of those recovering from mild disease (Long 274 et al., 2020a; Pollán et al., 2020) , which would be remarkably transient and very unusual for 275 acute viral infections, even other common coronaviruses (Callow et al., 1990; Reed, 1984) . 276
Although most N titers did not fall fully below our detection limits, we also observed such a 277 decline in some subjects. Yet encouragingly, neutralizing antibodies and those against RBD and 278 S2 reached a stable nadir after the initial expected decline, presumably as short-lived plasma 279 cells were replaced with long-lived antibody secreting cells. These data are consistent with 280 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020. . https://doi.org/10.1101/2020.08.14.20174490 doi: medRxiv preprint expectations for acute viral infections and with the conclusions of other studies currently on 281 preprint servers (Isho et al., 2020; Iyer et al., 2020; Wajnberg et al., 2020) . In this regard, the 282 primary data for S and neutralizing antibody responses seem consistent across several studies 283 The reasons for the differences in antibody responses across antigens are difficult to 291 explain, given the identical inflammatory environment in which these responses arose. One 292 possibility is that the avidities of germline precursors differ for N-and S-protein specificities. For 293 both memory and plasma cells, there appears to be a 'sweet spot' of antigen avidity that 294 promotes optimal responses (Abbott et al., 2018). A second possibility is that N-protein 295 responses are driven by cross-reactive memory, rather than naïve B cells. Memory B cells are 296 substantially more diverse than are plasma cells, thereby encoding a hidden repertoire that is 297 not represented in serum antibodies (Lavinder et al., 2014; Purtha et al., 2011; Smith et al., 298 1997) . Consistent with this possibility, N protein is more conserved across coronaviruses than is 299 RBD (Srinivasan et al., 2020) . Memory responses, especially by isotype-switched B cells, are 300 directed by fundamentally distinct transcriptional programs than those of naïve cells 301 (Bhattacharya et al., 2007; Jash et al., 2016; Wang et al., 2012; Zuccarino-Catania et al., 2014) . 302
For example, the transcription factor ZBTB32 specifically limits the magnitude and duration of 303 memory B cell responses, perhaps to keep chronic infections from overwhelming the system 304 (Jash et al., 2016 (Jash et al., , 2019 . It remains to be established whether such mechanisms may be 305 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020. . https://doi.org/10.1101/2020.08.14.20174490 doi: medRxiv preprint selectively operating on SARS-CoV-2 and other coronavirus N antibody responses due to their 306 antigenic similarity between strains. 307
Taken together, we have reported a highly specific serological assay for SARS-CoV-2 308 exposure that is usable in very low seroprevalence communities, and that returns positive 309 results that are highly co-incident with virus neutralization. Using this assay, we characterize the 310 responses in different subject populations by age, sex and disease severity, we demonstrate 311 that antibody production persists for at least 3 months, and we suggest explanations for some 312 reports that concluded otherwise. 313 314 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020 . . https://doi.org/10.1101 Limitations of current study: The above assay allowed us to examine the influence of age, 314 sex, and disease severity on levels of humoral immunity in our tested populations. Similar to 315 other studies (Qu et al., 2020; , we found that severe disease correlated 316 positively with levels of antibody immunity. While both older adults (>50 and even more >65 317 years of age) and males are more vulnerable to COVID-19 (Klein et al., 2020a , 2020b 318 Palaiodimos et al., 2020) , levels of humoral immunity did not reveal age or sex-related 319 differences that could explain such vulnerability. A caveat here is that our study had a limited 320 longitudinal component and that we could not determine whether there may have been a delay 321 or reduction in humoral immunity at earlier time points of the disease. A second related caveat 322 is that in our community testing cohort we may have missed individuals who were seropositive 323 initially but then seroreverted by the time of the antibody test. Finally, the latest timepoint post-324 disease onset in our study is 122 days. It remains possible that antibody titers will wane 325 substantially at later times. Additional serial sampling of PCR-confirmed mild cases will be 326 required to test these possibilities. CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
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The authors are indebted to the nurses in the intensive care units of Banner University Medical 336
Hughes) for facilitating the collection of samples in critically ill hospitalized patients with COVID- CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
The copyright holder for this preprint this version posted August 16, 2020. . https://doi.org/10.1101/2020.08.14. All other authors participated in collection of samples and patient care for the study. 347 348 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
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Unrelated intellectual property of D.B. and Washington University has been licensed by Sana 350 Biotechnology. J.N.Z. is on the scientific advisory board of and receives research funding from 351 Young Blood Inc. R.S. is a founder and chief scientific officer of Geneticure. R.W. is currently an 352 employee of Vir Biotechnology. 353 354 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
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The copyright holder for this preprint this version posted August 16, 2020. Figure IgM antibody titers were correlated to PRNT90 neutralization titers. R value was determined by 417
Pearson's Correlation. (B) Following inclusion of S2 as secondary screen, seropositivity results are 418
shown for individuals collected 1-7 days, 7-13 days, or >14 days post-PCR confirmation. Samples 419 match those used in Figure 1C . 420 421 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. (which was not certified by peer review)
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The copyright holder for this preprint this version posted August 16, 2020. . https://doi.org/10.1101/2020.08.14.20174490 doi: medRxiv preprint Table S1 . Demographics and essential clinical characteristics of subjects analyzed in this 430 study. Recruitment started in early April, 2020, and included the groups described above and in 431
Methods. Banner-UMC group was restricted to hospitalized subjects; Targeted Community included 432 subjects recruited via fliers and word-of-mouth within faculty, staff and contacts of University of 433
Arizona and Banner-UMC. Self-enrolled community were enrolled via website into the UArizona 434 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. (which was not certified by peer review)
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