A. SUMMARY This dataset shows San Francisco COVID-19 deaths by population characteristics. This data may not be immediately available for recently reported deaths. Data updates as more information becomes available. Because of this, death totals may increase or decrease.

Population characteristics are subgroups, or demographic cross-sections, like age, race, or gender. The City tracks how deaths have been distributed among different subgroups. This information can reveal trends and disparities among groups.

B. HOW THE DATASET IS CREATED As of January 1, 2023, COVID-19 deaths are defined as persons who had COVID-19 listed as a cause of death or a significant condition contributing to their death on their death certificate. This definition is in alignment with the California Department of Public Health and the national https://preparedness.cste.org/wp-content/uploads/2022/12/CSTE-Revised-Classification-of-COVID-19-associated-Deaths.Final_.11.22.22.pdf">Council of State and Territorial Epidemiologists. Death certificates are maintained by the California Department of Public Health.

Data on the population characteristics of COVID-19 deaths are from: *Case reports *Medical records *Electronic lab reports *Death certificates

Data are continually updated to maximize completeness of information and reporting on San Francisco COVID-19 deaths.

To protect resident privacy, we summarize COVID-19 data by only one population characteristic at a time. Data are not shown until cumulative citywide deaths reach five or more.

Data notes on select population characteristic types are listed below.

Race/ethnicity * We include all race/ethnicity categories that are collected for COVID-19 cases.

Gender * The City collects information on gender identity using these guidelines.

C. UPDATE PROCESS Updates automatically at 06:30 and 07:30 AM Pacific Time on Wednesday each week.

Dataset will not update on the business day following any federal holiday.

D. HOW TO USE THIS DATASET Population estimates are only available for age groups and race/ethnicity categories. San Francisco population estimates for race/ethnicity and age groups can be found in a dataset based on the San Francisco Population and Demographic Census dataset.These population estimates are from the 2018-2022 5-year American Community Survey (ACS).

This dataset includes several characteristic types. Filter the “Characteristic Type” column to explore a topic area. Then, the “Characteristic Group” column shows each group or category within that topic area and the number of cumulative deaths.

Cumulative deaths are the running total of all San Francisco COVID-19 deaths in that characteristic group up to the date listed.

To explore data on the total number of deaths, use the COVID-19 Deaths Over Time dataset.

E. CHANGE LOG

A. SUMMARY Case information on COVID-19 Laboratory testing. This data includes a daily count of test results reported, and how many of those were positive, negative, and indeterminate. Reported tests include tests with a positive, negative or indeterminate result. Indeterminate results, which could not conclusively determine whether COVID-19 virus was present, are not included in the calculation of percent positive. Testing for the novel coronavirus is available through commercial, clinical, and hospital laboratories, as well as the SFDPH Public Health Laboratory.

Tests are de-duplicated by an individual and date. This means that if a person gets tested multiple times on different dates in the last 30 days, all of those individual tests will be included in this data as individual tests (on each specimen collection date).

Total positive test results is not equal to the total number of COVID-19 cases in San Francisco.

B. HOW THE DATASET IS CREATED Laboratory test volume and positivity for COVID-19 is based on electronic laboratory test reports. Deduplication, quality assurance measures and other data verification processes maximize accuracy of laboratory test information.

C. UPDATE PROCESS Updates automatically at 05:00 Pacific Time each day. A redundant run is scheduled at 09:00 in case of pipeline failure.

D. HOW TO USE THIS DATASET Due to the high degree of variation in the time needed to complete tests by different labs there is a delay in this reporting. On March 24 the Health Officer ordered all labs in the City to report complete COVID-19 testing information to the local and state health departments. In order to track trends over time, a data user can analyze this data by "result_date" and see how the count of reported results and positivity rate have changed over time.

E. CHANGE LOG

• 4/10/2024 - An issue with our testing data was identified and corrected leading to a small increase in testing records over time.
• 6/21/2023 - A small number of additional COVID-19 testing records were released as part of our ongoing data cleaning efforts.
• 1/31/2023 - renamed column “last_updated_at” to “data_as_of”.
• 1/31/2023 - added columns “cumulative_tests”, “cumulative_positive_tests”, “cumulative_negative_tests”, “cumulative_indeterminate_tests”.
• 4/16/2021 - dataset updated to refresh with a five-day data lag.

Analysis of ‘COVID-19 Cases by Population Characteristics Over Time’ provided by Analyst-2 (analyst-2.ai), based on source dataset retrieved from https://catalog.data.gov/dataset/a3291d85-0076-43c5-a59c-df49480cdc6d on 13 February 2022.

--- Dataset description provided by original source is as follows ---

Note: On January 22, 2022, system updates to improve the timeliness and accuracy of San Francisco COVID-19 cases and deaths data were implemented. You might see some fluctuations in historic data as a result of this change. Due to the changes, starting on January 22, 2022, the number of new cases reported daily will be higher than under the old system as cases that would have taken longer to process will be reported earlier.

A. SUMMARY This dataset shows San Francisco COVID-19 cases by population characteristics and by specimen collection date. Cases are included on the date the positive test was collected.

Population characteristics are subgroups, or demographic cross-sections, like age, race, or gender. The City tracks how cases have been distributed among different subgroups. This information can reveal trends and disparities among groups.

Data is lagged by five days, meaning the most recent specimen collection date included is 5 days prior to today. Tests take time to process and report, so more recent data is less reliable.

B. HOW THE DATASET IS CREATED Data on the population characteristics of COVID-19 cases and deaths are from: * Case interviews * Laboratories * Medical providers

These multiple streams of data are merged, deduplicated, and undergo data verification processes. This data may not be immediately available for recently reported cases because of the time needed to process tests and validate cases. Daily case totals on previous days may increase or decrease. Learn more.

Data are continually updated to maximize completeness of information and reporting on San Francisco residents with COVID-19.

Data notes on each population characteristic type is listed below.

Race/ethnicity * We include all race/ethnicity categories that are collected for COVID-19 cases. * The population estimates for the "Other" or “Multi-racial” groups should be considered with caution. The Census definition is likely not exactly aligned with how the City collects this data. For that reason, we do not recommend calculating population rates for these groups.

Sexual orientation * Sexual orientation data is collected from individuals who are 18 years old or older. These individuals can choose whether to provide this information during case interviews. Learn more about our data collection guidelines. * The City began asking for this information on April 28, 2020.

Gender * The City collects information on gender identity using these guidelines.

Comorbidities * Underlying conditions are reported when a person has one or more underlying health conditions at the time of diagnosis or death.

Transmission type * Information on transmission of COVID-19 is based on case interviews with individuals who have a confirmed positive test. Individuals are asked if they have been in close contact with a known COVID-19 case. If they answer yes, transmission category is recorded as contact with a known case. If they report no contact with a known case, transmission category is recorded as community transmission. If the case is not interviewed or was not asked the question, they are counted as unknown.

Homelessness Persons are identified as homeless based on several data sources: * self-reported living situation
* the location at the time of testing * Department of Public Health homelessness and health databases * Residents in Single-Room Occupancy hotels are not included in these figures.
These methods serve as an estimate of persons experiencing homelessness. They may not meet other homelessness definitions.

Skilled Nursing Facility (SNF) occupancy * A Skilled Nursing

--- Original source retains full ownership of the source dataset ---

Between the weeks of February 3 and March 9, 2020, the DMA (Designated Market Area) in the United States with the highest increased in viewership of local news on major broadcast networks among adults aged 25 to 54 years old was San Francisco, with a 38.1 percent audience increase in March 2020 compared to the same week in February that year. The coronavirus spread rapidly across the United States in early to mid-March, sparking an increase the number of individuals self-isolating at home, quarantining, and turning to their preferred news sources to keep up to date with the outbreak. The West Coast of the U.S. was hit earlier than other parts of the country, explaining the high viewership increase in the key demographic in San Francisco, LA, and Seattle.

Replication material for Jackelyn Hwang & Bina Patel Shrimali (2022) Shared and Crowded Housing in the Bay Area: Where Gentrification and the Housing Crisis Meet COVID-19, Housing Policy Debate, DOI: 10.1080/10511482.2022.2099934

Paper Abstract: Amid the growing affordable housing crisis and widespread gentrification over the last decade, people have been moving less than before and increasingly live in shared and often crowded households across the U.S. Crowded housing has various negative health implications, including stress, sleep disorders, and infectious diseases. Difference-in- difference analysis of a unique, large-scale longitudinal consumer credit database of over 450,000 San Francisco Bay Area residents from 2002 to 2020 shows gentrification affects the probability of residents shifting to crowded households across the socioeconomic spectrum but in different ways than expected. Gentrification is negatively associated with low- socioeconomic status (SES) residents’ probability of entering crowded households, and this is largely explained by increased shifts to crowded households in neighborhoods outside of major cities showing early signs of gentrification. Conversely, gentrification is associated with increases in the probability that middle-SES residents enter crowded households, primarily in Silicon Valley. Lastly, crowding is positively associated with COVID-19 case rates, beyond density and socioeconomic and racial composition in neighborhoods, although the role of gentrification remains unclear. Housing policies that mitigate crowding can serve as early interventions in displacement prevention and reducing health inequities.

We examined the effect of social distancing on changes in visits to urban hotspot points of interest. In a pandemic situation, urban hotspots could be potential superspreader areas as visits to urban hotspots can increase the risk of contact and transmission of a disease among a population. We mapped origin-destination networks from census block groups to points of interest (POIs), such as restaurants, museums, and schools, in sixteen cities in the United States. We adopted a coarse-grain approach to examine patterns of visits to POIs among hotspots and non-hotspots from January to May 2020. Also, we conducted chi-square tests to identify POIs with significant flux-in changes during the analysis period. The results showed disparate patterns across cities in terms of reduction in hotspot POI visits. Sixteen cities are divided into two categories. In one category, which includes the cities of, San Francisco, Seattle, and Chicago, we observe a considerable decrease in hotspot POI visits, while in another category, including the cites of, Austin, Houston, and San Diego, the visits to hotspots did not greatly decrease. While all the cities exhibited overall decreasing visits to POIs, one category maintained the proportion of visits to hotspot POIs. The proportion of visits to some POIs (e.g., Restaurants) remained stable during the social distancing period, while some POIs had an increased proportion of visits (e.g., Grocery Stores). We also identified POIs with significant flux-in changes, showing that related businesses were greatly affected by social distancing.

Characteristics of mass COVID-19 “test and respond” event attendees from March-April 2021in two predominantly Latino, low-income communities in Northern California.

Multisystem inflammatory syndrome in children (MIS-C) is a severe, post-infectious sequela of SARS-CoV-2 infection, yet the pathophysiological mechanism connecting the infection to the broad inflammatory syndrome remains unknown. Here we leveraged a large set of MIS-C patient samples (n=199) to identify a distinct set of host proteins that are differentially targeted by patient autoantibodies relative to matched controls. We identified an autoreactive epitope within SNX8, a protein expressed primarily in immune cells that regulates an antiviral pathway associated with MIS-C pathogenesis. In parallel, we also probed the SARS-CoV-2 proteome-wide MIS-C patient antibody response and found it to be differentially reactive to a distinct domain of the SARS-CoV-2 nucleocapsid (N) protein relative to controls. This viral N region and the mapped SNX8 epitope bear remarkable biochemical similarity. Furthermore, we find that many children with anti-SNX8 autoantibodies also have T cells cross-reactive to both SNX8 and this distinct region of the SARS-CoV-2 N protein. Together, these findings suggest that MIS-C patients develop a characteristic immune response against the SARS-CoV-2 N protein that is associated with cross-reactivity to the self-protein SNX8, demonstrating a mechanistic link from the infection to the inflammatory syndrome with implications for better understanding a range of post-infectious autoinflammatory diseases. Methods Patients Patients were recruited through the prospectively enrolling multicenter Overcoming COVID-19 and Taking on COVID-19 Together study in the United States. The study was approved by the central Boston Children’s Hospital Institutional Review Board (IRB) and reviewed by IRBs of participating sites with CDC IRB reliance. A total of 292 patients were enrolled into 1 of the following independent cohorts between June 1, 2020 and September 9, 2021: 223 patients hospitalized with MIS-C (199 in the primary discovery cohort, 24 in a separate subsequent validation cohort), 29 patients hospitalized for COVID-19 in either an intensive care or step-down unit (referred to as severe acute COVID-19 in this study), and 45 outpatients (referred to as “at-risk controls” in this study) post-SARS-CoV-2 infections associated with mild or no symptoms. The demographic and clinical data are summarized in Table I, Extended Data Table 1, and Extended Data Table 2. The 2020 US Centers for Disease Control and Prevention case definition was used to define MIS-C(1). All patients with MIS-C had positive SARS-CoV-2 serology results and/or positive SARS-CoV-2 test results by reverse transcriptase quantitative PCR. All patients with severe COVID-19 or outpatient SARS-CoV-2 infections had a positive antigen test or nucleic acid amplification test for SARS-CoV-2. For outpatients, samples were collected from 36 to 190 days after the positive test (median, 70 days after the positive test; interquartile range, 56-81 days). For use as controls in the SARS-CoV-2 specific PhIP-Seq, plasma from 48 healthy, pre-COVID-19 controls was obtained as deidentified samples from the New York Blood Center. These samples were part of retention tubes collected at the time of blood donations from volunteer donors who provided informed consent for their samples to be used for research. Human proteome PhIP-Seq Human Proteome PhIP-Seq was performed following our previously published vacuum-based PhIP-Seq protocol (2) (https://www.protocols.io/view/scaled-high-throughput-vacuum-phip-protocol-ewov1459kvr2/v1). Our human peptidome library consists of a custom-designed phage library of 731,724 unique T7 bacteriophage each presenting a different 49 amino-acid peptide on its surface. Collectively these peptides tile the entire human proteome including all known isoforms (as of 2016) with 25 amino-acid overlaps. 1 milliliter of phage library was incubated with 1 microliter of human serum overnight at 4C and immunoprecipitated with 25 microliters of 1:1 mixed protein A and protein G magnetic beads (Thermo Fisher, Waltham, MA, #10008D and #10009D). These beads were then washed, and the remaining phage-antibody complexes were eluted in 1 milliliter of E.Coli (BLT5403, EMD Millipore, Burlington, MA) at 0.5-0.7 OD and amplified by growing in 37C incubator. This new phage library was then re-incubated with the same individual’s serum and the previously described protocol was repeated. DNA was then extracted from the final phage library, barcoded, and PCR-amplified, and Illumina adaptors were added. Next-generation sequencing was then performed using an Illumina sequencer (Illumina, San Diego, CA) to a read depth of approximately 1 million per sample. Human proteome PhIP-Seq analysis All human peptidome analysis (except when specifically stated otherwise) was performed at the gene level, in which all reads for all peptides mapping to the same gene were summed, and 0.5 reads were added to each gene to allow the inclusion of genes with zero reads in mathematical analyses. Within each individual sample, reads were normalized by converting to the percentage of total reads. To normalize each sample against background non-specific binding, a fold-change (FC) over mock-IP was calculated by dividing the sample read percentage for each gene by the mean read percentage of the same gene for the AG bead-only controls. This FC signal was then used for side-by-side comparison between samples and cohorts. FC values were also used to calculate z-scores for each MIS-C patient relative to controls and for each control sample by using all remaining controls. These z-scores were used for the logistic regression feature weighting. In instances of peptide-level analysis, raw reads were normalized by calculating the number of reads per 100,000 reads. SARS-CoV-2 proteome PhIP-Seq SARS-CoV-2 Proteome PhIP-Seq was performed as previously described(3). Briefly, 38 amino acid fragments tiling all open reading frames from SARS-CoV-2, SARS-CoV-1, and 7 other CoVs were expressed on T7 bacteriophage with 19 amino acid overlaps. 1 milliliter of phage library was incubated with 1 microliter of human serum overnight at 4C and immunoprecipitated with 25 microliters of 1:1 mixed protein A and protein G magnetic beads (Thermo Fisher, Waltham, MA, #10008D and #10009D). Beads were washed 5 times on a magnetic plate using a P1000 multichannel pipette. The remaining phage-antibody complexes were eluted in 1 milliliter of E.Coli (BLT5403, EMD Millipore, Burlington, MA) at 0.5-0.7 OD and amplified by growing in a 37°C incubator. This new phage library was then re-incubated with the same individual’s serum and the previously described protocol was repeated for a total of 3 rounds of immunoprecipitations. DNA was then extracted from the final phage library, barcoded, and PCR-amplified, and Illumina adaptors were added. Next-generation sequencing was then performed using an Illumina sequencer (Illumina, San Diego, CA) to a read depth of approximately 1 million per sample. Coronavirus proteome PhIP-Seq analysis To account for differing read depths between samples, the total number of reads for each peptide fragment was converted to the number of reads per 100k (RPK). To calculate normalized enrichment relative to pre-COVID controls (FC > Pre-COVID), the RPK for each peptide fragment within each sample was divided by the mean RPK of each peptide fragment among all pre-COVID controls. These FC > Pre-COVID values were used for all subsequent analyses as described in the text and figures.

HAN Archive - 00432 (2021). https://emergency.cdc.gov/han/2020/han00432.asp. S. E. Vazquez, S. A. Mann, A. Bodansky, A. F. Kung, Z. Quandt, E. M. N. Ferré, N. Landegren, D. Eriksson, P. Bastard, S.-Y. Zhang, J. Liu, A. Mitchell, I. Proekt, D. Yu, C. Mandel-Brehm, C.-Y. Wang, B. Miao, G. Sowa, K. Zorn, A. Y. Chan, V. M. Tagi, C. Shimizu, A. Tremoulet, K. Lynch, M. R. Wilson, O. Kämpe, K. Dobbs, O. M. Delmonte, R. Bacchetta, L. D. Notarangelo, J. C. Burns, J.-L. Casanova, M. S. Lionakis, T. R. Torgerson, M. S. Anderson, J. L. DeRisi, Autoantibody discovery across monogenic, acquired, and COVID-19-associated autoimmunity with scalable PhIP-seq. Elife 11 (2022). C. R. Zamecnik, J. V. Rajan, K. A. Yamauchi, S. A. Mann, R. P. Loudermilk, G. M. Sowa, K. C. Zorn, B. D. Alvarenga, C. Gaebler, M. Caskey, M. Stone, P. J. Norris, W. Gu, C. Y. Chiu, D. Ng, J. R. Byrnes, X. X. Zhou, J. A. Wells, D. F. Robbiani, M. C. Nussenzweig, J. L. DeRisi, M. R. Wilson, ReScan, a Multiplex Diagnostic Pipeline, Pans Human Sera for SARS-CoV-2 Antigens. Cell Rep Med 1, 100123 (2020).