COVID-19 Susceptibility By Race, Blood Type

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COVID-19 Susceptibility By Race, Blood Type Jun 20, 2020 2:20:05 GMT

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Post by Admin on Jun 20, 2020 2:20:05 GMT

The scientists opted for a GWAS methodology, in which common variants in a number of individuals, both without the disease (control groups) and with the disease (COVID-19 patients) are explored using arrays. Through this approach, genetic variants that are associated with the disease will be found at a higher frequency than in the control groups.

When COVID-19 reached a peak in Italy and Spain earlier in 2020, the research team recruited 835 patients and 1255 control participants from Italy and 775 patients and 950 control participants from Spain for the study.

In the patient cohort, a confirmed SARS-CoV-2 viral RNA polymerase-chain-reaction (PCR) test collected from nasopharyngeal swabs or alternative biologic fluids was required. Respiratory failure was defined in a simplistic manner as the use of oxygen supplementation or mechanical ventilation, and severity was graded according to the maximum respiratory support received at any one point during hospitalization. The COVID-19 participants were recruited from various hospitals across Spain and Italy.

The 2381 control participants were recruited from either blood donor banks or previous genotyping studies that had adopted the same array method.

Two genetic variants associated with COVID-19 respiratory failure

From the data, the scientists discovered two independent gene variants that appear to be associated with COVID-19 induced respiratory failure: rs11385942 at locus 3p21.31 and rs657152 at locus 9q34.2 – these were significant at the genome wide level (P<5×10−8).

Looking closer at chromosome 3p21.31, the peak association signal encompassed a cluster of six genes: SLC6A20, LZTFL1, CCR9, FYCO1, CXCR6, and XCR1. Whilst a causative gene cannot be drawn reliably from the current data, the authors highlighted SLC6A20 in the paper, a gene which encodes a transporter that interacts with the angiotensin-converting enzyme 2, the SARS-CoV-2 cell-surface receptor. The researchers also emphasize that these results align with those of the COVID-19 Host Genetics Consortium, whose preliminary data also suggest associations with the same locus at chromosome 3p21.31.

In the paper, the authors note: "It seems reasonable to conclude that the chromosome 3p21.31 locus is involved in Covid-19 [COVID-19] susceptibility per se, with a possible enrichment in patients with severe disease."

It's important to note that GWAS studies do not demonstrate a causal role for a specific genetic variant – rather, it points to associations. Commenting on the study, Dr Sakthivel Vaiyapuri, Associate Professor in Cardiovascular & Venom Pharmacology, University of Reading, said, "This is a high quality study on GWAS in relation to COVID-19. While a GWAS study is able to identify specific genes associated with COVID-19 in the wider population, it doesn’t link with the mechanistic details behind the disease progression or protection."

The potential role of blood type in COVID-19 susceptibility

A number of studies have pointed to the potential role that an individual's blood group may have on their susceptibility to COVID-19. To date, this has not been confirmed without reasonable doubt. However, data from this work suggests that further exploration of this potential factor is warranted.

The team found that the association signal at locus 9q34.2 coincided with the ABO blood group locus. A blood-group-specific analysis also demonstrated a higher risk in blood group A compared to other blood groups (P=1.48×10−4) in addition to a protective effect in blood group O when compared to other blood groups (P=1.06×10−5).

Sakthivel says: "This study doesn’t draw any strong conclusions about how different blood types may make someone susceptible or protective for COVID-19. They are only suggesting that they have identified genes in ABO blood group region and suggest that these might relate to someone’s susceptibility or protective nature based on their blood types."

Working under pressure during a global pandemic

The authors note that this research study performed at a critical time was a major undertaking, and as such, it is not without flaws.

For example, to enable fast and extensive recruitment of study participants, a bare minimum of clinical metadata was requested, the authors state in the paper. They add "For this reason, extensive genotype–phenotype elaboration of current findings could not be conducted, and adjustments for all potential sources of bias (e.g., underlying cardiovascular and metabolic factors relevant to Covid-19) could not be performed. Furthermore, we have limited information about the SARS-CoV-2 infection status in the control participants."

"People with A blood group should not panic about these results, and at the same time O blood group people should not be relaxed because they may not get this disease. Everyone should follow the guidelines provided by the health authorities and be extremely cautious to protect themselves and others around them." - Dr Sakthivel Vaiyapuri, Associate Professor in Cardiovascular & Venom Pharmacology, University of Reading.

References:
1. Ellinghaus et al. (2020). Genomewide Association Study of Severe Covid-19 with Respiratory Failure. The New England Journal of Medicine. DOI: 10.1056/NEJMoa2020283.

2. COVID-19 Host Genetics Initiative. (2020). The COVID-19 Host Genetics Initiative, a global initiative to elucidate the role of host genetic factors in susceptibility and severity of the SARS-CoV-2 virus pandemic. European Journal of Human Genetics. DOI: doi.org/10.1038/s41431-020-0636-6.

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COVID-19 Susceptibility By Race, Blood Type Jun 20, 2020 7:08:01 GMT

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Post by Admin on Jun 20, 2020 7:08:01 GMT

The COVID-19 Host Genetics Initiative, a global initiative to elucidate the role of host genetic factors in susceptibility and severity of the SARS-CoV-2 virus pandemic
The COVID-19 Host Genetics Initiative
European Journal of Human Genetics volume 28, 715–718(2020)

Introduction
The COVID-19 pandemic is a global crisis creating severe disruptions across the economy and health system. Insights into how to better understand and treat COVID-19 are desperately needed.

Early studies have focused on the clinical characteristics [1,2,3], epidemiology [1, 4, 5], and genomic characterization [6,7,8] of SARS-CoV-2 infection. These studies have also highlighted the value and importance of transparent data sharing across countries, which have enabled the live tracking of the disease widespread worldwide [9, 10]. The role of host genetics in impacting susceptibility and severity of COVID-19 has been less studied. Previous work has supported the role of human leukocyte antigen (HLA) in susceptibility [11] and severity [12] for several viral infections. Moreover, a synonymous variant in the IFN-induced transmembrane protein-3 gene has been reported to cause severe clinical outcomes in patients infected with H7N9 and H1N1 influenza viruses [13, 14], although results did not reach established P value thresholds (P < 5 × 10−8). In addition, candidate variant studies have suggested host factors that are critical for severe disease in other coronavirus infections, such as infections due to the related SARS-CoV [15].

Given the importance and urgency of exploring the role of the host genome in conjunction with COVID-19 clinical and genomic variability, and the recognition that this can only be achieved with the combined effort of the scientific community, we launched the ‘COVID-19 Host Genetics Initiative’. This initiative brings together the human genetics community to generate, share, and analyze data to learn the genetic determinants of COVID-19 susceptibility, severity, and outcomes. Such discoveries could help to identify individuals at unusually high or low risk, generate hypotheses for drug repurposing, and contribute to global knowledge of the biology of SARS-CoV-2 infection and disease. The initiative has three main goals:

1.
Provide an environment to foster the sharing of resources to facilitate COVID-19 host genetics research (e.g., protocols, questionnaires).

2.
Organize analytical activities across studies to identify genetic determinants of COVID-19 susceptibility and severity.

3.
Provide a platform to share the results from such activities, as well as the individual-level data where possible, to benefit the broader scientific community.

Approach
The COVID-19 host genetics initiative is a bottom-up initiative with a flexible, decentralized structure that is based on the following collaborative principles:

1.
Collaborate in an environment of honesty, fairness, and trust

2.
Promote early-career researchers

3.
Respect other groups’ data

4.
Operate transparently with a goal of no surprises

5.
Seek permission from each group to use results prior to public release

6.
Do not share another group’s results with other parties without permission

7.
The initiative should not inhibit any work being done within any individual studies (or between pairs of studies).

Studies that are interested in joining the initiative can register via the websiteFootnote1. We can categorize the participating studies in two main groups. Retrospective collections are typically biobanks with existing significant genetic data and active connections to health systems. In these studies, there is the opportunity to opportunistically and rapidly develop a genetic study on susceptibility and severity. For example, in Finland with the national network of biobanks covering each hospital district, it is possible to acquire almost ‘real-time’ updates on COVID-19 status of individuals that are already part of the FinnGen studyFootnote2. This group of studies is already connected and loosely structured via other initiatives such as the Global Biobank Meta-analysis InitiativeFootnote3.

The second group of studies includes prospective collection that have recently started to directly consent incoming COVID-19 patients. More than just the critical jump in scale for studying progression, severity, and outcomes, these studies bring important additional opportunities not only for deeper DNA studies, but potentially informative viral and antibody profiling and epitope mapping experiments which can be implemented in many sites with relatively small blood/plasma requirements.

Data sharing
We expect that a sizable fraction of the studies will be able to share individual-level data. Genetics and clinical data are submitted to the European Genome-phenome Archive (EGA) under controlled access, and this is coordinated with viral sequence deposition efforts and coordination of other biomolecular data with EU, EOSC, ELIXIR, and other institutions across the globe. Alternatively, studies are able to share summary statistics, which will be directly made available on the website and via the GWAS catalog [16].

The majority of the planning, discussion, and exchange of information between the participants study, analysts, and clinicians is done on a dedicated Slack workspace with the support of the International Common Disease Alliance (ICDA)Footnote4.

Phenotype and analysis
The initiative aims to support widespread sharing of data and knowledge across participants groups. Groups can connect and initiate collaborations focused on specific phenotypes. Few analyses that can benefit from maximal sample size are centralized. The primary analysis focuses on COVID-19 disease severity. There are challenges in defining COVID-19 severity across multiple studies and healthcare systems. We used a pragmatic approach which considers the use of invasive and noninvasive ventilation as an index of severity. The advantages of this approach is the possibility to easily retrieve this information from electronic health records and the widespread use of these procedures across healthcares. Studies that have collected detailed clinical information can perform secondary analyses using continuous markers of disease severity such as maximum respiratory rate during hospitalization or prior to invasive respiratory support.

Bioinformatic and statistical analysis will consider data generated from GWAS array, exome and genome sequencing, leveraging the impact of both common and rare variants. Key analysis will take into account differences between sexes, ancestries, and date of sample collection. The latter aspect is important to consider given the rapid changes in population screening procedures and hospital capacity with consequent impact on the severity of patients included in different studies.

Given the importance of the HLA genes system for the etiology of infectious diseases and autoimmune disorders, we will impute classical HLA alleles and the corresponding amino acid sequences. COVID indiscriminately affects populations from all around the world, and HLA variation is specific to different populations. Hence, we propose using a multiethnic HLA reference panel constructed using deep-coverage whole-genome sequencing data from 21,546 individuals of five different populations: European, African, Latino, Asian, and South Asian. This reference panel will capture much of the HLA variation around the world. This will allow to test each HLA allele and also each of the amino acid site position within HLA genes to assess if they explain COVID risk.

Participant studies
At time of writing 105 studies have joined the initiative, and participation is still expanding. The majority of studies are conducted in Europe (55%) and the US (28%), amongst which the United Kingdom (10%) and Italy (9%) are the largest. However there are also participants from Asia (Republic of Korea and Malaysia), Australia, the Middle-East (Kuwait, Pakistan, and Qatar), and Africa (Nigeria); Fig. 1, an updated list is available on the websiteFootnote5. Most studies (71%) have initiated a new prospective collection, 27% have done that on top of existing retrospective collections. Array-based genotyping is the most common approach, considered by 69% of the participant studies, while exome and genome sequencing are less common, (29%). Antibody and immune profiling are the two most common additional assays that are reported by the contributing studies.

Fig. 1: Map of the studies registered to the initiative by 13th of April 2020.

Conclusion
We initiated a global effort to study the relationship between host genome and SARS-CoV-2 infection. Our approach is inclusive, decentralized, and transparent. While providing novel scientific insights remains a priority of the initiative, we equally value the creation of an infrastructure that facilitates communication between studies with similar scientific goals. We expect the COVID-19 host genetics initiative to substantially contribute to the understanding of the variability of COVID-19 susceptibility, severity, and outcomes in the population within the next few months.

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COVID-19 Susceptibility By Race, Blood Type Jun 20, 2020 20:57:13 GMT

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Post by Admin on Jun 20, 2020 20:57:13 GMT

South Asian people are the most likely to die from coronavirus after being admitted to hospital in Great Britain, major analysis shows.

It is the only ethnic group to have a raised risk of death in hospital and is partly due to high levels of diabetes.

The study is hugely significant as it assessed data from four-in-10 of all hospital patients with Covid-19.

The researchers said policies such as protecting people at work and who gets a vaccine may now need to change.

Twenty-seven institutions across the UK, including universities and public health bodies, as well as 260 hospitals, were involved in the study.

The findings have been made public online ahead of being formally published in a medical journal.

However, the results were passed onto the UK government's scientific advisory group - Sage - more than a month ago.

The study tells us only what happens once somebody is admitted to hospital, not whether they were more likely to catch the virus.

It looked at nearly 35,000 Covid-19 patients in 260 hospitals across England, Scotland and Wales up until the middle of May.

"South Asians are definitely more likely to die from Covid-19 in hospital, but we don't see a strong effect in the black group," Prof Ewen Harrison, from the University of Edinburgh, told the BBC.

People from South Asian backgrounds were 20% more likely to die than white people. Other minority ethnic groups did not have a higher death rate.

The study, the largest of its type in the world, shows:

290 die out of every 1,000 white people needing hospital treatment for Covid-19
350 die out of every 1,000 South Asian people needing hospital treatment for Covid-19
The study also reveals profound differences in who is needing hospital care based on ethnicity.

"The South Asian population in hospital looks completely different to the white population," Prof Harrison said.

He added: "They're 12 years younger on average, that's a massive difference, and they tend not to have dementia, obesity or lung disease, but very high levels of diabetes."

Around 40% of South Asian patients had either type 1 or type 2 diabetes compared with 25% of white groups.

Diabetes has a dual effect of increasing the risk of infection and damaging the body's organs, which may affect the ability to survive a coronavirus infection.

Why are more people from BAME backgrounds dying from coronavirus?
This is thought to be a major factor in increasing the death rate in people of South Asian ethnicity, but the full picture has not yet been uncovered.

Other explanations could include poverty or subtle genetic differences that increase the risk of serious infection, the researchers say.

The report says ethnicity may now need to be considered alongside age and other health issues when deciding who gets a vaccine if one becomes available. The same issue crops up in deciding who should be shielding and whether some people need extra protection in the workplace.

"It does have far-reaching implications that are difficult to grapple with," Prof Harrison told the BBC.

"Should there be a different policy for a frontline South Asian nurse to a white nurse - that's what's really tricky."

The study showed all ethnic minorities were more likely to need intensive care than people from white backgrounds.

This may be partly due to the disease becoming more severe. However, another factor is white people were older and sicker so ventilation in intensive care may not be an option.

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COVID-19 Susceptibility By Race, Blood Type Jun 21, 2020 0:05:53 GMT

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Post by Admin on Jun 21, 2020 0:05:53 GMT

Ethnicity and Outcomes from COVID-19: The ISARIC CCP-UK Prospective Observational Cohort Study of Hospitalised Patients
41 Pages
Posted: 17 Jun 2020
Ewen M. Harrison
University of Edinburgh - Centre for Medical Informatics

Abstract
Background: Reports of ethnic inequalities in COVID-19 outcomes are conflicting and the reasons for any differences in outcomes are unclear. We investigated ethnic inequalities in critical care admission patterns, the need for invasive mechanical ventilation (IMV), and in-hospital mortality, among hospitalised patients with COVID-19.

Methods: We undertook a prospective cohort study in which dedicated research staff recruited hospitalised patients with suspected/confirmed COVID-19 from 260 hospitals across England, Scotland and Wales, collecting data directly and from records between 6th February and 8th May 2020 with follow-up until 22nd May 2020. Analysis used hierarchical regression models accounting for confounding, competing risks, and clustering of patients in hospitals. Potential mediators for death were explored with a three-way decomposition mediation analysis.

Findings: Of 34,986 patients enrolled, 30,693 (88%) had ethnicity recorded: South Asian (1,388, 5%), East Asian (266, 1%), Black (1,094, 4%), Other Ethnic Minority (2,398, 8%) (collectively Ethnic Minorities), and White groups (25,547, 83%). Ethnic Minorities were younger and more likely to have diabetes (type 1/type 2) but had fewer other comorbidities such as chronic heart disease or dementia than the White group. No difference was seen between ethnic groups in the time from symptom onset to hospital admission, nor in illness severity at admission. Critical care admission was more common in South Asian (odds ratio 1.28, 95% confidence interval 1.09 to 1.52), Black (1.36, 1.14 to 1.62), and Other Ethnic Minority (1.29, 1.13 to 1.47) groups compared to the White group, after adjusting for age, sex and location. This was broadly unchanged after adjustment for deprivation and comorbidities. Patterns were similar for IMV. Higher adjusted mortality was seen in the South Asian (hazard ratio 1.19, 1.05 to 1.36), but not East Asian (1.00, 0.74 to 1.35), Black (1.05, 0.91 to 1.26) or Other Ethnic Minority (0.99, 0.89 to 1.10) groups, compared to the White group. 18% (95% CI, 9% to 56%) of the excess mortality in South Asians was mediated by pre-existing diabetes.

Interpretation: Ethnic Minorities in hospital with COVID-19 were more likely to be admitted to critical care and receive IMV than Whites, despite similar disease severity on admission, similar duration of symptoms, and being younger with fewer comorbidities. South Asians are at greater risk of dying, due at least in part to a higher prevalence of pre-existing diabetes.

Trial Registration: The study was registered at www.isrctn.com/ISRCTN66726260.

Funding Statement: This work is supported by grants from: the National Institute for Health Research [award CO-CIN-01], the Medical Research Council [grant MC_PC_19059] and by the National Institute for Health Research Health Protection Research Unit (NIHR HPRU) in Emerging and Zoonotic Infections at University of Liverpool in partnership with Public Health England (PHE), in collaboration with Liverpool School of Tropical Medicine and the University of Oxford [NIHR award 200907], Wellcome Trust and Department for International Development [215091/Z/18/Z], and the Bill and Melinda Gates Foundation [OPP1209135], and Liverpool Experimental Cancer Medicine Centre for providing infrastructure support for this research (Grant Reference: C18616/A25153). JSN-V-T is seconded to the Department of Health and Social Care, England (DHSC).

Declaration of Interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf and declare: AB Docherty reports grants from Department of Health and Social Care, during the conduct of the study; grants from Wellcome Trust, outside the submitted work; CA Green reports grants from DHSC National Institute of Health Research UK, during the conduct of the study; PW Horby reports grants from Wellcome Trust / Department for International Development / Bill and Melinda Gates Foundation, grants from NIHR , during the conduct of the study; JS Nguyen-Van-Tam reports grants from Department of Health and Social Care, England, during the conduct of the study; and is seconded to the Department of Health and Social Care, England (DHSC); PJM Openshaw reports personal fees from consultancies and from European Respiratory Society; grants from MRC, MRC Global Challenge Research Fund, EU, NIHR Biomedical Research Centre, MRC/GSK, Wellcome Trust, NIHR (HPRU in Respiratory Infection), and NIHR Senior Investigator outside the submitted work. His role as President of the British Society for Immunology was unpaid but travel and accommodation at some meetings was provided by the Society. JK Baillie reports grants from Medical Research Council UK; MG Semple reports grants from DHSC National Institute of Health Research UK, grants from Medical Research Council UK, grants from Health Protection Research Unit in Emerging & Zoonotic Infections, University of Liverpool, during the conduct of the study; other from Integrum Scientific LLC, Greensboro, NC, USA, outside the submitted work. EM Harrison, H Ardwick, J Dunning, R Pius, L Norman, KA Holden, JM Read, G Carson, L Merson, J Lee, D Plotkin, L Sigfrid, S Halpin, C Jackson, and C Gamble, all declare: no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; and no other relationships or activities that could appear to have influenced the submitted work.

Ethics Approval Statement: Ethical approval was given by the South Central – Oxford C Research Ethics Committee in England (Ref: 13/SC/0149), and by the Scotland A Research Ethics Committee (Ref: 20/SS/0028).

papers.ssrn.com/sol3/papers.cfm?abstract_id=3618215

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COVID-19 Susceptibility By Race, Blood Type Jun 21, 2020 5:53:15 GMT

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Post by Admin on Jun 21, 2020 5:53:15 GMT

Introduction
The novel severe acute respiratory syndrome coronavirus SARS-CoV-2 has caused a pandemic, with 5.8
million reported as infected and over 360,000 reported to have died across the world.1 Studies from China,
Italy and the UK have consistently reported that advanced age, comorbidity, and male sex are associated
with increased mortality.2–4

COVID-19 deaths appear to disproportionately affect people from South Asian and Black ethnic backgrounds,
but it is unclear if the incidence of infection is greater, the prognosis is worse once infected, or both.5–8
Patients from Asian, Black and other Minority Ethnic backgrounds are reported to have accounted for 34% of
COVID-19 admissions to intensive care (ICU) in England, Wales and Northern Ireland, compared with only
12% for viral pneumonia (2017-2019), and a higher than expected proportion have required organ support
and have died.9 Of NHS staff known to have died with COVID-19, 63 (63%) were from an ethnic minority
background.10 In the USA, the mortality rate for Black African Americans is quoted as 2.4 times higher than
the rate for White Americans.11 It is unclear the extent to which differences in socioeconomic circumstances
or pre-existing conditions may account for some or all such differences in risk.12

Ethnicity and socioeconomic position were associated with poor health outcomes during previous
pandemics.13 The effect of ethnicity on outcome for pandemic influenza 2009 was explained in part by
socioeconomic status.14 Ethnic minority groups may be at greater risk of infection, severe disease, and poor
outcomes for multiple reasons. These include socioeconomic conditions that increase risks of transmission
and vulnerability, such as overcrowded housing,15 employment in essential frontline occupations,16 poverty,
healthcare seeking behaviours,17 and reliance on public transport.18 People living in more deprived areas in
the UK have experienced COVID-19 mortality rates more than double those living in less deprived areas.19
Theoretical biological mechanisms for differences by ethnicity include susceptibility due to common
comorbid illnesses such as diabetes and cardiovascular disease,20,21 or genetic factors associated with
susceptibility or disease progression. Susceptibility to infectious disease,22 including influenza,23 and viral
pneumonia,24 is strongly heritable, and early reports have suggested this is also true for COVID-19.25
Genetic variations in factors affecting viral entry26 or the host immune response27 may lead to differential
susceptibility according to genetic heritage. Behavioural differences by ethnicity may also account for
variability in healthcare outcomes.

In the wake of the A/H1N1pdm2009 influenza pandemic, the Clinical Characterisation Protocol UK (CCP-UK)
for Severe Emerging Infection was developed by the International Severe Acute Respiratory and emerging
Infections Consortium (ISARIC) and the World Health Organisation. As the pandemic potential of SARS-CoV-2 became apparent, the CCP was reactivated in the UK on 17th January 2020, in time to recruit the early
patients admitted to hospitals with COVID-19.4

Our aim was to assess how prognosis in relation to critical care admission, use of invasive mechanical
ventilation (IMV), and in-hospital mortality differs by ethnicity in the CCP-UK cohort of hospitalised patients
with COVID-19.

Results
Between 6th February and 8th May 2020, we enrolled 34,986 patients admitted to 260 hospitals with COVID-19 in England, Scotland, and Wales. This is estimated to represent 40.4% of all people admitted over that time period to hospital with COVID-19 in England, Scotland, and Wales.

Presentation at hospital
30,693 (88%) had ethnicity data recorded and were considered in the following groups: South Asians (n=1,388, 5%), East Asians (266, 1%), Black (1,094, 4%), Other Ethnic Minorities (2,398, 8%), and Whites (25,547, 83%) (Figure 1).

Ethnic Minorities were younger (White mean 72 years (y) [standard deviation 16], South Asian 60 y [17], East Asian 60 y [17], Black 61 y [17], Other Ethnic Minority 62 y [18]) and more likely to have diabetes (South Asian n=441 [39.4%], East Asian 71 [29.6%], Black 384 [38.8%], Other Ethnic Minority 636 [30.7%]) compared to the White group (5838 [25.1%]) (Table 1).

In unadjusted analysis, Whites were more likely than Ethnic Minorities to have other comorbidities such as chronic cardiac disease (White n=8228 [32.2%], South Asian 266 [19.2%], East Asian 47 [17.7%], Black 162 [14.8%], Other Ethnic Minority 467 [19.5%]; non-asthmatic chronic pulmonary disease (White 4751 [18.6%], South Asian 86 [6.2%], East Asian 18 [6.8%], Black 73 [6.7%], Other Ethnic Minority 218 [9.1%]); and dementia (White 4106 [16.1%], South Asian 60 [4.3%], East Asian 19 [7.1%], Black 74 [6.8%], Other Ethnic Minority 193 [8.0%]).

With age and sex adjustment, ethnic differences in comorbidity persisted with all Ethnic Minorities more likely to have diabetes (type 1 or type 2) and less likely to have non-asthmatic chronic pulmonary disease and obesity than the Whites (Figure 2). No difference in the likelihood of chronic cardiac disease was seen between South Asians and Whites.

No significant differences were seen in the distribution of severity scores (national early warning score 2 [NEWS2]) at admission between ethnic groups (figure 3A and figure 3C). In patients presenting to hospital with COVID-19, no differences were seen in the time from symptom onset to admission between ethnic groups (figure 3B) when modelled using Cox proportion hazards methods for the relative hazard of admission (figure 3D).

Last Edit: Jun 21, 2020 5:57:30 GMT by Admin