Trends in Cases, Hospitalizations, and Mortality Related to the Omicron BA.4/BA.5 Subvariants in South Africa

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Abstract

Background

In this study, we compared admission incidence risk and the risk of mortality in the Omicron BA.4/BA.5 wave to previous waves.

Methods

Data from South Africa's SARS-CoV-2 case linelist, national COVID-19 hospital surveillance system, and Electronic Vaccine Data System were linked and analyzed. Wave periods were defined when the country passed a weekly incidence of 30 cases/100 000 population. In-hospital case fatality ratios (CFRs) during the Delta, Omicron BA.1/BA.2, and Omicron BA.4/BA.5 waves were compared using post-imputation random effect multivariable logistic regression models.

Results

The CFR was 25.9% (N = 37 538 of 144 778), 10.9% (N = 6123 of 56 384), and 8.2% (N = 1212 of 14 879) in the Delta, Omicron BA.1/BA.2, and Omicron BA.4/BA.5 waves, respectively. After adjusting for age, sex, race, comorbidities, health sector, and province, compared with the Omicron BA.4/BA.5 wave, patients had higher risk of mortality in the Omicron BA.1/BA.2 wave (adjusted odds ratio [aOR], 1.3; 95% confidence interval [CI]: 1.2–1.4) and Delta wave (aOR, 3.0; 95% CI: 2.8–3.2). Being partially vaccinated (aOR, 0.9; 95% CI: .9–.9), fully vaccinated (aOR, 0.6; 95% CI: .6–.7), and boosted (aOR, 0.4; 95% CI: .4–.5) and having prior laboratory-confirmed infection (aOR, 0.4; 95% CI: .3–.4) were associated with reduced risks of mortality.

Conclusions

Overall, admission incidence risk and in-hospital mortality, which had increased progressively in South Africa's first 3 waves, decreased in the fourth Omicron BA.1/BA.2 wave and declined even further in the fifth Omicron BA.4/BA.5 wave. Mortality risk was lower in those with natural infection and vaccination, declining further as the number of vaccine doses increased.

Abstract

Admission incidence risk and in-hospital mortality decreased in the Omicron BA.1/BA.2 wave, reducing even further in the Omicron BA.4/BA.5 wave. Mortality risk was lower in those with natural infection and vaccination, declining further as the number of vaccine doses increased.

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Most cited references 33

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Comparative analysis of the risks of hospitalisation and death associated with SARS-CoV-2 omicron (B.1.1.529) and delta (B.1.617.2) variants in England: a cohort study

Tommy Nyberg, Neil M Ferguson, Sophie Nash … (2022)

Background The omicron variant (B.1.1.529) of SARS-CoV-2 has demonstrated partial vaccine escape and high transmissibility, with early studies indicating lower severity of infection than that of the delta variant (B.1.617.2). We aimed to better characterise omicron severity relative to delta by assessing the relative risk of hospital attendance, hospital admission, or death in a large national cohort. Methods Individual-level data on laboratory-confirmed COVID-19 cases resident in England between Nov 29, 2021, and Jan 9, 2022, were linked to routine datasets on vaccination status, hospital attendance and admission, and mortality. The relative risk of hospital attendance or admission within 14 days, or death within 28 days after confirmed infection, was estimated using proportional hazards regression. Analyses were stratified by test date, 10-year age band, ethnicity, residential region, and vaccination status, and were further adjusted for sex, index of multiple deprivation decile, evidence of a previous infection, and year of age within each age band. A secondary analysis estimated variant-specific and vaccine-specific vaccine effectiveness and the intrinsic relative severity of omicron infection compared with delta (ie, the relative risk in unvaccinated cases). Findings The adjusted hazard ratio (HR) of hospital attendance (not necessarily resulting in admission) with omicron compared with delta was 0·56 (95% CI 0·54–0·58); for hospital admission and death, HR estimates were 0·41 (0·39–0·43) and 0·31 (0·26–0·37), respectively. Omicron versus delta HR estimates varied with age for all endpoints examined. The adjusted HR for hospital admission was 1·10 (0·85–1·42) in those younger than 10 years, decreasing to 0·25 (0·21–0·30) in 60–69-year-olds, and then increasing to 0·47 (0·40–0·56) in those aged at least 80 years. For both variants, past infection gave some protection against death both in vaccinated (HR 0·47 [0·32–0·68]) and unvaccinated (0·18 [0·06–0·57]) cases. In vaccinated cases, past infection offered no additional protection against hospital admission beyond that provided by vaccination (HR 0·96 [0·88–1·04]); however, for unvaccinated cases, past infection gave moderate protection (HR 0·55 [0·48–0·63]). Omicron versus delta HR estimates were lower for hospital admission (0·30 [0·28–0·32]) in unvaccinated cases than the corresponding HR estimated for all cases in the primary analysis. Booster vaccination with an mRNA vaccine was highly protective against hospitalisation and death in omicron cases (HR for hospital admission 8–11 weeks post-booster vs unvaccinated: 0·22 [0·20–0·24]), with the protection afforded after a booster not being affected by the vaccine used for doses 1 and 2. Interpretation The risk of severe outcomes following SARS-CoV-2 infection is substantially lower for omicron than for delta, with higher reductions for more severe endpoints and significant variation with age. Underlying the observed risks is a larger reduction in intrinsic severity (in unvaccinated individuals) counterbalanced by a reduction in vaccine effectiveness. Documented previous SARS-CoV-2 infection offered some protection against hospitalisation and high protection against death in unvaccinated individuals, but only offered additional protection in vaccinated individuals for the death endpoint. Booster vaccination with mRNA vaccines maintains over 70% protection against hospitalisation and death in breakthrough confirmed omicron infections. Funding Medical Research Council, UK Research and Innovation, Department of Health and Social Care, National Institute for Health Research, Community Jameel, and Engineering and Physical Sciences Research Council.

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Early assessment of the clinical severity of the SARS-CoV-2 omicron variant in South Africa: a data linkage study

Nicole Wolter, Waasila Jassat, Sibongile Walaza … (2022)

Background The SARS-CoV-2 omicron variant of concern was identified in South Africa in November, 2021, and was associated with an increase in COVID-19 cases. We aimed to assess the clinical severity of infections with the omicron variant using S gene target failure (SGTF) on the Thermo Fisher Scientific TaqPath COVID-19 PCR test as a proxy. Methods We did data linkages for national, South African COVID-19 case data, SARS-CoV-2 laboratory test data, SARS-CoV-2 genome data, and COVID-19 hospital admissions data. For individuals diagnosed with COVID-19 via TaqPath PCR tests, infections were designated as either SGTF or non-SGTF. The delta variant was identified by genome sequencing. Using multivariable logistic regression models, we assessed disease severity and hospitalisations by comparing individuals with SGTF versus non-SGTF infections diagnosed between Oct 1 and Nov 30, 2021, and we further assessed disease severity by comparing SGTF-infected individuals diagnosed between Oct 1 and Nov 30, 2021, with delta variant-infected individuals diagnosed between April 1 and Nov 9, 2021. Findings From Oct 1 (week 39), 2021, to Dec 6 (week 49), 2021, 161 328 cases of COVID-19 were reported in South Africa. 38 282 people were diagnosed via TaqPath PCR tests and 29 721 SGTF infections and 1412 non-SGTF infections were identified. The proportion of SGTF infections increased from two (3·2%) of 63 in week 39 to 21 978 (97·9%) of 22 455 in week 48. After controlling for factors associated with hospitalisation, individuals with SGTF infections had significantly lower odds of admission than did those with non-SGTF infections (256 [2·4%] of 10 547 vs 121 [12·8%] of 948; adjusted odds ratio [aOR] 0·2, 95% CI 0·1–0·3). After controlling for factors associated with disease severity, the odds of severe disease were similar between hospitalised individuals with SGTF versus non-SGTF infections (42 [21%] of 204 vs 45 [40%] of 113; aOR 0·7, 95% CI 0·3–1·4). Compared with individuals with earlier delta variant infections, SGTF-infected individuals had a significantly lower odds of severe disease (496 [62·5%] of 793 vs 57 [23·4%] of 244; aOR 0·3, 95% CI 0·2–0·5), after controlling for factors associated with disease severity. Interpretation Our early analyses suggest a significantly reduced odds of hospitalisation among individuals with SGTF versus non-SGTF infections diagnosed during the same time period. SGTF-infected individuals had a significantly reduced odds of severe disease compared with individuals infected earlier with the delta variant. Some of this reduced severity is probably a result of previous immunity. Funding The South African Medical Research Council, the South African National Department of Health, US Centers for Disease Control and Prevention, the African Society of Laboratory Medicine, Africa Centers for Disease Control and Prevention, the Bill & Melinda Gates Foundation, the Wellcome Trust, and the Fleming Fund.

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SARS-CoV-2 Omicron variant replication in human bronchus and lung ex vivo

Kenrie P Y Hui, John C. W. Ho, Man-chun Cheung … (2022)

The emergence of SARS-CoV-2 variants of concern with progressively increased transmissibility between humans is a threat to global public health. The Omicron variant of SARS-CoV-2 also evades immunity from natural infection or vaccines1, but it is unclear whether its exceptional transmissibility is due to immune evasion or intrinsic virological properties. Here we compared the replication competence and cellular tropism of the wild-type virus and the D614G, Alpha (B.1.1.7), Beta (B.1.351), Delta (B.1.617.2) and Omicron (B.1.1.529) variants in ex vivo explant cultures of human bronchi and lungs. We also evaluated the dependence on TMPRSS2 and cathepsins for infection. We show that Omicron replicates faster than all other SARS-CoV-2 variants studied in the bronchi but less efficiently in the lung parenchyma. All variants of concern have similar cellular tropism compared to the wild type. Omicron is more dependent on cathepsins than the other variants of concern tested, suggesting that the Omicron variant enters cells through a different route compared with the other variants. The lower replication competence of Omicron in the human lungs may explain the reduced severity of Omicron that is now being reported in epidemiological studies, although determinants of severity are multifactorial. These findings provide important biological correlates to previous epidemiological observations.

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Author and article information

Contributors

Waasila Jassat

Salim S Abdool Karim

Lovelyn Ozougwu

Richard Welch

Caroline Mudara

Maureen Masha

Petro Rousseau

Milani Wolmarans

Anthony Selikow

Nevashan Govender

Sibongile Walaza

Anne von Gottberg

Nicole Wolter

Pedro Terrence Pisa

Ian Sanne

Sharlene Govender

Lucille Blumberg:

ORCID: https://orcid.org/0000-0002-6959-5749

Cheryl Cohen

Michelle J Groome

Journal

Journal ID (nlm-ta): Clin Infect Dis

Journal ID (iso-abbrev): Clin Infect Dis

Journal ID (publisher-id): cid

Title: Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America

Publisher: Oxford University Press (US )

ISSN (Print): 1058-4838

ISSN (Electronic): 1537-6591

Publication date Collection: 15 April 2023

Publication date (Electronic): 01 December 2022

Publication date PMC-release: 01 December 2022

Volume: 76

Issue: 8

Pages: 1468-1475

Affiliations

National Institute for Communicable Diseases, Division of the National Health Laboratory Service , Johannesburg, South Africa

Right to Care , Pretoria, South Africa

Centre for the AIDS Programme of Research in South Africa , Durban, South Africa

Department of Epidemiology, Mailman School of Public Health, Columbia University , New York, New York, USA

National Institute for Communicable Diseases, Division of the National Health Laboratory Service , Johannesburg, South Africa

Right to Care , Pretoria, South Africa

National Institute for Communicable Diseases, Division of the National Health Laboratory Service , Johannesburg, South Africa

Right to Care , Pretoria, South Africa

National Institute for Communicable Diseases, Division of the National Health Laboratory Service , Johannesburg, South Africa

Right to Care , Pretoria, South Africa

National Department of Health , Pretoria, South Africa

Council for Scientific and Industrial Research , Pretoria, South Africa

National Institute for Communicable Diseases, Division of the National Health Laboratory Service , Johannesburg, South Africa

School of Public Health, Faculty of Health Sciences, University of Witwatersrand , Johannesburg, South Africa

National Institute for Communicable Diseases, Division of the National Health Laboratory Service , Johannesburg, South Africa

School of Pathology, Faculty of Health Sciences, University of the Witwatersrand , Johannesburg, South Africa

National Institute for Communicable Diseases, Division of the National Health Laboratory Service , Johannesburg, South Africa

School of Pathology, Faculty of Health Sciences, University of the Witwatersrand , Johannesburg, South Africa

Right to Care , Pretoria, South Africa

Department of Human Nutrition and Dietetics, Faculty of Health Sciences, University of Pretoria , Pretoria, South Africa

Right to Care , Pretoria, South Africa

Clinical HIV Research Unit, Department of Internal Medicine, Faculty of Health Sciences, University of the Witwatersrand , Johannesburg, South Africa

Right to Care , Pretoria, South Africa

National Institute for Communicable Diseases, Division of the National Health Laboratory Service , Johannesburg, South Africa

Right to Care , Pretoria, South Africa

National Institute for Communicable Diseases, Division of the National Health Laboratory Service , Johannesburg, South Africa

School of Public Health, Faculty of Health Sciences, University of Witwatersrand , Johannesburg, South Africa

National Institute for Communicable Diseases, Division of the National Health Laboratory Service , Johannesburg, South Africa

School of Pathology, Faculty of Health Sciences, University of the Witwatersrand , Johannesburg, South Africa

Author notes

C. C. and M. J. G. contributed equally to this work.

Correspondence: Waasila Jassat, Division of Public Health Surveillance and Response, National Institute for Communicable Diseases, 1 Modderfontein Road, Sandringham, 2192 Johannesburg, South Africa ( WaasilaJ@ 123456nicd.ac.za ).

Potential conflicts of interest. S. S. A. K. reports grants or contracts unrelated to this work and paid to institution from the National Institutes of Health, South African Medical Research Council Cooperative Agreement, National Research Foundation/DST, USAID/Right to Care Cooperative agreement, the IQRAA Trust, and EDCTP; an unpaid role as a member of the World Health Organization (WHO) Science Council; a paid role as a member of the Bill and Melinda Gates Foundation (BMGF) Scientific Advisory Committee (meeting honorarium paid to author); and an unpaid role as vice-president of the International Science Council. C. C. reports grants or contracts unrelated to this work and paid to institution from the US Centers for Disease Control and Prevention (CDC), Wellcome Trust, Sanofi Pasteur, PATH, BMGF, and SA-Medical Research Council. A. v. G. reports grants unrelated to this work and paid to institution from the BMGF, Sanofi, CDC, WHO AFRO, Fleming Fund SEQAFRICA, SA MRC, the Solidarity Fund for Innovative Projects, NIH training grant, and ASLM PGI and a role as chair for the National Advisory Group for Immunisation. I. S. reports an institutional grant unrelated to this work from NIH DAIDS–WITS Helen Joseph Hospital CRS. M. J. G. reports grants or contracts unrelated to this work and paid to institution from the South African Medical Research Council and BMGF. N. W. reports grants paid to institution and unrelated to this work from the BMGF, Sanofi, and CDC. R. W. reports shareholding with Adcock Ingram Holdings Ltd, Dischem Pharmacies Ltd, Discovery Ltd, Netcare Ltd, and Aspen Pharmacare Holdings Ltd. S. W. reports grants unrelated to this work and paid to institution from the BMGF, Sanofi, CDC, and Welcome Trust. W. J. reports grants or contracts related to a long coronavirus disease 2019 study, paid to institution, from the BMGF. All remaining authors: No reported conflicts of interest. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.

Author information

Lucille Blumberg https://orcid.org/0000-0002-6959-5749

Article

Publisher ID: ciac921

DOI: 10.1093/cid/ciac921

PMC ID: 10110264

PubMed ID: 36453094

SO-VID: 291c8138-7181-40cf-a021-8602f8eeac0c

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence ( https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

History

Date received : 25 August 2022

Date: 22 November 2022

Date: 25 January 2023

Page count

Pages: 8

Funding

Funded by: NICD;

Funded by: NDoH, doi 10.13039/100009041;

Funded by: US Agency for International Development, doi 10.13039/100000200;

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Trends in Cases, Hospitalizations, and Mortality Related to the Omicron BA.4/BA.5 Subvariants in South Africa

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Abstract

Background

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Results

Conclusions

Abstract

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Most cited references 33

Comparative analysis of the risks of hospitalisation and death associated with SARS-CoV-2 omicron (B.1.1.529) and delta (B.1.617.2) variants in England: a cohort study

Early assessment of the clinical severity of the SARS-CoV-2 omicron variant in South Africa: a data linkage study

SARS-CoV-2 Omicron variant replication in human bronchus and lung ex vivo

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