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1.
Preprint en Inglés | medRxiv | ID: ppmedrxiv-21268116

RESUMEN

BackgroundThe SARS-CoV-2 Omicron variant of concern (VOC) almost completely replaced other variants in South Africa during November 2021, and was associated with a rapid increase in COVID-19 cases. We aimed to assess clinical severity of individuals infected with Omicron, using S Gene Target Failure (SGTF) on the Thermo Fisher Scientific TaqPath COVID-19 PCR test as a proxy. MethodsWe performed data linkages for (i) SARS-CoV-2 laboratory tests, (ii) COVID-19 case data, (iii) genome data, and (iv) the DATCOV national hospital surveillance system for the whole of South Africa. For cases identified using Thermo Fisher TaqPath COVID-19 PCR, infections were designated as SGTF or non-SGTF. Disease severity was assessed using multivariable logistic regression models comparing SGTF-infected individuals diagnosed between 1 October to 30 November to (i) non-SGTF in the same period, and (ii) Delta infections diagnosed between April and November 2021. ResultsFrom 1 October through 6 December 2021, 161,328 COVID-19 cases were reported nationally; 38,282 were tested using TaqPath PCR and 29,721 SGTF infections were identified. The proportion of SGTF infections increased from 3% in early October (week 39) to 98% in early December (week 48). On multivariable analysis, after controlling for factors associated with hospitalisation, individuals with SGTF infection had lower odds of being admitted to hospital compared to non-SGTF infections (adjusted odds ratio (aOR) 0.2, 95% confidence interval (CI) 0.1-0.3). Among hospitalised individuals, after controlling for factors associated with severe disease, the odds of severe disease did not differ between SGTF-infected individuals compared to non-SGTF individuals diagnosed during the same time period (aOR 0.7, 95% CI 0.3-1.4). Compared to earlier Delta infections, after controlling for factors associated with severe disease, SGTF-infected individuals had a lower odds of severe disease (aOR 0.3, 95% CI 0.2-0.5). ConclusionEarly analyses suggest a reduced risk of hospitalisation among SGTF-infected individuals when compared to non-SGTF infected individuals in the same time period. Once hospitalised, risk of severe disease was similar for SGTF- and non-SGTF infected individuals, while SGTF-infected individuals had a reduced risk of severe disease when compared to earlier Delta-infected individuals. Some of this reducton is likely a result of high population immunity.

2.
Raquel Viana; Sikhulile Moyo; Daniel Gyamfi Amoako; Houriiyah Tegally; Cathrine Scheepers; Richard J Lessells; Jennifer Giandhari; Nicole Wolter; Josie Everatt; Andrew Rambaut; Christian Althaus; Eduan Wilkinson; Adriano Mendes; Amy Strydom; Michaela Davids; Simnikiwe Mayaphi; Simani Gaseitsiwe; Wonderful T Choga; Dorcas Maruapula; Boitumelo Zuze; Botshelo Radibe; Legodile Koopile; Roger Shapiro; Shahin Lockman; Mpaphi B. Mbulawa; Thongbotho Mphoyakgosi; Pamela Smith-Lawrence; Mosepele Mosepele; Mogomotsi Matshaba; Kereng Masupu; Mohammed Chand; Charity Joseph; Lesego Kuate-Lere; Onalethatha Lesetedi-Mafoko; Kgomotso Moruisi; Lesley Scott; Wendy Stevens; Constantinos Kurt Wibmer; Anele Mnguni; Arshad Ismail; Boitshoko Mahlangu; Darren P. Martin; Verity Hill; Rachel Colquhoun; Modisa S. Motswaledi; James Emmanuel San; Noxolo Ntuli; Gerald Motsatsi; Sureshnee Pillay; Thabo Mohale; Upasana Ramphal; Yeshnee Naidoo; Naume Tebeila; Marta Giovanetti; Koleka Mlisana; Carolyn Williamson; Nei-yuan Hsiao; Nokukhanya Msomi; Kamela Mahlakwane; Susan Engelbrecht; Tongai Maponga; Wolfgang Preiser; Zinhle Makatini; Oluwakemi Laguda-Akingba; Lavanya Singh; Ugochukwu J. Anyaneji; Monika Moir; Stephanie van Wyk; Derek Tshiabuila; Yajna Ramphal; Arisha Maharaj; Sergei Pond; Alexander G Lucaci; Steven Weaver; Maciej F Boni; Koen Deforche; Kathleen Subramoney; Diana Hardie; Gert Marais; Deelan Doolabh; Rageema Joseph; Nokuzola Mbhele; Luicer Olubayo; Arash Iranzadeh; Alexander E Zarebski; Joseph Tsui; Moritz UG Kraemer; Oliver G Pybus; Dominique Goedhals; Phillip Armand Bester; Martin M Nyaga; Peter N Mwangi; Allison Glass; Florette Treurnicht; Marietjie Venter; Jinal N. Bhiman; Anne von Gottberg; Tulio de Oliveira.
Preprint en Inglés | medRxiv | ID: ppmedrxiv-21268028

RESUMEN

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) epidemic in southern Africa has been characterised by three distinct waves. The first was associated with a mix of SARS-CoV-2 lineages, whilst the second and third waves were driven by the Beta and Delta variants respectively1-3. In November 2021, genomic surveillance teams in South Africa and Botswana detected a new SARS-CoV-2 variant associated with a rapid resurgence of infections in Gauteng Province, South Africa. Within three days of the first genome being uploaded, it was designated a variant of concern (Omicron) by the World Health Organization and, within three weeks, had been identified in 87 countries. The Omicron variant is exceptional for carrying over 30 mutations in the spike glycoprotein, predicted to influence antibody neutralization and spike function4. Here, we describe the genomic profile and early transmission dynamics of Omicron, highlighting the rapid spread in regions with high levels of population immunity.

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