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1.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-22274406

Résumé

South Africas fourth COVID-19 wave was driven predominantly by three lineages (BA.1, BA.2 and BA.3) of the SARS-CoV-2 Omicron variant of concern. We have now identified two new lineages, BA.4 and BA.5. The spike proteins of BA.4 and BA.5 are identical, and comparable to BA.2 except for the addition of 69-70del, L452R, F486V and the wild type amino acid at Q493. The 69-70 deletion in spike allows these lineages to be identified by the proxy marker of S-gene target failure with the TaqPath COVID-19 qPCR assay. BA.4 and BA.5 have rapidly replaced BA.2, reaching more than 50% of sequenced cases in South Africa from the first week of April 2022 onwards. Using a multinomial logistic regression model, we estimate growth advantages for BA.4 and BA.5 of 0.08 (95% CI: 0.07 - 0.09) and 0.12 (95% CI: 0.09 - 0.15) per day respectively over BA.2 in South Africa.

2.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-22274477

Résumé

The SARS-CoV-2 Omicron (B.1.1.529) variant first emerged as the BA.1 sub-lineage, with extensive escape from neutralizing immunity elicited by previous infection with other variants, vaccines, or combinations of both1,2. Two new sub-lineages, BA.4 and BA.5, are now emerging in South Africa with changes relative to BA.1, including L452R and F486V mutations in the spike receptor binding domain. We isolated live BA.4 and BA.5 viruses and tested them against neutralizing immunity elicited to BA.1 infection in participants who were Omicron/BA.1 infected but unvaccinated (n=24) and participants vaccinated with Pfizer BNT162b2 or Johnson and Johnson Ad26.CoV.2S with breakthrough Omicron/BA.1 infection (n=15). In unvaccinated individuals, FRNT50, the inverse of the dilution for 50% neutralization, declined from 275 for BA.1 to 36 for BA.4 and 37 for BA.5, a 7.6 and 7.5-fold drop, respectively. In vaccinated BA.1 breakthroughs, FRNT50 declined from 507 for BA.1 to 158 for BA.4 (3.2-fold) and 198 for BA.5 (2.6-fold). Absolute BA.4 and BA.5 neutralization levels were about 5-fold higher in this group versus unvaccinated BA.1 infected participants. The observed escape of BA.4 and BA.5 from BA.1 elicited immunity is more moderate than of BA.1 against previous immunity1,3. However, the low absolute neutralization levels for BA.4 and BA.5, particularly in the unvaccinated group, are unlikely to protect well against symptomatic infection4.This may indicate that, based on neutralization escape, BA.4 and BA.5 have potential to result in a new infection wave.

3.
Houriiyah Tegally; James E. San; Matthew Cotten; Bryan Tegomoh; Gerald Mboowa; Darren P. Martin; Cheryl Baxter; Monika Moir; Arnold Lambisia; Amadou Diallo; Daniel G. Amoako; Moussa M. Diagne; Abay Sisay; Abdel-Rahman N. Zekri; Abdelhamid Barakat; Abdou Salam Gueye; Abdoul K. Sangare; Abdoul-Salam Ouedraogo; Abdourahmane SOW; Abdualmoniem O. Musa; Abdul K. Sesay; Adamou LAGARE; Adedotun-Sulaiman Kemi; Aden Elmi Abar; Adeniji A. Johnson; Adeola Fowotade; Adewumi M. Olubusuyi; Adeyemi O. Oluwapelumi; Adrienne A. Amuri; Agnes Juru; Ahmad Mabrouk Ramadan; Ahmed Kandeil; Ahmed Mostafa; Ahmed Rebai; Ahmed Sayed; Akano Kazeem; Aladje Balde; Alan Christoffels; Alexander J. Trotter; Allan Campbell; Alpha Kabinet KEITA; Amadou Kone; Amal Bouzid; Amal Souissi; Ambrose Agweyu; Ana V. Gutierrez; Andrew J. Page; Anges Yadouleton; Anika Vinze; Anise N. Happi; Anissa Chouikha; Arash Iranzadeh; Arisha Maharaj; Armel Landry Batchi-Bouyou; Arshad Ismail; Augustina Sylverken; Augustine Goba; Ayoade Femi; Ayotunde Elijah Sijuwola; Azeddine Ibrahimi; Baba Marycelin; Babatunde Lawal Salako; Bamidele S. Oderinde; Bankole Bolajoko; Beatrice Dhaala; Belinda L. Herring; Benjamin Tsofa; Bernard Mvula; Berthe-Marie Njanpop-Lafourcade; Blessing T. Marondera; Bouh Abdi KHAIREH; Bourema Kouriba; Bright Adu; Brigitte Pool; Bronwyn McInnis; Cara Brook; Carolyn Williamson; Catherine Anscombe; Catherine B. Pratt; Cathrine Scheepers; Chantal G. Akoua-Koffi; Charles N. Agoti; Cheikh Loucoubar; Chika Kingsley Onwuamah; Chikwe Ihekweazu; Christian Noel MALAKA; Christophe Peyrefitte; Chukwuma Ewean Omoruyi; Clotaire Donatien Rafai; Collins M. Morang'a; D. James Nokes; Daniel Bugembe Lule; Daniel J. Bridges; Daniel Mukadi-Bamuleka; Danny Park; David Baker; Deelan Doolabh; Deogratius Ssemwanga; Derek Tshiabuila; Diarra Bassirou; Dominic S.Y. Amuzu; Dominique Goedhals; Donald S. Grant; Donwilliams O. Omuoyo; Dorcas Maruapula; Dorcas Waruguru Wanjohi; Ebenezer Foster-Nyarko; Eddy K. Lusamaki; Edgar Simulundu; Edidah M. Ong'era; Edith N. Ngabana; Edward O. Abworo; Edward Otieno; Edwin Shumba; Edwine Barasa; EL BARA AHMED; Elmostafa EL FAHIME; Emmanuel Lokilo; Enatha Mukantwari; Erameh Cyril; Eromon Philomena; Essia Belarbi; Etienne Simon-Loriere; Etile A. Anoh; Fabian Leendertz; Fahn M. Taweh; Fares Wasfi; Fatma Abdelmoula; Faustinos T. Takawira; Fawzi Derrar; Fehintola V Ajogbasile; Florette Treurnicht; Folarin Onikepe; Francine Ntoumi; Francisca M. Muyembe; FRANCISCO NGIAMBUDULU; Frank Edgard ZONGO Ragomzingba; Fred Athanasius DRATIBI; Fred-Akintunwa Iyanu; Gabriel K. Mbunsu; Gaetan Thilliez; Gemma L. Kay; George O. Akpede; George E Uwem; Gert van Zyl; Gordon A. Awandare; Grit Schubert; Gugu P. Maphalala; Hafaliana C. Ranaivoson; Hajar Lemriss; Hannah E Omunakwe; Harris Onywera; Haruka Abe; HELA KARRAY; Hellen Nansumba; Henda Triki; Herve Alberic ADJE KADJO; Hesham Elgahzaly; Hlanai Gumbo; HOTA mathieu; Hugo Kavunga-Membo; Ibtihel Smeti; Idowu B. Olawoye; Ifedayo Adetifa; Ikponmwosa Odia; Ilhem Boutiba-Ben Boubaker; Isaac Ssewanyana; Isatta Wurie; Iyaloo S Konstantinus; Jacqueline Wemboo Afiwa Halatoko; James Ayei; Janaki Sonoo; Jean Bernard LEKANA-DOUKI; Jean-Claude C. Makangara; Jean-Jacques M. Tamfum; Jean-Michel Heraud; Jeffrey G. Shaffer; Jennifer Giandhari; Jennifer Musyoki; Jessica N. Uwanibe; Jinal N. Bhiman; Jiro Yasuda; Joana Morais; Joana Q. Mends; Jocelyn Kiconco; John Demby Sandi; John Huddleston; John Kofi Odoom; John M. Morobe; John O. Gyapong; John T. Kayiwa; Johnson C. Okolie; Joicymara Santos Xavier; Jones Gyamfi; Joseph Humphrey Kofi Bonney; Joseph Nyandwi; Josie Everatt; Jouali Farah; Joweria Nakaseegu; Joyce M. Ngoi; Joyce Namulondo; Judith U. Oguzie; Julia C. Andeko; Julius J. Lutwama; Justin O'Grady; Katherine J Siddle; Kathleen Victoir; Kayode T. Adeyemi; Kefentse A. Tumedi; Kevin Sanders Carvalho; Khadija Said Mohammed; Kunda G. Musonda; Kwabena O. Duedu; Lahcen Belyamani; Lamia Fki-Berrajah; Lavanya Singh; Leon Biscornet; Leonardo de Oliveira Martins; Lucious Chabuka; Luicer Olubayo; Lul Lojok Deng; Lynette Isabella Ochola-Oyier; Madisa Mine; Magalutcheemee Ramuth; Maha Mastouri; Mahmoud ElHefnawi; Maimouna Mbanne; Maitshwarelo I. Matsheka; Malebogo Kebabonye; Mamadou Diop; Mambu Momoh; Maria da Luz Lima Mendonca; Marietjie Venter; Marietou F Paye; Martin Faye; Martin M. Nyaga; Mathabo Mareka; Matoke-Muhia Damaris; Maureen W. Mburu; Maximillian Mpina; Claujens Chastel MFOUTOU MAPANGUY; Michael Owusu; Michael R. Wiley; Mirabeau Youtchou Tatfeng; Mitoha Ondo'o Ayekaba; Mohamed Abouelhoda; Mohamed Amine Beloufa; Mohamed G Seadawy; Mohamed K. Khalifa; Mohammed Koussai DELLAGI; Mooko Marethabile Matobo; Mouhamed Kane; Mouna Ouadghiri; Mounerou Salou; Mphaphi B. Mbulawa; Mudashiru Femi Saibu; Mulenga Mwenda; My V.T. Phan; Nabil Abid; Nadia Touil; Nadine Rujeni; Nalia Ismael; Ndeye Marieme Top; Ndongo Dia; Nedio Mabunda; Nei-yuan Hsiao; Nelson Borico Silochi; Ngonda Saasa; Nicholas Bbosa; Nickson Murunga; Nicksy Gumede; Nicole Wolter; Nikita Sitharam; Nnaemeka Ndodo; Nnennaya A. Ajayi; Noel Tordo; Nokuzola Mbhele; Norosoa H Razanajatovo; Nosamiefan Iguosadolo; Nwando Mba; Ojide C. Kingsley; Okogbenin Sylvanus; Okokhere Peter; Oladiji Femi; Olumade Testimony; Olusola Akinola Ogunsanya; Oluwatosin Fakayode; Onwe E. Ogah; Ousmane Faye; Pamela Smith-Lawrence; Pascale Ondoa; Patrice Combe; Patricia Nabisubi; Patrick Semanda; Paul E. Oluniyi; Paulo Arnaldo; Peter Kojo Quashie; Philip Bejon; Philippe Dussart; Phillip A. Bester; Placide K. Mbala; Pontiano Kaleebu; Priscilla Abechi; Rabeh El-Shesheny; Rageema Joseph; Ramy Karam Aziz; Rene Ghislain Essomba; Reuben Ayivor-Djanie; Richard Njouom; Richard O. Phillips; Richmond Gorman; Robert A. Kingsley; Rosemary Audu; Rosina A.A. Carr; Saad El Kabbaj; Saba Gargouri; Saber Masmoudi; Safietou Sankhe; Sahra Isse Mohamed; Salma MHALLA; Salome Hosch; Samar Kamal Kassim; Samar Metha; Sameh Trabelsi; Sanaa Lemriss; Sara Hassan Agwa; Sarah Wambui Mwangi; Seydou Doumbia; Sheila Makiala-Mandanda; Sherihane Aryeetey; Shymaa S. Ahmed; SIDI MOHAMED AHMED; Siham Elhamoumi; Sikhulile Moyo; Silvia Lutucuta; Simani Gaseitsiwe; Simbirie Jalloh; Soafy Andriamandimby; Sobajo Oguntope; Solene Grayo; Sonia Lekana-Douki; Sophie Prosolek; Soumeya Ouangraoua; Stephanie van Wyk; Stephen F. Schaffner; Stephen Kanyerezi; Steve AHUKA-MUNDEKE; Steven Rudder; Sureshnee Pillay; Susan Nabadda; Sylvie Behillil; Sylvie L. Budiaki; Sylvie van der Werf; Tapfumanei Mashe; Tarik Aanniz; Thabo Mohale; Thanh Le-Viet; Thirumalaisamy P. Velavan; Tobias Schindler; Tongai Maponga; Trevor Bedford; Ugochukwu J. Anyaneji; Ugwu Chinedu; Upasana Ramphal; Vincent Enouf; Vishvanath Nene; Vivianne Gorova; Wael H. Roshdy; Wasim Abdul Karim; William K. Ampofo; Wolfgang Preiser; Wonderful T. Choga; Yahaya ALI ALI AHMED; Yajna Ramphal; Yaw Bediako; Yeshnee Naidoo; Yvan Butera; Zaydah R. de Laurent; Ahmed E.O. Ouma; Anne von Gottberg; George Githinji; Matshidiso Moeti; Oyewale Tomori; Pardis C. Sabeti; Amadou A. Sall; Samuel O. Oyola; Yenew K. Tebeje; Sofonias K. Tessema; Tulio de Oliveira; Christian Happi; Richard Lessells; John Nkengasong; Eduan Wilkinson.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-22273906

Résumé

Investment in Africa over the past year with regards to SARS-CoV-2 genotyping has led to a massive increase in the number of sequences, exceeding 100,000 genomes generated to track the pandemic on the continent. Our results show an increase in the number of African countries able to sequence within their own borders, coupled with a decrease in sequencing turnaround time. Findings from this genomic surveillance underscores the heterogeneous nature of the pandemic but we observe repeated dissemination of SARS-CoV-2 variants within the continent. Sustained investment for genomic surveillance in Africa is needed as the virus continues to evolve, particularly in the low vaccination landscape. These investments are very crucial for preparedness and response for future pathogen outbreaks. One-Sentence SummaryExpanding Africa SARS-CoV-2 sequencing capacity in a fast evolving pandemic.

4.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-22270789

Résumé

The SARS-CoV-2 Omicron variant escapes neutralizing antibodies elicited by vaccines or infection. However, whether Omicron triggers cross-reactive humoral responses to other variants of concern (VOCs) remains unknown. We use plasma from 20 unvaccinated and seven vaccinated individuals infected by Omicron BA.1 to test binding, Fc effector function and neutralization against VOCs. In unvaccinated individuals, Fc effector function and binding antibodies target Omicron and other VOCs at comparable levels. However, Omicron BA.1-triggered neutralization is not extensively cross-reactive for VOCs (14 to 31-fold titer reduction) and we observe 4-fold decreased titers against Omicron BA.2. In contrast, vaccination followed by breakthrough Omicron infection was associated with improved cross-neutralization of VOCs, with titers exceeding 1:2,100. This has important implications for vulnerability of unvaccinated Omicron-infected individuals to reinfection by circulating and emerging VOCs. While Omicron-based immunogens may be adequate boosters, they are unlikely to be superior to existing vaccines for priming in SARS-CoV-2 naive individuals.

5.
Preprint Dans Anglais | bioRxiv | ID: ppbiorxiv-476382

Résumé

Among the 30 non-synonymous nucleotide substitutions in the Omicron S-gene are 13 that have only rarely been seen in other SARS-CoV-2 sequences. These mutations cluster within three functionally important regions of the S-gene at sites that will likely impact (i) interactions between subunits of the Spike trimer and the predisposition of subunits to shift from down to up configurations, (ii) interactions of Spike with ACE2 receptors, and (iii) the priming of Spike for membrane fusion. We show here that, based on both the rarity of these 13 mutations in intrapatient sequencing reads and patterns of selection at the codon sites where the mutations occur in SARS-CoV-2 and related sarbecoviruses, prior to the emergence of Omicron the mutations would have been predicted to decrease the fitness of any genomes within which they occurred. We further propose that the mutations in each of the three clusters therefore cooperatively interact to both mitigate their individual fitness costs, and adaptively alter the function of Spike. Given the evident epidemic growth advantages of Omicron over all previously known SARS-CoV-2 lineages, it is crucial to determine both how such complex and highly adaptive mutation constellations were assembled within the Omicron S-gene, and why, despite unprecedented global genomic surveillance efforts, the early stages of this assembly process went completely undetected.

6.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-22268646

Résumé

COVID-19 was first diagnosed in Egypt on 14 February 2020. By the end of November 2021, over 333,840 cases and 18,832 deaths had been reported. As part of national genomic surveillance, 1,027 SARS-CoV-2 near whole-genomes had been generated and published by the end of May 2021. Here we describe the genomic epidemiology of SARS-CoV-2 in Egypt over this period using a subset of 976 high-quality Egyptian genomes analysed together with a representative set of global sequences within a phylogenetic framework. We show that a single lineage, C.36, introduced early in the pandemic was responsible for most cases in Egypt. Furthermore, we show that to remain dominant in the face of mounting immunity from previous infection and vaccination, this lineage evolved into various sub-lineages acquiring several mutations known to confer adaptive advantage and pathogenic properties. These results highlight the value of continuous genomic surveillance in regions where VOCs are not predominant and enforcement of public health measures to prevent expansion of existing lineages.

7.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21268309

Résumé

The COVID-19 epidemic in Brazil was driven mainly by the spread of Gamma (P.1), a locally emerged Variant of Concern (VOC) that was first detected in early January 2021. This variant was estimated to be responsible for more than 96% of cases reported between January and June 2021, being associated with increased transmissibility and disease severity, a reduction in neutralization antibodies and effectiveness of treatments or vaccines, as well as diagnostic detection failure. Here we show that, following several importations predominantly from the USA, the Delta variant rapidly replaced Gamma after July 2021. However, in contrast to what was seen in other countries, the rapid spread of Delta did not lead to a large increase in the number of cases and deaths reported in Brazil. We suggest that this was likely due to the relatively successful early vaccination campaign coupled with natural immunity acquired following prior infection with Gamma. Our data reinforces reports of the increased transmissibility of the Delta variant and, considering the increasing concern due to the recently identified Omicron variant, argues for the necessity to strengthen genomic monitoring on a national level to quickly detect and curb the emergence and spread of other VOCs that might threaten global health.

8.
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 Dans Anglais | medRxiv | ID: ppmedrxiv-21268028

Résumé

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.

9.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21267417

Résumé

The emergence of SARS-CoV-2 Omicron, first identified in Botswana and South Africa, may compromise vaccine effectiveness and the ability of antibodies triggered by previous infection to protect against re-infection (1). Here we investigated whether Omicron escapes antibody neutralization in South Africans, either previously SARS-CoV-2 infected or uninfected, who were vaccinated with Pfizer BNT162b2. We also investigated if Omicron requires the ACE2 receptor to infect cells. We isolated and sequence confirmed live Omicron virus from an infected person in South Africa and compared plasma neutralization of this virus relative to an ancestral SARS-CoV-2 strain with the D614G mutation, observing that Omicron still required ACE2 to infect. For neutralization, blood samples were taken soon after vaccination, so that vaccine elicited neutralization was close to peak. Neutralization capacity of the D614G virus was much higher in infected and vaccinated versus vaccinated only participants but both groups had 22-fold Omicron escape from vaccine elicited neutralization. Previously infected and vaccinated individuals had residual neutralization predicted to confer 73% protection from symptomatic Omicron infection, while those without previous infection were predicted to retain only about 35%. Both groups were predicted to have substantial protection from severe disease. These data support the notion that high neutralization capacity elicited by a combination of infection and vaccination, and possibly boosting, could maintain reasonable effectiveness against Omicron. A waning neutralization response is likely to decrease vaccine effectiveness below these estimates. However, since protection from severe disease requires lower neutralization levels and involves T cell immunity, such protection may be maintained.

10.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21266298

Résumé

Outbreaks of COVID at university campuses can spread rapidly and threaten the broader community. We describe the management of an outbreak at a Malawian university in April-May 2021 during Malawis second wave. Classes were suspended following detection of infections by routine testing and campus-wide PCR mass testing was conducted. Fifty seven cases were recorded, 55 among students, two among staff. Classes resumed 28 days after suspension following two weeks without cases. Just 6.3% of full-time staff and 87.4% of outsourced staff tested while 65% of students at the main campus and 74% at the extension campus were tested. Final year students had significantly higher positivity and lower testing coverage compared to freshmen. All viruses sequenced were beta variant and at least four separate virus introductions onto campus were observed. These findings are useful for development of campus outbreak responses and indicate the need to emphasize staff, males and senior students in testing. Article Summary LineSuccessful management of a campus outbreak using test trace and isolate approach with resumption within a month following suspension of all in-person classes. Trends in voluntary testing by gender, age and year of study that can help in formation of future management approaches.

11.
Marta Giovanetti; Svetoslav Nanev Slavov; Vagner Fonseca; Eduan Wilkinson; Houriiyah Tegally; Jose Patane; Vincent Louis Viala; Emmanuel James San; Evandra Strazza Rodrigues; Elaine Vieira Santos; Flavia Aburjaile; Joilson Xavier; Hegger Fritsch; Talita Emile Ribeiro Adelino; Felicidade Pereira; Arabela Leal; Felipe Campos de Melo Iani; Glauco de Carvalho Pereira; Cynthia Vazquez; Gladys Mercedes Estigarribia Sanabria; Elaine Cristina de Oliveira; Luiz Demarchi; Julio Croda; Rafael Dos Santos Bezerra Sr.; Loyze Paola Oliveira de Lima; Antonio Jorge Martins; Claudia Renata dos Santos Barros; Elaine Cristina Marqueze; Jardelina de Souza Todao Bernardino; Debora Botequio Moretti; Ricardo Augusto Brassaloti; Raquel de Lello Rocha Campos Cassano; Pilar Drummond Sampaio Correa Mariani; Joao Paulo Kitajima; Bibiana Santos; Rodrigo Proto Siqueira; Vlademir Vicente Cantarelli; Stephane Tosta; Vanessa Brandao Nardy; Luciana Reboredo de Oliveira da Silva; Marcela Kelly Astete Gomez; Jaqueline Gomes Lima; Adriana Aparecida Ribeiro; Natalia Rocha Guimaraes; Luiz Takao Watanabe; Luana Barbosa Da Silva; Raquel da Silva Ferreira; Mara Patricia F. da Penha; Maria Jose Ortega; Andrea Gomez de la Fuente; Shirley Villalba; Juan Torales; Maria Liz Gamarra; Carolina Aquino; Gloria Patricia Martinez Figueredo; Wellington Santos Fava; Ana Rita C. Motta Castro; James Venturini; Sandra Maria do Vale Leone de Oliveira; Crhistinne Cavalheiro Maymone Goncalves; Maria do Carmo Debur Rossa; Guilherme Nardi Becker; Mayra Marinho Presibella; Nelson Quallio Marques; Irina Nastassja Riediger; Sonia Raboni; Gabriela Mattoso; Allan D. Cataneo; Camila Zanluca; Claudia N Duarte dos Santos; Patricia Akemi Assato; Felipe Allan da Silva da Costa; Mirele Daiana Poleti; Jessika Cristina Chagas Lesbon; Elisangela Chicaroni Mattos; Cecilia Artico Banho; Livia S Sacchetto; Marilia Mazzi Moraes; Rejane Maria Tommasini Grotto; Jayme A. Souza-Neto; Mauricio L Nogueira; Heidge Fukumasu; Luiz Lehmann Coutinho; Rodrigo Tocantins Calado; Raul Machado Neto; Ana Maria Bispo de Filippis; Rivaldo Venancio da Cunha; Carla Freitas; Cassio Roberto Leonel Peterka; Cassia de Fatima Rangel Fernandes; Wildo Navegantes; Rodrigo Fabiano do Carmo Said; Maria Almiron; Carlos F Campelo de A e Melo; Jose Lourenco; Tulio de Oliveira; Edward C Holmes; Ricardo Haddad; Sandra Coccuzzo Sampaio; Maria Carolina Elias; Simone Kashima; Luiz Carlos Junior Alcantara; Dimas Tadeu Covas.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21264644

Résumé

Brazil has experienced some of the highest numbers of COVID-19 cases and deaths globally and from May 2021 made Latin America a pandemic epicenter. Although SARS-CoV-2 established sustained transmission in Brazil early in the pandemic, important gaps remain in our understanding of virus transmission dynamics at the national scale. Here, we describe the genomic epidemiology of SARS-CoV-2 using near-full genomes sampled from 27 Brazilian states and a bordering country - Paraguay. We show that the early stage of the pandemic in Brazil was characterised by the co-circulation of multiple viral lineages, linked to multiple importations predominantly from Europe, and subsequently characterized by large local transmission clusters. As the epidemic progressed under an absence of effective restriction measures, there was a local emergence and onward international spread of Variants of Concern (VOC) and Variants Under Monitoring (VUM), including Gamma (P.1) and Zeta (P.2). In addition, we provide a preliminary genomic overview of the epidemic in Paraguay, showing evidence of importation from Brazil. These data reinforce the usefulness and need for the implementation of widespread genomic surveillance in South America as a toolkit for pandemic monitoring that provides a means to follow the real-time spread of emerging SARS-CoV-2 variants with possible implications for public health and immunization strategies.

12.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21264408

Résumé

Routine SARS-CoV-2 surveillance in the Western Cape region of South Africa (January-August 2021) found a reduced PCR amplification efficiency of the RdRp gene target of the Seegene, Allplex 2019-nCoV diagnostic assay when detecting the Delta variant. We propose that this can be used as a surrogate for variant detection.

13.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21263564

Résumé

Characterizing SARS-CoV-2 evolution in specific geographies may help predict the properties of variants coming from these regions. We mapped neutralization of a SARS-CoV-2 strain that evolved over 6 months from the ancestral virus in a person with advanced HIV disease. Infection was before the emergence of the Beta variant first identified in South Africa, and the Delta variant. We compared early and late evolved virus to the ancestral, Beta, Alpha, and Delta viruses and tested against convalescent plasma from ancestral, Beta, and Delta infections. Early virus was similar to ancestral, whereas late virus was similar to Beta, exhibiting vaccine escape and, despite pre-dating Delta, strong escape of Delta-elicited neutralization. This example is consistent with the notion that variants arising in immune-compromised hosts, including those with advanced HIV disease, may evolve immune escape of vaccines and enhanced escape of Delta immunity, with implications for vaccine breakthrough and reinfections. HighlightsO_LIA prolonged ancestral SARS-CoV-2 infection pre-dating the emergence of Beta and Delta resulted in evolution of a Beta-like serological phenotype C_LIO_LISerological phenotype includes strong escape from Delta infection elicited immunity, intermediate escape from ancestral virus immunity, and weak escape from Beta immunity C_LIO_LIEvolved virus showed substantial but incomplete escape from antibodies elicited by BNT162b2 vaccination C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=110 SRC="FIGDIR/small/21263564v2_ufig1.gif" ALT="Figure 1"> View larger version (18K): org.highwire.dtl.DTLVardef@1194bfdorg.highwire.dtl.DTLVardef@1cbe318org.highwire.dtl.DTLVardef@aa74f8org.highwire.dtl.DTLVardef@e57969_HPS_FORMAT_FIGEXP M_FIG C_FIG

14.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21262393

Résumé

Genomic sequencing provides critical information to track the evolution and spread of SARS-CoV-2, optimize molecular tests, treatments and vaccines, and guide public health responses. To investigate the spatiotemporal heterogeneity in the global SARS-CoV-2 genomic surveillance, we estimated the impact of sequencing intensity and turnaround times (TAT) on variant detection in 167 countries. Most countries submit genomes >21 days after sample collection, and 77% of low and middle income countries sequenced <0.5% of their cases. We found that sequencing at least 0.5% of the cases, with a TAT <21 days, could be a benchmark for SARS-CoV-2 genomic surveillance efforts. Socioeconomic inequalities substantially impact our ability to quickly detect SARS-CoV-2 variants, and undermine the global pandemic preparedness. One-Sentence SummarySocioeconomic inequalities impacted the SARS-CoV-2 genomic surveillance, and undermined the global pandemic preparedness.

15.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21262342

Résumé

Global genomic surveillance of SARS-CoV-2 has identified variants associated with increased transmissibility, neutralization resistance and disease severity. Here we report the emergence of the PANGO lineage C.1.2, detected at low prevalence in South Africa and eleven other countries. The emergence of C.1.2, associated with a high substitution rate, includes changes within the spike protein that have been associated with increased transmissibility or reduced neutralization sensitivity in SARS-CoV-2 VOC/VOIs. Like Beta and Delta, C.1.2 shows significantly reduced neutralization sensitivity to plasma from vaccinees and individuals infected with the ancestral D614G virus. In contrast, convalescent donors infected with either Beta or Delta showed high plasma neutralization against C.1.2. These functional data suggest that vaccine efficacy against C.1.2 will be equivalent to Beta and Delta, and that prior infection with either Beta or Delta will likely offer protection against C.1.2.

16.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21259017

Résumé

Mauritius, a small island in the Indian Ocean, has had a unique experience of the SARS-CoV-2 pandemic. In March 2020, Mauritius endured a small first wave and quickly implemented control measures which allowed elimination of local transmission of SARS-CoV-2. When borders to the island reopened, it was accompanied by mandatory quarantine and testing of incoming passengers to avoid reintroduction of the virus into the community. As variants of concern (VOCs) emerged elsewhere in the world, Mauritius began using genomic surveillance to keep track of quarantined cases of these variants. In March 2021, another local outbreak occurred, and sequencing was used to investigate this new wave of local infections. Here, we analyze 154 SARS-CoV-2 viral genomes from Mauritius, which represent 12% of all the infections seem in Mauritius, these were both from specimens of incoming passengers before March 2021 and those of cases during the second wave. Our findings indicate that despite the presence of known VOCs Beta (B.1.351) and Alpha (B.1.1.7) among quarantined passengers, the second wave of local SARS-CoV-2 infections in Mauritius was caused by a single introduction and dominant circulation of the B.1.1.318 virus. The B.1.1.318 variant is characterized by fourteen non-synonymous mutations in the S-gene, with five encoded amino acid substitutions (T95I, E484K, D614G, P681H, D796H) and one deletion (Y144del) in the Spike glycoprotein. This variant seems to be increasing in prevalence and it is now present in 34 countries. This study highlights that despite having stopped the introduction of more transmissible VOCs by travel quarantines, a single undetected introduction of a B.1.1.318 lineage virus was enough to initiate a large local outbreak in Mauritius and demonstrated the need for continuous genomic surveillance to fully inform public health decisions.

17.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21258307

Résumé

SARS-CoV-2 variants have emerged that escape neutralization and potentially impact vaccine efficacy. T cell responses play a role in protection from reinfection and severe disease, but the potential for spike mutations to affect T cell immunity is poorly studied. We assessed both neutralizing antibody and T cell responses in 44 South African COVID-19 patients infected either with B.1.351, now dominant in South Africa, or infected prior to its emergence ( first wave), to provide an overall measure of immune evasion. We show for the first time that robust spike-specific CD4 and CD8 T cell responses were detectable in B.1.351-infected patients, similar to first wave patients. Using peptides spanning only the B.1.351 mutated regions, we identified CD4 T cell responses targeting the wild type peptides in 12/22 (54.5%) first wave patients, all of whom failed to recognize corresponding B.1.351-mutated peptides (p=0.0005). However, responses to the mutated regions formed only a small proportion (15.7%) of the overall CD4 response, and few patients (3/44) mounted CD8 responses that targeted the mutated regions. First wave patients showed a 12.7 fold reduction in plasma neutralization of B.1.351. This study shows that despite loss of recognition of immunodominant CD4 epitope(s), overall CD4 and CD8 T cell responses to B.1.351 are preserved. These observations may explain why, despite substantial loss of neutralizing antibody activity against B.1.351, several vaccines have retained the ability to protect against severe COVID-19 disease. One Sentence SummaryT cell immunity to SARS-CoV-2 B.1.351 is preserved despite some loss of variant epitope recognition by CD4 T cells.

18.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21258228

Résumé

While most people effectively clear SARS-CoV-2, there are several reports of prolonged infection in immunosuppressed individuals. Here we present a case of prolonged infection of greater than 6 months with shedding of high titter SARS-CoV-2 in an individual with advanced HIV and antiretroviral treatment failure. Through whole genome sequencing at multiple time-points, we demonstrate the early emergence of the E484K substitution associated with escape from neutralizing antibodies, followed by other escape mutations and the N501Y substitution found in most variants of concern. This provides support to the hypothesis of intra-host evolution as one mechanism for the emergence of SARS-CoV-2 variants with immune evasion properties.

19.
Preprint Dans Anglais | bioRxiv | ID: ppbiorxiv-446516

Résumé

Viruses increase the efficiency of close-range transmission between cells by manipulating cellular physiology and behavior, and SARS-CoV-2 uses cell fusion as one mechanism for cell-to-cell spread. Here we visualized infection using time-lapse microscopy of a human lung cell line and used live virus neutralization to determine the sensitivity of SARS-CoV-2 cell-to-cell spread to neutralizing antibodies. SARS-CoV-2 infection rapidly led to cell fusion, forming multinucleated cells with clustered nuclei which started to be detected at 6h post-infection. To compare sensitivity of cell-to-cell spread to neutralization, we infected either with cell-free virus or with single infected cells expressing on their surface the SARS-CoV-2 spike protein. We tested two variants of SARS-CoV-2: B.1.117 containing only the D614G substitution, and the escape variant B.1.351. We used the much smaller area of single infected cells relative to infection foci to exclude any input infected cells which did not lead to transmission. The monoclonal antibody and convalescent plasma we tested neutralized cell-free SARS-CoV-2, with the exception of B.1.351 virus, which was poorly neutralized with plasma from non-B.1.351 infections. In contrast, cell-to-cell spread of SARS-CoV-2 showed no sensitivity to monoclonal antibody or convalescent plasma neutralization. These observations suggest that, once cells are infected, SARS-CoV-2 may be more difficult to neutralize in cell types and anatomical compartments permissive for cell-to-cell spread.

20.
Eduan Wilkinson; Marta Giovanetti; Houriiyah Tegally; James E San; Richard Lessels; Diego Cuadros; Darren P Martin; Abdel-Rahman N Zekri; Abdoul Sangare; Abdoul Salam Ouedraogo; Abdul K Sesay; Adnene Hammami; Adrienne A Amuri; Ahmad Sayed; Ahmed Rebai; Aida Elargoubi; Alpha K Keita; Amadou A Sall; Amadou Kone; Amal Souissi; Ana V Gutierrez; Andrew Page; Arnold Lambisia; Arash Iranzadeh; Augustina Sylverken; Azeddine Ibrahimi; Bourema Kouriba; Bronwyn Kleinhans; Beatrice Dhaala; Cara Brook; Carolyn Williamson; Catherine B Pratt; Chantal G Akoua-Koffi; Charles Agoti; Collins M Moranga; James D Nokes; Daniel J Bridges; Daniel L Bugembe; Deelan Doolabh; Deogratius Ssemwanga; Derek Tshabuila; Diarra Bassirou; Dominic S.Y. Amuzu; Dominique Goedhals; Dorcas Maruapula; Edith N Ngabana; Eddy Lusamaki; Edidah Moraa; Elmostafa El Fahime; Emerald Jacob; Emmanuel Lokilo; Enatha Mukantwari; Essia Belarbi; Etienne Simon-Loriere; Etile A Anoh; Fabian Leendertz; Faida Ajili; Fares Wasfi; Faustinos T Takawira; Fawzi Derrar; Feriel Bouzid; Francisca M Muyembe; Frank Tanser; Gabriel Mbunsu; Gaetan Thilliez; Gert van Zyl; Grit Schubert; George Githinji; Gordon A Awandare; Haruka Abe; Hela H Karray; Hellen Nansumba; Hesham A Elgahzaly; Hlanai Gumbo; Ibtihel Smeti; Ikhlass B Ayed; Imed Gaaloul; Ilhem B.B. Boubaker; Inbal Gazy; Isaac Ssewanyana; Jean B Lekana-Douk; Jean-Claude C Makangara; Jean-Jacques M Tamfum; Jean M Heraud; Jeffrey G Shaffer; Jennifer Giandhari; Jingjing Li; Jiro Yasuda; Joana Q Mends; Jocelyn Kiconco; Jonathan A Edwards; John Morobe; John N Nkengasong; John Gyapong; John T Kayiwa; Jones Gyamfi; Jouali Farah; Joyce M Ngoi; Joyce Namulondo; Julia C Andeko; Julius J Lutwama; Justin O Grady; Kefenstse A Tumedi; Khadija Said; Kim Hae-Young; Kwabena O Duedu; Lahcen Belyamani; Lavanya Singh; Leonardo de O. Martins; Madisa Mine; Mahmoud el Hefnawi; Mahjoub Aouni; Maha Mastouri; Maitshwarelo I Matsheka; Malebogo Kebabonye; Manel Turki; Martin Nyaga; Matoke Damaris; Matthew Cotten; Maureen W Mburu; Maximillian Mpina; Michael R Wiley; Mohamed A Ali; Mohamed K Khalifa; Mohamed G Seadawy; Mouna Ouadghiri; Mulenga Mwenda; Mushal Allam; My V.T. Phan; Nabil Abid; Nadia Touil; Najla Kharrat; Nalia Ismael; Nedio Mabunda; Nei-yuan Hsiao; Nelson Silochi; Ngonda Saasa; Nicola Mulder; Patrice Combe; Patrick Semanda; Paul E Oluniyi; Paulo Arnaldo; Peter K Quashie; Reuben Ayivor-Djanie; Philip A Bester; Philippe Dussart; Placide K Mbala; Pontiano Kaleebu; Richard Njouom; Richmond Gorman; Robert A Kingsley; Rosina A.A. Carr; Saba Gargouri; Saber Masmoudi; Samar Kassim; Sameh Trabelsi; Sami Kammoun; Sanaa Lemriss; Sara H Agwa; Sebastien Calvignac-Spencer; Seydou Doumbia; Sheila M Madinda; Sherihane Aryeetey; Shymaa S Ahmed; Sikhulile Moyo; Simani Gaseitsiwe; Edgar Simulundu; Sonia Lekana-Douki; Soumeya Ouangraoua; Steve A Mundeke; Sumir Panji; Sureshnee Pillay; Susan Engelbrecht; Susan Nabadda; Sylvie Behillil; Sylvie van der Werf; Tarik Aanniz; Tapfumanei Mashe; Thabo Mohale; Thanh Le-Viet; Tobias Schindler; Upasana Ramphal; Magalutcheemee Ramuth; Vagner Fonseca; Vincent Enouf; Wael H Roshdy; William Ampofo; Wolfgang Preiser; Wonderful T Choga; Yaw Bediako; Yenew K. Tebeje; Yeshnee Naidoo; Zaydah de Laurent; Sofonias K Tessema; Tulio de Oliveira.
Preprint Dans Anglais | medRxiv | ID: ppmedrxiv-21257080

Résumé

The progression of the SARS-CoV-2 pandemic in Africa has so far been heterogeneous and the full impact is not yet well understood. Here, we describe the genomic epidemiology using a dataset of 8746 genomes from 33 African countries and two overseas territories. We show that the epidemics in most countries were initiated by importations, predominantly from Europe, which diminished following the early introduction of international travel restrictions. As the pandemic progressed, ongoing transmission in many countries and increasing mobility led to the emergence and spread within the continent of many variants of concern and interest, such as B.1.351, B.1.525, A.23.1 and C.1.1. Although distorted by low sampling numbers and blind-spots, the findings highlight that Africa must not be left behind in the global pandemic response, otherwise it could become a breeding ground for new variants.

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