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1.
Tegally, H.; San, J. E.; Cotten, M.; Moir, M.; Tegomoh, B.; Mboowa, G.; Martin, D. P.; Baxter, C.; Lambisia, A. W.; Diallo, A.; Amoako, D. G.; Diagne, M. M.; Sisay, A.; Zekri, A. N.; Gueye, A. S.; Sangare, A. K.; Ouedraogo, A. S.; Sow, A.; Musa, A. O.; Sesay, A. K.; Abias, A. G.; Elzagheid, A. I.; Lagare, A.; Kemi, A. S.; Abar, A. E.; Johnson, A. A.; Fowotade, A.; Oluwapelumi, A. O.; Amuri, A. A.; Juru, A.; Kandeil, A.; Mostafa, A.; Rebai, A.; Sayed, A.; Kazeem, A.; Balde, A.; Christoffels, A.; Trotter, A. J.; Campbell, A.; Keita, A. K.; Kone, A.; Bouzid, A.; Souissi, A.; Agweyu, A.; Naguib, A.; Gutierrez, A. V.; Nkeshimana, A.; Page, A. J.; Yadouleton, A.; Vinze, A.; Happi, A. N.; Chouikha, A.; Iranzadeh, A.; Maharaj, A.; Batchi-Bouyou, A. L.; Ismail, A.; Sylverken, A. A.; Goba, A.; Femi, A.; Sijuwola, A. E.; Marycelin, B.; Salako, B. L.; Oderinde, B. S.; Bolajoko, B.; Diarra, B.; Herring, B. L.; Tsofa, B.; Lekana-Douki, B.; Mvula, B.; Njanpop-Lafourcade, B. M.; Marondera, B. T.; Khaireh, B. A.; Kouriba, B.; Adu, B.; Pool, B.; McInnis, B.; Brook, C.; Williamson, C.; Nduwimana, C.; Anscombe, C.; Pratt, C. B.; Scheepers, C.; Akoua-Koffi, C. G.; Agoti, C. N.; Mapanguy, C. M.; Loucoubar, C.; Onwuamah, C. K.; Ihekweazu, C.; Malaka, C. N.; Peyrefitte, C.; Grace, C.; Omoruyi, C. E.; Rafaï, C. D.; Morang'a, C. M.; Erameh, C.; Lule, D. B.; Bridges, D. J.; Mukadi-Bamuleka, D.; Park, D.; Rasmussen, D. A.; Baker, D.; Nokes, D. J.; Ssemwanga, D.; Tshiabuila, D.; Amuzu, D. S. Y.; Goedhals, D.; Grant, D. S.; Omuoyo, D. O.; Maruapula, D.; Wanjohi, D. W.; Foster-Nyarko, E.; Lusamaki, E. K.; Simulundu, E.; Ong'era, E. M.; Ngabana, E. N.; Abworo, E. O.; Otieno, E.; Shumba, E.; Barasa, E.; Ahmed, E. B.; Ahmed, E. A.; Lokilo, E.; Mukantwari, E.; Philomena, E.; Belarbi, E.; Simon-Loriere, E.; Anoh, E. A.; Manuel, E.; Leendertz, F.; Taweh, F. M.; Wasfi, F.; Abdelmoula, F.; Takawira, F. T.; Derrar, F.; Ajogbasile, F. V.; Treurnicht, F.; Onikepe, F.; Ntoumi, F.; Muyembe, F. M.; Ragomzingba, F. E. Z.; Dratibi, F. A.; Iyanu, F. A.; Mbunsu, G. K.; Thilliez, G.; Kay, G. L.; Akpede, G. O.; van Zyl, G. U.; Awandare, G. A.; Kpeli, G. S.; Schubert, G.; Maphalala, G. P.; Ranaivoson, H. C.; Omunakwe, H. E.; Onywera, H.; Abe, H.; Karray, H.; Nansumba, H.; Triki, H.; Kadjo, H. A. A.; Elgahzaly, H.; Gumbo, H.; Mathieu, H.; Kavunga-Membo, H.; Smeti, I.; Olawoye, I. B.; Adetifa, I. M. O.; Odia, I.; Ben Boubaker, I. B.; Mohammad, I. A.; Ssewanyana, I.; Wurie, I.; Konstantinus, I. S.; Halatoko, J. W. A.; Ayei, J.; Sonoo, J.; Makangara, J. C.; Tamfum, J. M.; Heraud, J. M.; Shaffer, J. G.; Giandhari, J.; Musyoki, J.; Nkurunziza, J.; Uwanibe, J. N.; Bhiman, J. N.; Yasuda, J.; Morais, J.; Kiconco, J.; Sandi, J. D.; Huddleston, J.; Odoom, J. K.; Morobe, J. M.; Gyapong, J. O.; Kayiwa, J. T.; Okolie, J. C.; Xavier, J. S.; Gyamfi, J.; Wamala, J. F.; Bonney, J. H. K.; Nyandwi, J.; Everatt, J.; Nakaseegu, J.; Ngoi, J. M.; Namulondo, J.; Oguzie, J. U.; Andeko, J. C.; Lutwama, J. J.; Mogga, J. J. H.; O'Grady, J.; Siddle, K. J.; Victoir, K.; Adeyemi, K. T.; Tumedi, K. A.; Carvalho, K. S.; Mohammed, K. S.; Dellagi, K.; Musonda, K. G.; Duedu, K. O.; Fki-Berrajah, L.; Singh, L.; Kepler, L. M.; Biscornet, L.; de Oliveira Martins, L.; Chabuka, L.; Olubayo, L.; Ojok, L. D.; Deng, L. L.; Ochola-Oyier, L. I.; Tyers, L.; Mine, M.; Ramuth, M.; Mastouri, M.; ElHefnawi, M.; Mbanne, M.; Matsheka, M. I.; Kebabonye, M.; Diop, M.; Momoh, M.; Lima Mendonça, M. D. L.; Venter, M.; Paye, M. F.; Faye, M.; Nyaga, M. M.; Mareka, M.; Damaris, M. M.; Mburu, M. W.; Mpina, M. G.; Owusu, M.; Wiley, M. R.; Tatfeng, M. Y.; Ayekaba, M. O.; Abouelhoda, M.; Beloufa, M. A.; Seadawy, M. G.; Khalifa, M. K.; Matobo, M. M.; Kane, M.; Salou, M.; Mbulawa, M. B.; Mwenda, M.; Allam, M.; Phan, M. V. T.; Abid, N.; Rujeni, N.; Abuzaid, N.; Ismael, N.; Elguindy, N.; Top, N. M.; Dia, N.; Mabunda, N.; Hsiao, N. Y.; Silochi, N. B.; Francisco, N. M.; Saasa, N.; Bbosa, N.; Murunga, N.; Gumede, N.; Wolter, N.; Sitharam, N.; Ndodo, N.; Ajayi, N. A.; Tordo, N.; Mbhele, N.; Razanajatovo, N. H.; Iguosadolo, N.; Mba, N.; Kingsley, O. C.; Sylvanus, O.; Femi, O.; Adewumi, O. M.; Testimony, O.; Ogunsanya, O. A.; Fakayode, O.; Ogah, O. E.; Oludayo, O. E.; Faye, O.; Smith-Lawrence, P.; Ondoa, P.; Combe, P.; Nabisubi, P.; Semanda, P.; Oluniyi, P. E.; Arnaldo, P.; Quashie, P. K.; Okokhere, P. O.; Bejon, P.; Dussart, P.; Bester, P. A.; Mbala, P. K.; Kaleebu, P.; Abechi, P.; El-Shesheny, R.; Joseph, R.; Aziz, R. K.; Essomba, R. G.; Ayivor-Djanie, R.; Njouom, R.; Phillips, R. O.; Gorman, R.; Kingsley, R. A.; Neto Rodrigues, Rmdesa, Audu, R. A.; Carr, R. A. A.; Gargouri, S.; Masmoudi, S.; Bootsma, S.; Sankhe, S.; Mohamed, S. I.; Femi, S.; Mhalla, S.; Hosch, S.; Kassim, S. K.; Metha, S.; Trabelsi, S.; Agwa, S. H.; Mwangi, S. W.; Doumbia, S.; Makiala-Mandanda, S.; Aryeetey, S.; Ahmed, S. S.; Ahmed, S. M.; Elhamoumi, S.; Moyo, S.; Lutucuta, S.; Gaseitsiwe, S.; Jalloh, S.; Andriamandimby, S. F.; Oguntope, S.; Grayo, S.; Lekana-Douki, S.; Prosolek, S.; Ouangraoua, S.; van Wyk, S.; Schaffner, S. F.; Kanyerezi, S.; Ahuka-Mundeke, S.; Rudder, S.; Pillay, S.; Nabadda, S.; Behillil, S.; Budiaki, S. L.; van der Werf, S.; Mashe, T.; Mohale, T.; Le-Viet, T.; Velavan, T. P.; Schindler, T.; Maponga, T. G.; Bedford, T.; Anyaneji, U. J.; Chinedu, U.; Ramphal, U.; George, U. E.; Enouf, V.; Nene, V.; Gorova, V.; Roshdy, W. H.; Karim, W. A.; Ampofo, W. K.; Preiser, W.; Choga, W. T.; Ahmed, Y. A.; Ramphal, Y.; Bediako, Y.; Naidoo, Y.; Butera, Y.; de Laurent, Z. R.; Ouma, A. E. O.; von Gottberg, A.; Githinji, G.; Moeti, M.; Tomori, O.; Sabeti, P. C.; Sall, A. A.; Oyola, S. O.; Tebeje, Y. K.; Tessema, S. K.; de Oliveira, T.; Happi, C.; Lessells, R.; Nkengasong, J.; Wilkinson, E..
Science ; : eabq5358, 2022.
Article in English | PubMed | ID: covidwho-2029459

ABSTRACT

Investment in SARS-CoV-2 sequencing in Africa over the past year has led to a major increase in the number of sequences generated, now exceeding 100,000 genomes, used to track the pandemic on the continent. Our results show an increase in the number of African countries able to sequence domestically, and highlight that local sequencing enables faster turnaround time and more regular routine surveillance. Despite limitations of low testing proportions, findings from this genomic surveillance study underscore the heterogeneous nature of the pandemic and shed light on the distinct dispersal dynamics of Variants of Concern, particularly Alpha, Beta, Delta, and Omicron, on the continent. Sustained investment for diagnostics and genomic surveillance in Africa is needed as the virus continues to evolve, while the continent faces many emerging and re-emerging infectious disease threats. These investments are crucial for pandemic preparedness and response and will serve the health of the continent well into the 21st century.

2.
Giovanetti, M.; Slavov, S. N.; Fonseca, V.; Wilkinson, E.; Tegally, H.; Patané, J. S. L.; Viala, V. L.; San, E. J.; Rodrigues, E. S.; Santos, E. V.; Aburjaile, F.; Xavier, J.; Fritsch, H.; Adelino, T. E. R.; Pereira, F.; Leal, A.; Iani, F. C. M.; de Carvalho Pereira, G.; Vazquez, C.; Sanabria, G. M. E.; Oliveira, E. C.; Demarchi, L.; Croda, J.; Dos Santos Bezerra, R.; Paola Oliveira de Lima, L.; Martins, A. J.; Renata Dos Santos Barros, C.; Marqueze, E. C.; de Souza Todao Bernardino, J.; Moretti, D. B.; Brassaloti, R. A.; de Lello Rocha Campos Cassano, R.; Mariani, Pdsc, Kitajima, J. P.; Santos, B.; Proto-Siqueira, R.; Cantarelli, V. V.; Tosta, S.; Nardy, V. B.; Reboredo de Oliveira da Silva, L.; Gómez, M. K. A.; Lima, J. G.; Ribeiro, A. A.; Guimarães, N. R.; Watanabe, L. T.; Barbosa Da Silva, L.; da Silva Ferreira, R.; da Penha, M. P. F.; Ortega, M. J.; de la Fuente, A. G.; Villalba, S.; Torales, J.; Gamarra, M. L.; Aquino, C.; Figueredo, G. P. M.; Fava, W. S.; Motta-Castro, A. R. C.; Venturini, J.; do Vale Leone de Oliveira, S. M.; Gonçalves, C. C. M.; do Carmo Debur Rossa, M.; Becker, G. N.; Giacomini, M. P.; Marques, N. Q.; Riediger, I. N.; Raboni, S.; Mattoso, G.; Cataneo, A. D.; Zanluca, C.; Duarte Dos Santos, C. N.; Assato, P. A.; Allan da Silva da Costa, F.; Poleti, M. D.; Lesbon, J. C. C.; Mattos, E. C.; Banho, C. A.; Sacchetto, L.; Moraes, M. M.; Grotto, R. M. T.; Souza-Neto, J. A.; Nogueira, M. L.; Fukumasu, H.; Coutinho, L. L.; Calado, R. T.; Neto, R. M.; Bispo de Filippis, A. M.; Venancio da Cunha, R.; Freitas, C.; Peterka, C. R. L.; de Fátima Rangel Fernandes, C.; Navegantes, W.; do Carmo Said, R. F.; Campelo de, A. E. Melo C. F.; Almiron, M.; Lourenço, J.; de Oliveira, T.; Holmes, E. C.; Haddad, R.; Sampaio, S. C.; Elias, M. C.; Kashima, S.; Junior de Alcantara, L. C.; Covas, D. T..
Nat Microbiol ; 2022.
Article in English | PubMed | ID: covidwho-1991610

ABSTRACT

The high numbers of COVID-19 cases and deaths in Brazil have made Latin America an epicentre of the pandemic. SARS-CoV-2 established sustained transmission in Brazil early in the pandemic, but important gaps remain in our understanding of virus transmission dynamics at a national scale. We use 17,135 near-complete genomes sampled from 27 Brazilian states and bordering country Paraguay. From March to November 2020, we detected co-circulation of multiple viral lineages that were linked to multiple importations (predominantly from Europe). After November 2020, we detected large, local transmission clusters within the country. In the absence of effective restriction measures, the epidemic progressed, and in January 2021 there was emergence and onward spread, both within and abroad, of variants of concern and variants under monitoring, including Gamma (P.1) and Zeta (P.2). We also characterized a genomic overview of the epidemic in Paraguay and detected evidence of importation of SARS-CoV-2 ancestor lineages and variants of concern from Brazil. Our findings show that genomic surveillance in Brazil enabled assessment of the real-time spread of emerging SARS-CoV-2 variants.

3.
Giovanetti, M.; Slavov, S. N.; Fonseca, V.; Wilkinson, E.; Tegally, H.; Patané, J. S. L.; Viala, V. L.; San, J. E.; Rodrigues, E. S.; Vieira Santos, E.; Aburjaile, F.; Xavier, J.; Fritsch, H.; Ribeiro Adelino, T. E.; Pereira, F.; Leal, A.; Campos de Melo Iani, F.; de Carvalho Pereira, G.; Vazquez, C.; Mercedes Estigarribia Sanabria, G.; de Oliveira, E. C.; Demarchi, L.; Croda, J.; Dos Santos Bezerra, R.; Oliveira de Lima, L. P.; Martins, A. J.; Dos Santos Barros, C. R.; Marqueze, E. C.; de Souza Todao Bernardino, J.; Moretti, D. B.; Brassaloti, R. A.; de Lello Rocha Campos Cassano, R.; Drummond Sampaio Corrêa Mariani, P.; Kitajima, J. P.; Santos, B.; Proto-Siqueira, R.; Cantarelli, V. V.; Tosta, S.; Brandão Nardy, V.; Reboredo de Oliveira da Silva, L.; Astete Gómez, M. K.; Lima, J. G.; Ribeiro, A. A.; Guimarães, N. R.; Watanabe, L. T.; Barbosa Da Silva, L.; da Silva Ferreira, R.; MP, F. da Penha, Ortega, M. J.; Gómez de la Fuente, A.; Villalba, S.; Torales, J.; Gamarra, M. L.; Aquino, C.; Martínez Figueredo, G. P.; Fava, W. S.; Motta-Castro, A. R. C.; Venturini, J.; do Vale Leone de Oliveira, S. M.; Cavalheiro Maymone Gonçalves, C.; Debur Rossa, M. D. C.; Becker, G. N.; Presibella, M. M.; Marques, N. Q.; Riediger, I. N.; Raboni, S.; Coelho, G. M.; Cataneo, A. H. D.; Zanluca, C.; Dos Santos, C. N. D.; Assato, P. A.; Allan da Silva da Costa, F.; Poleti, M. D.; Chagas Lesbon, J. C.; Mattos, E. C.; Banho, C. A.; Sacchetto, L.; Moraes, M. M.; Tommasini Grotto, R. M.; Souza-Neto, J. A.; Nogueira, M. L.; Fukumasu, H.; Coutinho, L. L.; Calado, R. T.; Neto, R. M.; Bispo de Filippis, A. M.; Venancio da Cunha, R.; Freitas, C.; Leonel Peterka, C. R.; Rangel Fernandes, C. F.; de Araújo, W. N.; do Carmo Said, R. F.; Almiron, M.; Campelo de Albuquerque, E. Melo C. F.; Lourenço, J.; de Oliveira, T.; Holmes, E. C.; Haddad, R.; Sampaio, S. C.; Elias, M. C.; Kashima, S.; de Alcantara, L. C. J.; Covas, D. T..
PubMed; 2022.
Preprint in English | PubMed | ID: ppcovidwho-332259

ABSTRACT

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.

4.
PubMed; 2021.
Preprint in English | PubMed | ID: ppcovidwho-330706

ABSTRACT

With the emergence of SARS-CoV-2 variants that may increase transmissibility and/or cause escape from immune responses 1-3 , there is an urgent need for the targeted surveillance of circulating lineages. It was found that the B.1.1.7 (also 501Y.V1) variant first detected in the UK 4,5 could be serendipitously detected by the ThermoFisher TaqPath COVID-19 PCR assay because a key deletion in these viruses, spike DELTA69-70, would cause a "spike gene target failure" (SGTF) result. However, a SGTF result is not definitive for B.1.1.7, and this assay cannot detect other variants of concern that lack spike DELTA69-70, such as B.1.351 (also 501Y.V2) detected in South Africa 6 and P.1 (also 501Y.V3) recently detected in Brazil 7 . We identified a deletion in the ORF1a gene (ORF1a DELTA3675-3677) in all three variants, which has not yet been widely detected in other SARS-CoV-2 lineages. Using ORF1a DELTA3675-3677 as the primary target and spike DELTA69-70 to differentiate, we designed and validated an open source PCR assay to detect SARS-CoV-2 variants of concern 8 . Our assay can be rapidly deployed in laboratories around the world to enhance surveillance for the local emergence spread of B.1.1.7, B.1.351, and P.1.

5.
Embase;
Preprint in English | EMBASE | ID: ppcovidwho-327015

ABSTRACT

Omicron has been shown to be highly transmissible and have extensive evasion of neutralizing antibody immunity elicited by vaccination and previous SARS-CoV-2 infection. Omicron infections are rapidly expanding worldwide often in the face of high levels of Delta infections. Here we characterized developing immunity to Omicron and investigated whether neutralizing immunity elicited by Omicron also enhances neutralizing immunity of the Delta variant. We enrolled both previously vaccinated and unvaccinated individuals who were infected with SARS-CoV-2 in the Omicron infection wave in South Africa soon after symptom onset. We then measured their ability to neutralize both Omicron and Delta virus at enrollment versus a median of 14 days after enrollment. Neutralization of Omicron increased 14-fold over this time, showing a developing antibody response to the variant. Importantly, there was an enhancement of Delta virus neutralization, which increased 4.4-fold. The increase in Delta variant neutralization in individuals infected with Omicron may result in decreased ability of Delta to re-infect those individuals. Along with emerging data indicating that Omicron, at this time in the pandemic, is less pathogenic than Delta, such an outcome may have positive implications in terms of decreasing the Covid-19 burden of severe disease.

6.
Embase;
Preprint in English | EMBASE | ID: ppcovidwho-326897

ABSTRACT

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.

7.
MEDLINE;
Preprint in English | MEDLINE | ID: ppcovidwho-325667

ABSTRACT

Omicron variant (B.1.1.529) infections are rapidly expanding worldwide, often in settings where the Delta variant (B.1.617.2) was dominant. We investigated whether neutralizing immunity elicited by Omicron infection would also neutralize the Delta variant and the role of prior vaccination. We enrolled 23 South African participants infected with Omicron a median of 5 days post-symptoms onset (study baseline) with a last follow-up sample taken a median of 23 days post-symptoms onset. Ten participants were breakthrough cases vaccinated with Pfizer BNT162b2 or Johnson and Johnson Ad26.CoV2.S. In vaccinated participants, neutralization of Omicron increased from a geometric mean titer (GMT) FRNT50 of 28 to 378 (13.7-fold). Unvaccinated participants had similar Omicron neutralization at baseline but increased from 26 to only 113 (4.4-fold) at follow-up. Delta virus neutralization increased from 129 to 790, (6.1-fold) in vaccinated but only 18 to 46 (2.5-fold, not statistically significant) in unvaccinated participants. Therefore, in Omicron infected vaccinated individuals, Delta neutralization was 2.1-fold higher at follow-up relative to Omicron. In a separate group previously infected with Delta, neutralization of Delta was 22.5-fold higher than Omicron. Based on relative neutralization levels, Omicron re-infection would be expected to be more likely than Delta in Delta infected individuals, and in Omicron infected individuals who are vaccinated. This may give Omicron an advantage over Delta which may lead to decreasing Delta infections in regions with high infection frequencies and high vaccine coverage.

9.
PubMed; 2021.
Preprint in English | PubMed | ID: ppcovidwho-296585

ABSTRACT

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. Highlights: A prolonged ancestral SARS-CoV-2 infection pre-dating the emergence of Beta and Delta resulted in evolution of a Beta-like serological phenotypeSerological phenotype includes strong escape from Delta infection elicited immunity, intermediate escape from ancestral virus immunity, and weak escape from Beta immunityEvolved virus showed substantial but incomplete escape from antibodies elicited by BNT162b2 vaccination. Graphical abstract:

10.
PubMed; 2021.
Preprint in English | PubMed | ID: ppcovidwho-296584

ABSTRACT

The emergence of the SARS-CoV-2 Omicron variant, first identified in South Africa, may compromise the ability of vaccine and previous infection (1) elicited immunity to protect against new infection. Here we investigated whether Omicron escapes antibody neutralization elicited by the Pfizer BNT162b2 mRNA vaccine in people who were vaccinated only or vaccinated and previously infected. We also investigated whether the virus still requires binding to the ACE2 receptor to infect cells. We isolated and sequence confirmed live Omicron virus from an infected person in South Africa. We then compared neutralization of this virus relative to an ancestral SARS-CoV-2 strain with the D614G mutation. Neutralization was by blood plasma from South African BNT162b2 vaccinated individuals. We observed that Omicron still required the ACE2 receptor to infect but had extensive escape of Pfizer elicited neutralization. However, 5 out of 6 of the previously infected, Pfizer vaccinated individuals, all of them with high neutralization of D614G virus, showed residual neutralization at levels expected to confer protection from infection and severe disease (2). While vaccine effectiveness against Omicron is still to be determined, these data support the notion that high neutralization capacity elicited by a combination of infection and vaccination, and possibly by boosting, could maintain reasonable effectiveness against Omicron. If neutralization capacity is lower or wanes with time, protection against infection is likely to be low. However, protection against severe disease, requiring lower neutralization levels and involving T cell immunity, would likely be maintained.

11.
O'Toole, A.; Hill, V.; Pybus, O. G.; Watts, A.; Bogoch, II, Khan, K.; Messina, J. P.; consortium, Covid- Genomics UK, Network for Genomic Surveillance in South, Africa, Brazil, U. K. Cadde Genomic Network, Tegally, H.; Lessells, R. R.; Giandhari, J.; Pillay, S.; Tumedi, K. A.; Nyepetsi, G.; Kebabonye, M.; Matsheka, M.; Mine, M.; Tokajian, S.; Hassan, H.; Salloum, T.; Merhi, G.; Koweyes, J.; Geoghegan, J. L.; de Ligt, J.; Ren, X.; Storey, M.; Freed, N. E.; Pattabiraman, C.; Prasad, P.; Desai, A. S.; Vasanthapuram, R.; Schulz, T. F.; Steinbruck, L.; Stadler, T.; Swiss Viollier Sequencing, Consortium, Parisi, A.; Bianco, A.; Garcia de Viedma, D.; Buenestado-Serrano, S.; Borges, V.; Isidro, J.; Duarte, S.; Gomes, J. P.; Zuckerman, N. S.; Mandelboim, M.; Mor, O.; Seemann, T.; Arnott, A.; Draper, J.; Gall, M.; Rawlinson, W.; Deveson, I.; Schlebusch, S.; McMahon, J.; Leong, L.; Lim, C. K.; Chironna, M.; Loconsole, D.; Bal, A.; Josset, L.; Holmes, E.; St George, K.; Lasek-Nesselquist, E.; Sikkema, R. S.; Oude Munnink, B.; Koopmans, M.; Brytting, M.; Sudha Rani, V.; Pavani, S.; Smura, T.; Heim, A.; Kurkela, S.; Umair, M.; Salman, M.; Bartolini, B.; Rueca, M.; Drosten, C.; Wolff, T.; Silander, O.; Eggink, D.; Reusken, C.; Vennema, H.; Park, A.; Carrington, C.; Sahadeo, N.; Carr, M.; Gonzalez, G.; Diego, Search Alliance San, National Virus Reference, Laboratory, Seq, Covid Spain, Danish Covid-19 Genome, Consortium, Communicable Diseases Genomic, Network, Dutch National, Sars-CoV-surveillance program, Division of Emerging Infectious, Diseases, de Oliveira, T.; Faria, N.; Rambaut, A.; Kraemer, M. U. G..
Wellcome Open Research ; 6:121, 2021.
Article in English | MEDLINE | ID: covidwho-1450989

ABSTRACT

Late in 2020, two genetically-distinct clusters of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) with mutations of biological concern were reported, one in the United Kingdom and one in South Africa. Using a combination of data from routine surveillance, genomic sequencing and international travel we track the international dispersal of lineages B.1.1.7 and B.1.351 (variant 501Y-V2). We account for potential biases in genomic surveillance efforts by including passenger volumes from location of where the lineage was first reported, London and South Africa respectively. Using the software tool grinch (global report investigating novel coronavirus haplotypes), we track the international spread of lineages of concern with automated daily reports, Further, we have built a custom tracking website (cov-lineages.org/global_report.html) which hosts this daily report and will continue to include novel SARS-CoV-2 lineages of concern as they are detected.

12.
Topics in Antiviral Medicine ; 29(1):89, 2021.
Article in English | EMBASE | ID: covidwho-1250005

ABSTRACT

Background: New SARS-CoV-2 variants with mutations in the spike glycoprotein have arisen independently at multiple locations and may have functional significance. The combination of mutations in the 501Y.V2 variant first detected in South Africa include the N501Y, K417N, and E484K mutations in the receptor binding domain (RBD) as well as mutations in the N-terminal domain (NTD). Here we address whether the 501Y.V2 variant could escape the neutralizing antibody response elicited by natural infection with earlier variants. Methods: We were the first to outgrow two variants of 501Y.V2 from South Africa, designated 501Y.V2.HV001 and 501Y.V2.HVdF002. We examined the neutralizing effect of convalescent plasma collected from adults hospitalized with COVID-19 using a microneutralization assay with live (authentic) virus. Whole genome sequencing of the infecting virus of the plasma donors confirmed the absence of the spike mutations which characterize 501Y.V2. We infected with 501Y.V2.HV001 and 501Y.V2.HVdF002 and compared plasma neutralization to first wave virus which contained the D614G mutation but no RBD or NTD mutations. Results: We observed a reduction in antibody activity ranging from 6-fold to knockout for the 501Y.V2 (B.1.351) relative to the B.1.1 variant derived from the first wave of the pandemic in South Africa. Conclusion: This observation indicates that 501Y.V2 may escape the neutralizing antibody response elicited by prior natural infection. It raises a concern of potential reduced protection against re-infection and by vaccines designed to target the spike protein of earlier SARS-CoV-2 variants.

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