Genomic surveillance of severe acute respiratory syndrome coronavirus 2 in Burundi, from May 2021 to January 2022.
The emergence and rapid spread of new severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) variants have challenged the control of the COVID-19 pandemic globally. Burundi was not spared by that pandemic, but the genetic diversity, evolution, and epidemiology of those variants in the country remained poorly understood. The present study sought to investigate the role of different SARS-COV-2 variants in the successive COVID-19 waves experienced in Burundi and the impact of their evolution on the course of that pandemic. We conducted a cross-sectional descriptive study using positive SARS-COV-2 samples for genomic sequencing. Subsequently, we performed statistical and bioinformatics analyses of the genome sequences in light of available metadata.
In total, we documented 27 PANGO lineages of which BA.1, B.1.617.2, AY.46, AY.122, and BA.1.1, all VOCs, accounted for 83.15% of all the genomes isolated in Burundi from May 2021 to January 2022. Delta (B.1.617.2) and its descendants predominated the peak observed in July-October 2021. It replaced the previously predominant B.1.351 lineage. It was itself subsequently replaced by Omicron (B.1.1.529, BA.1, and BA.1.1). Furthermore, we identified amino acid mutations including E484K, D614G, and L452R known to increase infectivity and immune escape in the spike proteins of Delta and Omicron variants isolated in Burundi. The SARS-COV-2 genomes from imported and community-detected cases were genetically closely related.
The global emergence of SARS-COV-2 VOCs and their subsequent introductions in Burundi was accompanied by new peaks (waves) of COVID-19. The relaxation of travel restrictions and the mutations occurring in the virus genome played an important role in the introduction and the spread of new SARS-COV-2 variants in the country. It is of utmost importance to strengthen the genomic surveillance of SARS-COV-2, enhance the protection by increasing the SARS-COV-2 vaccine coverage, and adjust the public health and social measures ahead of the emergence or introduction of new SARS-COV-2 VOCs in the country.
Nduwimana C
，Nzoyikorera N
，Ndihokubwayo A
，Ihorimbere T
，Nibogora C
，Ndoreraho A
，Hajayandi O
，Bizimana JC
，Diawara I
，Niyonizigiye D
，Nyandwi J
... -
《BMC GENOMICS》
SARS-CoV-2 genomic surveillance in Malaysia: displacement of B.1.617.2 with AY lineages as the dominant Delta variants and the introduction of Omicron during the fourth epidemic wave.
This study reported SARS-CoV-2 whole genome sequencing results from June 2021 to January 2022 from seven genome sequencing centers in Malaysia as part of the national surveillance program.
COVID-19 samples that tested positive by reverse transcription polymerase chain reaction and with cycle threshold values <30 were obtained throughout Malaysia. Sequencing of SARS-CoV-2 complete genomes was performed using Illumina, Oxford Nanopore, or Ion Torrent platforms. A total of 6163 SARS-CoV-2 complete genome sequences were generated over the surveillance period. All sequences were submitted to the Global Initiative on Sharing All Influenza Data database.
From June 2021 to January 2022, Malaysia experienced the fourth wave of COVID-19 dominated by the Delta variant of concern, including the original B.1.617.2 lineage and descendant AY lineages. The B.1.617.2 lineage was identified as the early dominant circulating strain throughout the country but over time, was displaced by AY.59 and AY.79 lineages in Peninsular (west) Malaysia, and the AY.23 lineage in east Malaysia. In December 2021, pilgrims returning from Saudi Arabia facilitated the introduction and spread of the BA.1 lineage (Omicron variant of concern) in the country.
The changing trends of circulating SARS-CoV-2 lineages were identified, with differences observed between west and east Malaysia. This initiative highlighted the importance of leveraging research expertise in the country to facilitate pandemic response and preparedness.
Azami NAM
，Perera D
，Thayan R
，AbuBakar S
，Sam IC
，Salleh MZ
，Isa MNM
，Ab Mutalib NS
，Aik WK
，Suppiah J
，Tan KK
，Chan YF
，Teh LK
，Azzam G
，Rasheed ZBM
，Chan JCJ
，Kamel KA
，Tan JY
，Khalilur Rahman O
，Lim WF
，Johari NA
，Ishak M
，Yunos RIM
，Anasir MI
，Wong JE
，Fu JYL
，Noorizhab MNF
，Sapian IS
，Mokhtar MFM
，Md Shahri NAA
，Ghafar K
，Yusuf SNHM
，Noor YM
，Jamal R
，Malaysia COVID-19 Genomics Surveillance Consortium
... -
《-》
A high scale SARS-CoV-2 profiling by its whole-genome sequencing using Oxford Nanopore Technology in Kazakhstan.
Severe acute respiratory syndrome (SARS-CoV-2) is responsible for the worldwide pandemic, COVID-19. The original viral whole-genome was sequenced by a high-throughput sequencing approach from the samples obtained from Wuhan, China. Real-time gene sequencing is the main parameter to manage viral outbreaks because it expands our understanding of virus proliferation, spread, and evolution. Whole-genome sequencing is critical for SARS-CoV-2 variant surveillance, the development of new vaccines and boosters, and the representation of epidemiological situations in the country. A significant increase in the number of COVID-19 cases confirmed in August 2021 in Kazakhstan facilitated a need to establish an effective and proficient system for further study of SARS-CoV-2 genetic variants and the development of future Kazakhstan's genomic surveillance program. The SARS-CoV-2 whole-genome was sequenced according to SARS-CoV-2 ARTIC protocol (EXP-MRT001) by Oxford Nanopore Technologies at the National Laboratory Astana, Kazakhstan to track viral variants circulating in the country. The 500 samples kindly provided by the Republican Diagnostic Center (UMC-NU) and private laboratory KDL "Olymp" were collected from individuals in Nur-Sultan city diagnosed with COVID-19 from August 2021 to May 2022 using real-time reverse transcription-quantitative polymerase chain reaction (RT-qPCR). All samples had a cycle threshold (Ct) value below 20 with an average Ct value of 17.03. The overall average value of sequencing depth coverage for samples is 244X. 341 whole-genome sequences that passed quality control were deposited in the Global initiative on sharing all influenza data (GISAID). The BA.1.1 (n = 189), BA.1 (n = 15), BA.2 (n = 3), BA.1.15 (n = 1), BA.1.17.2 (n = 1) omicron lineages, AY.122 (n = 119), B.1.617.2 (n = 8), AY.111 (n = 2), AY.126 (n = 1), AY.4 (n = 1) delta lineages, one sample B.1.1.7 (n = 1) belongs to alpha lineage, and one sample B.1.637 (n = 1) belongs to small sublineage were detected in this study. This is the first study of SARS-CoV-2 whole-genome sequencing by the ONT approach in Kazakhstan, which can be expanded for the investigation of other emerging viral or bacterial infections on the country level.
Kairov U
，Amanzhanova A
，Karabayev D
，Rakhimova S
，Aitkulova A
，Samatkyzy D
，Kalendar R
，Kozhamkulov U
，Molkenov A
，Gabdulkayum A
，Sarbassov D
，Akilzhanova A
... -
《Frontiers in Genetics》
A bioinformatic analysis of T-cell epitope diversity in SARS-CoV-2 variants: association with COVID-19 clinical severity in the United States population.
Long-term immunity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) requires the identification of T-cell epitopes affecting host immunogenicity. In this computational study, we explored the CD8+ epitope diversity estimated in 27 of the most common HLA-A and HLA-B alleles, representing most of the United States population. Analysis of 16 SARS-CoV-2 variants [B.1, Alpha (B.1.1.7), five Delta (AY.100, AY.25, AY.3, AY.3.1, AY.44), and nine Omicron (BA.1, BA.1.1, BA.2, BA.4, BA.5, BQ.1, BQ.1.1, XBB.1, XBB.1.5)] in analyzed MHC class I alleles revealed that SARS-CoV-2 CD8+ epitope conservation was estimated at 87.6%-96.5% in spike (S), 92.5%-99.6% in membrane (M), and 94.6%-99% in nucleocapsid (N). As the virus mutated, an increasing proportion of S epitopes experienced reduced predicted binding affinity: 70% of Omicron BQ.1-XBB.1.5 S epitopes experienced decreased predicted binding, as compared with ~3% and ~15% in the earlier strains Delta AY.100-AY.44 and Omicron BA.1-BA.5, respectively. Additionally, we identified several novel candidate HLA alleles that may be more susceptible to severe disease, notably HLA-A*32:01, HLA-A*26:01, and HLA-B*53:01, and relatively protected from disease, such as HLA-A*31:01, HLA-B*40:01, HLA-B*44:03, and HLA-B*57:01. Our findings support the hypothesis that viral genetic variation affecting CD8 T-cell epitope immunogenicity contributes to determining the clinical severity of acute COVID-19. Achieving long-term COVID-19 immunity will require an understanding of the relationship between T cells, SARS-CoV-2 variants, and host MHC class I genetics. This project is one of the first to explore the SARS-CoV-2 CD8+ epitope diversity that putatively impacts much of the United States population.
Kim GJ
，Elnaggar JH
，Varnado M
，Feehan AK
，Tauzier D
，Rose R
，Lamers SL
，Sevalia M
，Nicholas N
，Gravois E
，Fort D
，Crabtree JS
，Miele L
... -
《Frontiers in Immunology》
ResearchGate
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