Centre for Epidemic Response and Innovation (CERI)
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The Centre for Epidemic Response and Innovation (CERI) is an academic and research entity that is located within the School for Data Science and Computational Thinking in the Faculty of Science at Stellenbosch University and the laboratories are situated at the state-of-the art facilities at the Tygerberg Medical Campus. CERI’s mission is to strengthen Africa’s capacity to quickly identify and control its own epidemics and pandemics.
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- ItemBA.2.12.1, BA.4 and BA.5 escape antibodies elicited by Omicron infection(Springer Nature, 2022-06-17) Cao, Yunlong; Yisimayi, Ayijiang; Jian, Fanchong; Song, Weiliang; Xiao, Tianhe; Wang, Lei; Du, Shuo; Wang, Jing; Li, Qianqian; Chen, Xiaosu; Yu, Yuanling; Wang, Peng; Zhang, Zhiying; Liu, Pulan; An, Ran; Hao, Xiaohua; Wang, Yao; Wang, Jing; Feng, Rui; Sun, Haiyan; Zhao, Lijuan; Zhang, Wen; Zhao, Dong; Zheng, Jiang; Yu, Lingling; Li, Can; Zhang, Na; Wang, Rui; Niu, Xiao; Yang, Sijie; Song, Xuetao; Chai, Yangyang; Hu, Ye; Shi, Yansong; Zheng, Linlin; Li, Zhiqiang; Gu, Qingqing; Shao, Fei; Huang, Weijin; Jin, Ronghua; Shen, Zhongyang; Wang, Youchun; Wang, Xiangxi; Xiao, Junyu; Xie, Xiaoliang SunneySevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron sublineages BA.2.12.1, BA.4 and BA.5 exhibit higher transmissibility than the BA.2 lineage1. The receptor binding and immune-evasion capability of these recently emerged variants require immediate investigation. Here, coupled with structural comparisons of the spike proteins, we show that BA.2.12.1, BA.4 and BA.5 (BA.4 and BA.5 are hereafter referred collectively to as BA.4/BA.5) exhibit similar binding affinities to BA.2 for the angiotensin-converting enzyme 2 (ACE2) receptor. Of note, BA.2.12.1 and BA.4/BA.5 display increased evasion of neutralizing antibodies compared with BA.2 against plasma from triple-vaccinated individuals or from individuals who developed a BA.1 infection after vaccination. To delineate the underlying antibody-evasion mechanism, we determined the escape mutation profiles2, epitope distribution3 and Omicron-neutralization efficiency of 1,640 neutralizing antibodies directed against the receptor-binding domain of the viral spike protein, including 614 antibodies isolated from people who had recovered from BA.1 infection. BA.1 infection after vaccination predominantly recalls humoral immune memory directed against ancestral (hereafter referred to as wild-type (WT)) SARS-CoV-2 spike protein. The resulting elicited antibodies could neutralize both WT SARS-CoV-2 and BA.1 and are enriched on epitopes on spike that do not bind ACE2. However, most of these cross-reactive neutralizing antibodies are evaded by spike mutants L452Q, L452R and F486V. BA.1 infection can also induce new clones of BA.1-specific antibodies that potently neutralize BA.1. Nevertheless, these neutralizing antibodies are largely evaded by BA.2 and BA.4/BA.5 owing to D405N and F486V mutations, and react weakly to pre-Omicron variants, exhibiting narrow neutralization breadths. The therapeutic neutralizing antibodies bebtelovimab4 and cilgavimab5 can effectively neutralize BA.2.12.1 and BA.4/BA.5, whereas the S371F, D405N and R408S mutations undermine most broadly sarbecovirus-neutralizing antibodies. Together, our results indicate that Omicron may evolve mutations to evade the humoral immunity elicited by BA.1 infection, suggesting that BA.1-derived vaccine boosters may not achieve broad-spectrum protection against new Omicron variants.
- ItemClimate change & epidemics 2023: climade consortium report; summary for policymakers COP28(Centre for Epidemic Response and Innovation, 2023) The Core Writing Team ; De Oliveira, Tulio; Baxter, Cheryl; Huguet, AlexisINTRODUCTION: As the world endeavours to recover from the COVID-19 pandemic, it is crucial to recognize that another crisis, unfolding at an alarming pace, demands our immediate attention. Climate change has assumed a dominant role our lives, causing unprecedented levels of distress. Populations across the globe are grappling with the devastating consequences of extreme climatic events, necessitating efforts to control wildfires, rebuild infrastructure damaged by floods, and adapt to a progressively hotter and more perilous environment. Regrettably, amidst these challenges, there is a looming threat that is being overlooked—the intricate interaction between climate change and infectious diseases. A review has revealed that climate change has the potential to aggravate over 50% of known human pathogens. This distressing phenomenon is not a distant projection but a stark reality currently unfolding before us.