Molecular Epidemiology of Omicron CH.1.1 Lineage: Genomic and Phenotypic Data Perspective

Yasir Mohammed A. Al Qurashi,Jawaher A. Abdulhakim,Samia S. Alkhalil, Maymuna Alansari, Renad Almutiri, Rageed Alabbasi,Manal S. Fawzy

CUREUS JOURNAL OF MEDICAL SCIENCE(2024)

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Abstract
Background: The Omicron variant (B.1.1.529 lineage) of SARS-CoV-2 represents a substantial global health challenge due to its high transmissibility and potential resistance to immunity from vaccines or previous infections. Among the rapidly evolving Omicron lineages, the BA.2.75 and the emerging CH.1.1 have garnered attention. While BA.2.75 is marked by mutations that may enhance immune evasion, CH.1.1 is distinguished by the S: L452R mutation, linked to increased pathogenicity and transmission. Initially identified in India by the end of 2021, these variants have exhibited global dissemination, signaling an urgent need to track and analyze their progression. Methods: In this study, the genomic and geographical distribution data of CH.1.1 were collected from the Global Initiative on Sharing Avian Influenza Data (GISAID), PANGOLIN, CoV-Spectrum, and NextStrain databases. Due to the unavailability of epidemiological and genomic data of the CH.1.1 lineage, PubMed and ScienceDirect were used as sources of the phenotypic data of the lineage variations. Amino acid variations utilized in the data mining included S: R346T, S: K444T, S: L452R, and S: F486S. Results: The current epidemiological data indicate that CH.1.1 is more likely to become one of the dominant spreading lineages in the United Kingdom, New Zealand, Australia, and the United States based on a 32% growth advantage, present CH.1.1 lineage cases number, and the amino acid variation's impact. Conclusion: A significant increase in the newly detected lineage CH.1.1 is highly anticipated. The rise in the detected sequences number from 13,231 on January 21, 2023, to 23,181 on February 6, 2023, supports the prediction and growth advantage of the lineage detected cases. Increases in viral transmissibility caused by higher affinity to ACE2 receptors and immune evasion are deduced from amino acid variations analyzed in the study.
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Key words
s,k444t,f486s,r346t,l452r,ba.2.75,ch.1.1 lineage
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