People have different susceptibilities to SARS-CoV-2, the virus behind the COVID-19 pandemic, and develop varying degrees of fever, fatigue, and breathing problems—common symptoms of the illness. What might explain this variation?
Scientists at the University of California, Riverside, and University of Southern California may have an answer to this mystery.
In a paper published in Informatics in Medicine Unlocked, the researchers show for the first time that the observed COVID-19 variability may have underlying molecular sources. The finding could help in the development of effective prophylactic and therapeutic strategies against the disease.
“Based on biomarkers and molecular profiles of individuals, one would hope to develop better medical tests to accommodate these variations in monitoring virus transmission and disease pathology, which helps guide mitigation and treatment options,” said Sika Zheng, an associate professor of biomedical sciences at the UC Riverside School of Medicine, who led the study.
The SARS-CoV-2 virus hijacks human host molecules for fusion and virus replication, attacking human cellular functions. These human host molecules are collectively called SARS-CoV-2 host genes. The researchers systematically analyzed SARS-CoV-2 host gene expression, their variations, and age- and sex-dependency in the human population using large-scale genomics, transcriptomics, and proteomics.
They first found similarity of host gene expression is generally correlated with tissue vulnerability to SARS-CoV-2 infection. Among the six most variably expressed genes in the population they identified ACE2, CLEC4G, and CLEC4M, which are known to interact with the spike protein of SARS-CoV-2. Higher expression of these genes likely increases the possibility of being infected and of developing severe symptoms. Other variable genes include SLC27A2 and