Molecular features similarities between SARS-CoV-2, SARS, MERS and key human genes could favour the viral infections and trigger collateral effects
Lucas L. Maldonado, Laura Kamenetzky
Received date: 17th September 2020
In December 2019, rising pneumonia cases caused by a novel β-coronavirus (SARS-CoV-2) occurred in Wuhan, China, which has rapidly spread worldwide, causing thousands of deaths. The WHO declared the SARS-CoV-2 outbreak as a public health emergency of international concern, since then several scientists are dedicated to its study. In this work, we analysed 91 molecular features and codon usage patterns for 339 viral genes and 463 human genes that consisted of 677873 codon positions. Human viruses have codon usage biases that match highly expressed proteins in the tissues they infect, therefore, they depend on the host cell machinery for the replication and co-evolution. We selected the highly expressed genes from human lung tissue to perform computational studies that permit to compare their molecular features with those of SARS, SARS-CoV-2 and MERS genes. Hereby, the integrated analysis of all the features revealed that certain viral genes and overexpressed human genes have similar codon usage patterns. The main pattern was the A/T bias that together with other features, could propitiate the viral infection, enhanced by a host dependant specialization of the translation machinery of only some genes. The envelope protein E, the membrane glycoprotein M and ORF7 are further benefited. This could be the key for a facilitated translation and viral replication conducting to different comorbidities depending on the genetic variability of population due to the host translation machinery. This is the first codon usage approach that reveals how codon usage similarities between the host and the viral genes could cause deregulation in the genes translation when the virus is already inside the human cells of the lung tissues. In addition, we provided a list of human genes whose molecular features match those of the viruses and should be considered for genetic association studies to evaluate the susceptibility to respiratory viral infections caused by these viruses. This work leaded to the identification of additional highly expressed human genes which are not the usual suspects but might play a role in the viral infection and settle the basis for further research in the field of human genetics associated with new viral infections.
This is an abstract of a preprint hosted on a preprint server, which is currently undergoing peer review at Scientific Reports. The findings have yet to be thoroughly evaluated, nor has a decision on ultimate publication been made. Therefore, the results reported should not be considered conclusive, and these findings should not be used to inform clinical practice, or public health policy, or be promoted as verified information.