SARS-CoV-2 codon usage bias downregulates host expressed genes with similar codon usage

L. DIAMBRA; ALONSO, ANDRES M.

Cold Spring Harbor

Congreso; COVID/SARS CoV2 Rapid Research Reports #3; 2020

Cold Spring Harbor Laboratory

ABSTRACTSARS-CoV-2 is the pathogenic agent of COVID-19 which infects pulmonary cells with great effectiveness. In this study we focus on the codoncomposition for the viral proteins and its relationship with the proteins synthesis of the host. SARS-CoV-2 preferred codons have poor representationof G or C nucleotides in the third position, a characteristic which could conduct to an unbalance in the tRNAs pools of the infected cells with seriousimplications in host protein synthesis. By integrating this observation with proteomic data from infected cells, we observe a reduced translation rateof host proteins associated with highly expressed genes, and that they share the codon usage bias of the virus. The functional analysis of thesegenes suggests that this mechanism of epistasis can contribute to understanding how this virus evades the immune response, and the etiology ofsome deleterious collateral effect, as results of the viral replication. The concomitant paper was published.