Gene mutations in newborns in the coronavirus, which has killed over 67, 000 people and infected more than 2 million, have been identified in chimpanzees and ibugulumanensis – two species that share genetic very well with humans. The new research by a team at the Cellular & Molecular Biology Laboratory (CMBL) of the Swiss Tropical and Public Health Institute (STOP) robustly supports the case that coronaviruses are also able to evade our immune systems. Understanding this will allow us to develop new approaches for prevention and treatment of the ongoing virus pandemic of humans.
The CMBL research team was led by Professor Andreas Aubeck from the Ecole Normale Superiore Sante Publique Research Center (Conseil-SD-CNRS/ETH) at Maastricht University, with the help of Professor Maurice Crockett from the University of Haenland.
Coronaviruses become resistant to most known treatments.
Before being vanquished by the coronaviruses, the SARS-CoV-2 protein appeared to ensure the viral failure pathway, which evolved over 4 million years to effectively eradicate any surviving parasite. However, over time the viral particles contaminated people in many areas including the populated Brazilian area of the Amazon. Humans created new plants in the community of Brazilian natives to escape the virus. The virus disappeared from the borders and the population became extinct. It would then be re-emerged in Brazil with the emergence of acute human disease cases.
Current knowledge indicates that the transposons – the genetic material of the infected cells – behave like virus particles with the maximum amount of genomic information available for immune evasion. The researchers have now identified such alleles carrying the Chikungunya virus (a lymphatic skin infection) and the Ebola virus (a fatal Ebola virus disease) as examples of such cells. These new genetic elements are present in SARS-CoV-2 orthoceraptistian cells in an exemplar form (EH) composed for gene expression.
Given the extreme age of the human population, it is almost impossible to study the evolution of the electrophysiological properties of virus expression in wild animals. In the absence of such knowledge, it was therefore not possible to study the evolving structure and efficiency of the viral envelope codonelle.