SARS-CoV-2 “Mexican variant” sequence analysed by researchers

A research group has analysed over one million SARS-CoV-2 genome sequences, identifying a new variant that over the past weeks has been spreading mostly in Mexico but has also been found in Europe. With the scientific name T478K, the team found that like other strains, this variant presents a mutation in the Spike (S) protein, which allows coronaviruses to attach to and penetrate their targeted cells.

The study was conducted at the Department of Pharmacy and Biotechnology of the University of Bologna, Italy. 

“This variant has been increasingly spreading among people in North America, particularly in Mexico. To date, this variant covers more than 50 percent of the existing viruses in this area. The rate and speed of the spread recall those of the ‘British variant’,” said Professor Federico Giorgi, the study co-ordinator. “The mutation of the S protein is structurally located in the region of interaction with human receptor angiotensin-converting enzyme 2 (ACE2). Coronaviruses attach to this receptor to infect cells, thus spreading the infection with more efficacy.”

The researchers started from the analysis of almost 1.2 million sequenced samples of the SARS-CoV-2 genome found in international databases until 27 April 2021. The new T478K variant was detected in 11,435 samples. This is double the number of samples that presented the same variant just a month earlier. Such an increase since the beginning of 2021 alarmed the researchers.

T478K spreads evenly across males and females and age ranges. This variant represents 52.8 percent of all sequenced coronaviruses in Mexico, whereas in the US it shows up only in 2.7 percent of the sequenced samples. In Europe, this variant has spread feebly in Germany, Sweden and Switzerland. In Italy is virtually non-existent with only four reported cases.

The researchers tested the action of the T478K S protein with in silico simulations and found out that this mutated protein can alter the superficial electrostatic charge. Consequently, it can change not only the interaction with the ACE2 human protein but also with the antibodies of the immune system and thus hinder drug efficacy.

“Thanks to the great amount of data available in international databases, we can hold an almost real-time control over the situation by monitoring the spread of coronavirus variants across different geographical areas,” concluded Giorgi. “Keeping up this effort in the next months will be crucial to act promptly and with efficient means.”

The study was published in the Journal of Medical Virology.