Moscow, Aug 16 : A team of researchers has assessed the effectiveness of the T-cell immune response to 11 variants of SARS-CoV-2 and used their results to develop the T-cell Covid-19 Atlas portal (T-CoV). The findings, published in the journal Nucleic Acids Research, indicates that the continuing emergence of new SARS-CoV-2 mutations allows the virus to spread more effectively and evade the antibodies. However, it is unclear whether new strains are capable of evading T-cell immunity, one of the body's main lines of defence against Covid-19, said the researchers, including Stepan Nersisyan, Faculty of Biology and Biotechnology at HSE University in Moscow, Russia. The development of a T-cell immune response is largely governed by genetic factors, including variations in the genes of the major histocompatibility complex (HLA), the researchers said. Each HLA gene variant has a corresponding molecule that identifies a specific set of peptides (protein) of a virus. There are a huge number of such gene variations, and each person has a unique set of them, added the findings. The effectiveness of the development of T-cell immunity to Covid-19 strains varies from person to person. Depending on the set of HLA molecules, some people's immune systems will identify and destroy a mutated virus with the same efficacy as they would the base form of the virus. In others, the response is less effective. For the study, the team assessed the genetic features of the development of T-cell immunity to 11 main SARS-CoV-2 variants by analyzing the most common HLA gene variants. The researchers used bioinformatics to assess the binding affinities of hundreds of HLA molecule variations and tens of thousands of virus peptides of the main SARS-CoV-2 variants (Alpha, Beta, Gamma, Delta, Epsilon, Zeta, Eta, Theta, Iota, Kappa and Lambda). The team identified the HLA alleles that displayed the most significantly changed set of identified virus peptides. According to scientists, mutated variants may pose a higher risk to people with these alleles. /IANS