Most scientists are still unable to successfully stop the spread of Coronavirus Disease or prevent infection. Regardless of COVID-19's alterations, HLA-A*01:01 allele bearers' immune systems appear to be better at memorising and recognising it. This indicates that there may be a hereditary basis to severe. In adults with COVID-19, it has been observed that CD4+ and CD8+ T-cell subsets frequently drop in the early phases of the disease. This might have a significant impact on pathogenicity and symptom severity in some people. Innate immunity is crucial to prevent viral replication and elimination, as well as to trigger tissue regeneration and a prolonged immune response. Type I interferons (IFN-I) are necessary in this situation for conferring antiviral activity in host cells. To circumvent IFN antiviral activity, SARS-CoV-2 appears to have developed new mechanisms. Given the complexity of COVID-19 pathophysiology, type I interferons, however, might play different roles at different stages of infection or in mild vs. severe COVID-19 patients. The adaptive immune response, which is primarily composed of B and T cells and plays a crucial role in determining the prognosis of the COVID-19 disease, supports the vaccine's effectiveness. T cells play a critical role in reducing viral loads and suppressing the infection .T cells may detect a wide variety of viral proteins and offer a variety of protection, particularly in perspective of the advent of novel SARSCoV-2 variants. The two main signs of the severe disease, on the other hand, have been identified as being the hyperactivation of effector T cells and a decrease in lymphocytes. The immunity mechanism in COVID-19 is not clearly understood despite these findings.