COVID-19: A state of art on immunological responses, mutations, and treatment modalities in riposte

Abstract

Over the last few years, the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) unleashed a global public health catastrophe that had a substantial influence on human physical and mental health, the global economy, and socio-political dynamics. SARS-CoV-2 is a respiratory pathogen and the cause of ongoing COVID-19 pandemic, which testified how unprepared humans are for pandemics. Scientists and policymakers continue to face challenges in developing ideal therapeutic agents and vaccines, while at the same time deciphering the pathology and immunology of SARS-CoV-2. Challenges in the early part of the pandemic included the rapid development of diagnostic assays, vaccines, and therapeutic agents. The ongoing transmission of COVID-19 is coupled with the emergence of viral variants that differ in their transmission efficiency, virulence, and vaccine susceptibility, thus complicating the spread of the pandemic. Our understanding of how the human immune system responds to these viruses as well as the patient groups (such as the elderly and immunocompromised individuals) who are often more susceptible to serious illness have both been aided by this epidemic. COVID-19 causes different symptoms to occur at different stages of infection, making it difficult to determine distinct treatment regimens employed for the various clinical phases of the disease. Unsurprisingly, determining the efficacy of currently available medications and developing novel therapeutic strategies have been a process of trial and error. The global scientific community collaborated to research and develop vaccines at a neck-breaking speed. This review summarises the overall picture of the COVID-19 pandemic, different mutations in SARS-CoV-2, immune response, and the treatment modalities against SARS-CoV-2.

Keywords: COVID-19; Immunological responses; Mutations; Treatment modalities; Vaccines.

Fig. 1

Illustration of four important structural proteins of SARS-CoV-2.

Fig. 2

: The immune response during the SARS-CoV-2 infection. Where the immune cells and cytokines activate to fight the viral infection, the virus infects an epithelial cell by attaching to the ACE2 receptor with help from the TMPRSS2 receptor. The natural killer (NK) cell recognises an infected cell and releases perforin and granzyme, causing apoptosis. Some viruses get phagocytosed by antigen-presenting cells and present the viral antigen (APC) on their surface. CD8 T-lymphocyte recognises the viral antigen presented on the infected cell surface or the APC, while CD4 + T-lymphocyte recognises the viral antigen presented on the APC and release cytokines causing chain reactions further downstream in the immune system.

Fig. 3

: The immune response during a cytokine storm where the immune system causes damage to the body due to the SARS-CoV-2 infection. During SARS-CoV-2 infection, some infected cells die causing necrosis and releasing damage-associated molecular patterns (DAMPs). The macrophages react to the DAMPs and release cytokines which suppress regulatory T-cells (Treg) and activate other immune cells. This results in a chain reaction of hyper-inflammatory response and causes damage and stress to the body.

Fig. 4

: Type of COVID-19 treatment being studied. Corresponds to the number of safe to proceed INDs. Excludes INDs related to vaccines.

Fig. 5

: Percentage of vaccine candidates in different phases of development.