Emergence of Novel Coronavirus and COVID-19: whether to stay or die out?

Abstract

The last century has witnessed several assaults from RNA viruses, resulting in millions of death throughout the world. The 21st century appears no longer an exception, with the trend continued with escalated fear of SARS coronavirus in 2002 and further concern of influenza H5N1 in 2003. A novel influenza virus created the first pandemic of the 21st century, the pandemic flu in 2009 preceded with the emergence of another deadly virus, MERS-CoV in 2012. A novel coronavirus "SARS-CoV-2" (and the disease COVID-19) emerged suddenly, causing a rapid outbreak with a moderate case fatality rate. This virus is continuing to cause health care providers grave concern due to the lack of any existing immunity in the human population, indicating their novelty and lack of previous exposure. The big question is whether this novel virus will be establishing itself in an endemic form or will it eventually die out? Endemic viruses during circulation may acquire mutations to infect naïve, as well as individual with pre-existing immunity. Continuous monitoring is strongly advisable, not only to the newly infected individuals, but also to those recovered individuals who were infected by SARS-CoV-2 as re-infection may lead to the selection of escape mutants and subsequent dissemination to the population.

Keywords: COVID-19; Coronavirus; SARS; SARS-CoV-2; pre existing immunity.

Figure 1.

Relationship between high and low CFR virus infection and outbreak outcome. When viruses with low CFR infect an individual, gradually, it induces the host immune system. The induced immunity may enable the spread of mutant viruses in the population, whereas viruses with high CFR causes robust infection and rapid immune responses leading to death. Imprisonment of the different viral species within the dead host will lead to a reduction in the diverse or mutant virus population in the circulation result the outbreak to its conclusion.

Figure 2.

Schematic presentation of coronavirus genome orientation. SARS-coronavirus (SARS-CoV), MERS-coronavirus (MERS-CoV) and novel coronavirus (SARS-CoV-2).

Figure 3.

Phylogenetic analysis of coronaviruses. Phylogenetic tree constructed based on the spike gene using MEGA 6 software with the neighbor-joining method and 1000 bootstrap values. Novel coronavirus, SARS-CoV-2 symbolises as a solid circle and bat-derived coronaviruses symbolises as a solid hexagonal shape.

Figure 4.

Immunopathogenesis of Coronavirus infection. Robust viral replication in the lung causes activation of alveolar macrophages and epithelial cell damages which, results in the induction of inflammatory cytokines and release upon activation through innate immune receptors. Cyclic amplification of inflammatory responses lead to pneumonia and hypoxia as depicted in figure. Alveolar Epithelial Cells (AEC); Red Blood Cells (RBCs).

Figure 5.

Viral selection during an outbreak. Host induces immune response when infected by the virus, which can protect the individual from the same virus but not from the mutated one. Reservoir host allows the virus to replicate and mutate, leading to an expansion in viral diversity with altered antigenicity within the viral pool. The antigenically mutated virus can be selected when it infects a host with pre-existing immunity towards the earlier strain. This will allow the selection of mutated viruses within a host and dissemination if the mutant virus remains contagious.

Figure 6.

Transmission pattern of SARS-coronavirus (SARS-CoV), MERS-coronavirus (MERS-CoV and novel coronavirus, SARS-CoV-2.