Coronavirus disease (COVID-19) outbreak

Mechanism for SARS-CoV and SARS-CoV-2

The infected ratio of the COVID-19 has been remarkable compared to SARs-CoV. One of the proteins which are present in COVID-19, known as Nsp2 & 3 protein; mainly consists of mutation attached with the ability of the Coronavirus to be more infectious. Moreover, some proteins are very much different from COVID-19 proteins i.e. orf8 & orf10. These types of proteins are mostly easy to understand the living function of the particular protein structures. According to a study, a cleavage locus is observed in the COVID-19 virus (furin), which is not present in the SARS-CoV. So, this may be the dialectics behind the raised virulence of COVID-19 viruses.

The coronavirus especially, beta-coronaviruses goes through with some processes to enroll in host cells and initiate the affecting host cells. The main reason behind this mechanism is the Novel coronaviruses tether with the ACE2 receptor located in the alveoli of the lungs and respiratory tract. The main mechanism behind the SARS-CoV is the protease cut the Spike protein into S1 & S2 domains, and that cleavage evokes a structural modification that initiates the S2 domain. And this whole process is followed by the enroll of FP into the membrane cells which promote the entry of the virus into cells. And it is also possible that Novel coronaviruses use the same process or mechanism to enroll the viral cells into host cells.

According to this mechanism, if the virus enrolls in the host cell, ACE2 will cleaved through ADAM17 into the extra membrane matrix and leads to alveoli bruises & increase permeability. And this might be done by the ACE2 which converts angiotensin 1 to angiotensin II. Further, once the virus enters into proteins of the cell, the protein known as ORF3a is produced and cipher the calcium ion channels which is very much similar to SARS and Novel coronaviruses. TRAF3 & ORF3a both are responsible for the inflammasome complex which leads to the second signal like caspases inactivation, free radical productions, and interleukins productions in Cytokines. In this mechanism, all these molecular pathways combined together which targeting the respiratory problems, the main symptoms of COVID-19. In viral infection mechanism, the main part is the interaction of viral cells with the host cell nucleases. And a study reveals that COVID-19 may use protease which is familiar to SARS-CoV like Plasmin and Furin in the cleavage of the S protein to enroll the virus into host cells.

In case of MERS (Middle East Respiratory Syndrome), the enrollment of MERS-CoV to the host cells through its type-1 transmembrane glycoprotein also known as S protein or spike protein. MERS can also enter the cells by an auxiliary pathway via cell surface transmembrane protease. The host protease cleaves the Spike protein into 2 functional domains which are distinctive from each other, denoted as S1 subunit & S2 subunit and the transmembrane domains. The fusion of the membrane is conciliated through main structural changes which showed the fusion peptide resulting in the production of a six-helix bundle. The depth of 6HB made up of triple-stranded coiled like structure constructed by 3 Spike subunits which formed the trimmers. The main part of the Life cycle of MERS is fusion with plasma membrane i.e. the fusion of spike protein to the membrane of the host for the formation of the double-membrane vesicle in the host cells. The RNA of the virus undergoes multiplication process and initiates transcription followed by a translation mechanism. After assembly and packaging of viral cells and lastly through exocytosis and MERS-CoV is released out of the host cells