**3.2 Replication**

Untranslated regions of RNA (UTRs) have 5′ and 3′ viruses that carry RNA-specific signals. The 5′ capped coronavirus genome compromise a 3' UTR *SARS-CoV-2 and Coronavirus Ancestors under a Molecular Scope DOI: http://dx.doi.org/10.5772/intechopen.95102*

**Figure 5.** *Phylogenetic tree of 160 SARS-CoV-2 genomes [33].*

consisting of 300 to 500 nucleotides) in addition to a poly(A) tail. Host-related factors involving two class-II viruses bovine coronavirus (BCV) and Mouse Hepatitis Coronavirus (MHV) were studied, in order to better understand coronavirus replication. Using gel mobility shift assays unique host protein interactions were identified with BCV 3' UTR [287 nt plus poly(A) tail]. The MHV 3′ -UTR [301 nt in addition to poly(A) tail] rivalry indicates that interactivity for the two viruses are preserved. UV cross-linking studies observed proteins with molecular masses of 99, 95 and 73 kDa. The ranges 40- to 50 and 30 kDa even contained less heavily labeled proteins. For binding the 73-kDa protein a poly(A) tail was needed. The 73 kDa proteins have been identified as cytoplasmic poly(A)-binding protein (PABP) by an Immuno-precipitation of UV-cross-linked proteins. To define the significance of the poly(A) tail, the replication of the impaired genomes BCV Drep and MHV MIDI-C was used alongside with several mutants. After transfection to the supporting virus-infected cells, the defect genomes with shortened, 5- or 10-A poly(A) tails have been replicated. BCV Drep RNA lacking a poly(A) tail did not replicate while MHV MIDI-C RNA replication was detected with a deleted tail after multiple mutations of the virus. The kinetics of replication is delayed in both mutants. Noticeable extension or addition of the poly(A) tail in mutants in the replication assay associated with the presence of these RNAs. RNAs exhibit less in vitro PABP binding in shorted Poly(A) tails, indicating decreased RNA replication interactions with protein. The data show strongly that the poly(A) tail is a significant indication for the replication of coronavirus [34]. The virus initiates replication and assembly of protein that is followed by the release of new infectious particles into novel target cells. These events are followed by proinflammation chemokines and cytokines producing and triggering which lead to significant pulmonary damage-causing atypical pneumonia with quick abnormalities and failure [35, 36].
