The conserved L1089 in the S2 subunit of avian infectious bronchitis virus determines viral kidney tropism by disrupting virus-cell fusion

The S2 Subunit of Infectious Bronchitis Virus Affects Abl2-Mediated Syncytium Formation

“…Despite the mutation to rare amino acids in rSczy3S2 -G543S-Q544S-S553T-F557Y at the cleavage site in the front part of the protein, this process may cause a decrease in the performance of the S2 protein and result in a decrease in the formation of syncytia. The mutations G543S, Q544S, S553T, and F557Y, which are all from the non-adapted strain CN of CEKs and are situated near the S1/S2 cleavage site, might be responsible for this activity [ 5 ]. The mutations of S2 subunit change its conformation or function, which could impede the activity of ABI1 and NCKAP1 pathway, likely causing the lessening of syncytia ( Figure 5 B).…”

“…As previously mentioned, CN is a type of infectious bronchitis virus (IBV) that is unable to infect CEKs. Following a sequence assessment and investigation, CN strain of IBV was used as the benchmark for the mutations G543S, Q544S, S553T, and F557Y in rSczy3, leading to the generation of rSczy3S2 -G543S-Q544S-S553T-F557Y (TCID 50 /mL = 10 3.5 ) [ 5 ]. Successive passages of Sczy3 with CEKs 100 times led to the creation of zy100, which is a variant of zy30 with a distinct S2 subunit that could generate bigger and greater numbers of syncytia when infected with CEKs.…”

“…The fusion peptides located on the S2 subunit point to its involvement in membrane fusion processes, the creation of viral syncytia, and cytophilicity [ 4 ]. The S2 subunit of IBV is essential for the fusion of the viral envelope with the host cell membrane, which permits the virus to discharge its genome into the host cell [ 5 ]. IBV mainly enters through clathrin-mediated endocytosis (CME), and viral particles move forward along the classical endosomal/lysosomal pathway, where viral particles can penetrate the cell and cause active cytoskeletal rearrangements [ 6 ].…”

“…[ 7 ]. Our earlier studies revealed that S2 mutated strains had dissimilar viral titers, generated irregular syncytia, and showed various levels of pathogenicity in living organism trials [ 5 , 8 ].However, the cause of this phenomenon was not fully elucidated due to a lack of investigation into the role of the S2 subunit. Gaining insight into how S2 subunit mutations affect viral infection can be facilitated through studying the contribution of the S2 subunit to syncytium formation.…”

Global Emergence of Infectious Bronchitis Virus Variants: Evolution, Immunity, and Vaccination Challenges

“…The S2 subunit is a highly conserved part formed primarily by the heptad repeat regions, HRP1 and HRP2, and a fusion peptide that is responsible mainly for the viral entry and membrane fusion [48]. Research has shown that the S2 subunit is responsible for viral adaptation to various cell lines [52][53][54][55][56][57][58]. The S2 subunit also contains some minor neutralizing epitopes and contributes to the avidity and specificity of virus attachment, and thus viral host range [51].…”