The emergence of subgenotype ON‐1 of Human orthopneumovirus type A in Riyadh, Saudi Arabia: A new episode of the virus epidemiological dynamic

Abstract

Lower respiratory tract infections caused by Human orthopneumovirus are still a threat to the pediatric population worldwide. To date, the molecular epidemiology of the virus in Saudi Arabia has not been adequately charted. In this study, a total of 205 nasopharyngeal aspirate samples were collected from hospitalized children with lower respiratory tract symptoms during the winter seasons of 2014/15 and 2015/16. Human orthopneumovirus was detected in 89 (43.4%) samples, of which 56 (27.3%) were positive for type A and 33 (16.1%) were positive for type B viruses. The fragment that spans the two hypervariable regions (HVR1 and HVR2) of the G gene of Human orthopneumovirus A was amplified and sequenced. Sequence and phylogenetic analyses have revealed a genotype shift from NA1 to ON‐1, which was prevalent during the winter seasons of 2007/08 and 2008/09. Based on the intergenotypic p‐distance values, ON‐1 was reclassified as a subgenotype of the most predominant genotype GA2. Three conserved N‐glycosylation sites were observed in the HVR2 of Saudi ON‐1 strains. The presence of a 23 amino acid duplicated region in ON‐1 strains resulted in a higher number of O‐glycosylation sites as compared to other genotypes. The data presented in this report outlined the replacement of NA1 and NA2 subgenotypes in Saudi Arabia with ON‐1 within 7 to 8 years. The continuous evolution of Human orthopneumovirus through point mutations and nucleotide duplication may explain its ability to cause recurrent infections.

ON-1 and BA-IX Are the Dominant Sub-Genotypes of Human Orthopneumovirus A&B in Riyadh, Saudi Arabia

“…In the present study, genotype ON1 strains remained the dominant HOPV-A genotype in two epidemic seasons (2019/2020 and 2021/2022). These observations, are in parallel with our previous study where majority of HOPV-A strains were found to be that of ON-1 sub-genotype in Riyadh during winter seasons 2014/2015 and 2015/2016 [ 13 ]. An earlier study reported that 26% of the positive samples clustered in ON-1 sub-genotype in Riyadh between October and December, 2014 [ 30 ].…”

“…These observations are consistent with our previous study where out of 175 samples analyzed, 39 (22.3%) were positive for HOPV (59%) type A and (41%) type B in Riyadh during the winter-spring seasons of 2007/2008 and 2008/2009 [ 12 ]. Furthermore, we also reported that HOPV was found in 89 of 205 (43.4%) samples of which 56 (27.3%) were type A and 33 (16.1%) were type B viruses during the winter seasons of 2014/2015 and 2015/2016 [ 13 ]. In agreement with these findings, the prevalence of HOPV was between 0.2–54% in the children during 1991–2015 in Saudi Arabia [ 29 ].…”

“…Although HOPV-A and B co-circulate during the epidemic type A is slightly more prevalent than B [ 10 ]. We have previously shown that in Saudi Arabia, HOPV-A and B are major circulating subtypes with a slight predominance of HOPV-A responsible for lower respiratory tract infection in hospitalized children (19.3–45.4%) [ 11 , 12 , 13 ].…”

“…We have previously reported that all of the Saudi HOPV-B strains clustered in the BA-IX genotype [ 12 ]. We also reported a genotype shift from NA1 to ON-1 in HOPV-A, which was prevalent during the winter seasons of 2007/2008 and 2008/2009 [ 12 , 13 ]. Here, we examined predominant HOPV subtypes and their genotype variation in the clinical samples collected during two winter seasons of 2019–2020 and 2021–2022 in Riyadh.…”

Sequence and phylogentic analysis of MERS-CoV in Saudi Arabia, 2012–2019

“…Both N-and O-linked oligosaccharides may mask epitopes in certain cases and hence enables the virus to escape the immune system [40,41]. In a previous study, we have reported that the variation in the glycosylation pattern of Saudi HRSV-A strains had a deep impact on virus infectivity and immunogenicity [42]. Here, we report a total of 13 potential N-glycosylation and from 2 to 4 O-linked glycosylation sites in the spike protein.…”