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The emergence of subgenotype ON‐1 of Human orthopneumovirus type A in Riyadh, Saudi Arabia: A new episode of the virus epidemiological dynamic
Author(s) -
Farrag Mohamed A.,
Amer Haitham M.,
Aziz Ibrahim M.,
Alsaleh Asma N.,
Almajhdi Fahad N.
Publication year - 2020
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.25643
Subject(s) - hypervariable region , genotype , biology , molecular epidemiology , virology , phylogenetic tree , population , virus , respiratory tract infections , genetics , gene , medicine , respiratory system , environmental health , anatomy
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.