Emergence of a novel swine-origin influenza A virus (S-OIV) H1N1 virus in humans

Abstract

A recently emerged novel influenza A H1N1 virus continues to spread globally. The virus contains a novel constellation of gene segments, the nearest known precursors being viruses found in swine and it likely arose through reassortment of two or more viruses of swine origin. H1N1, H1N2 and H3N2 subtype swine influenza viruses have occasionally infected humans before but such zoonotic transmission-events did not lead to sustained human-to-human transmission in the manner this swine-origin influenza virus (S-OIV) has done. Its transmission among humans appears to be higher than that observed with seasonal influenza. Children and young adults appear to those most affected and also those who appear to maintain transmission. Clinical disease generally appears mild but complications leading to hospitalization can occur, especially in those with underlying lung or cardiac disease, diabetes or those on immunosuppresive therapies. There are concerns that the virus may reassort with existing human influenza virus giving rise to more transmissible or more pathogenic viruses. The virus appears to retain the potential to transmit back to swine and thus continued reassortment with swine viruses is a cause for concern.

Naturally Occurring Mutations in the PA Gene Are Key Contributors to Increased Virulence of Pandemic H1N1/09 Influenza Virus in Mice

“…he outbreak of H1N1/09 influenza in North America in April 2009 marked the global spread of the virus as the first pandemic of the 21st century (1,2). Although most H1N1/09 infections were mild (1,3), experts estimated that 284,500 people died from the virus in the first 12 months of its circulation (4).…”

Molecular Docking Study of Naturally-derived Neuraminidase Inhibitors Isolated from Phellinus Baumii

“…The subtypes of Influenza A virus are classified based on the combination of the virus coat glycoproteins on its surface namely Hemagglutinin (HA) and Neuraminidase (NA) which are essential for the infectious cycle of influenza virus. There are 16 different HA antigens (H1-H16) and 9 different NA antigens (N1-N9) for Influenza A virus [1,2] . Hemagglutinin is a lectin that binds sialic acid on host cell membrane.…”

Crucial role of PA in virus life cycle and host adaptation of influenza A virus

“…Further [118][119][120] PA-svRNA Promotes genome replication and maintains segment balance through allosteric modulation of polymerase activity [121,122] PA-MCM Acts as a scaffold between the nascent RNA chains and the viral polymerase to promote viral replication [123] PA-HAX1 Impedes nuclear transportation of PA and inhibits viral replication [124,125] PA-PB1-RanBP5 Acts as an import factor for the newly synthesized polymerase by targeting the PB1-PA dimer to the nucleus [126] PA-CPSF30-NS1A Stabilizes the CPSF30-NS1A complex that inhibits the 3′-end processing of all cellular pre-mRNAs [127] study demonstrated that not only the well-established virulence marker PB2 627K but also PA F666L implicates in the virulence discrepancy of these two viruses. except for the contribution of the adaptive mutations, the whole PA segment also affects IAv adaptation in mammals, especially during genetic reassortment [61][62][63][64][65][66][67]. In some cases, co-existence of homologous PB2 and PA is required for efficient virus replication, suggesting the functional cooperation between these two proteins during the generation of viable reassortant viruses [61][62][63][64].…”