Inactivated IAV H7N9 Antigen

The Influenza A virus (IAV) from the Orthomyxoviridae family serves as the leading pathogen behind seasonal flu outbreaks and pandemic occurrences. IAV infects a variety of animal species such as birds, pigs and horses while IBV affects only humans which makes IAV a major public health threat because of its ability to spread between different species. The influenza virus produces seasonal outbreaks through antigenic changes but causes worldwide pandemics through genetic reassortment leading to antigenic shift. Infection with IAV leads to an incubation period of 1 to 5 days which then presents as acute high fevers over 38.5°C and symptoms including coughing, throat pain, muscle soreness and overall tiredness. Upper respiratory infections usually heal without any medical intervention yet some patients advance to viral pneumonia or secondary bacterial pneumonia which cause severe complications like ARDS and multi-organ failure. Encephalitis and myocarditis represent the rare serious complications that may affect children and immunocompromised individuals.

The IAV virus consists of eight single-stranded negative-sense RNA segments which encode 11 proteins including HA and NA glycoproteins that define virus subtypes like H1N1 or H3N2. The viral particle which can be spherical or filamentous has diameters from 80 to 120 nm and features a host-derived envelope that holds the HA and NA glycoproteins as well as the M2 ion channel protein. The HA protein binds to sialic acid receptors on host cells to enter the cell while NA protein cleaves those receptors to enable viral release. The viral genetic material RNA becomes encapsulated by nucleoprotein (NP) which together with the polymerase complex (PB1, PB2, PA) forms viral ribonucleoprotein complexes (vRNPs) needed for genome replication. IAV has more HA and NA subtype diversity than IBV with 16 HA and 9 NA subtypes and keeps an animal reservoir in waterfowl which supports its pandemic potential.

Figure 1. The structure of influenza A virus
(Source: Jung HE, et al. 2020)

The eight RNA segments of IAV encode both structural proteins and nonstructural proteins. The viral polymerase uses cap-snatching to steal the 5' cap structure from host mRNA during replication to start viral mRNA synthesis with the help of the host RNA polymerase II system. The HA/NA genes undergo point mutations that cause antigenic drift which leads to seasonal vaccine failures while antigenic shift results from gene reassortment between different subtypes in co-infected hosts producing new subtypes that can trigger pandemics.

Inactivated Influenza A virus H7N9 Antigen