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Review
. 2018 Sep 6;9:1941.
doi: 10.3389/fmicb.2018.01941. eCollection 2018.

A Comprehensive Review on Equine Influenza Virus: Etiology, Epidemiology, Pathobiology, Advances in Developing Diagnostics, Vaccines, and Control Strategies

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Free PMC article
Review

A Comprehensive Review on Equine Influenza Virus: Etiology, Epidemiology, Pathobiology, Advances in Developing Diagnostics, Vaccines, and Control Strategies

Raj K Singh et al. Front Microbiol. .
Free PMC article

Abstract

Among all the emerging and re-emerging animal diseases, influenza group is the prototype member associated with severe respiratory infections in wide host species. Wherein, Equine influenza (EI) is the main cause of respiratory illness in equines across globe and is caused by equine influenza A virus (EIV-A) which has impacted the equine industry internationally due to high morbidity and marginal morality. The virus transmits easily by direct contact and inhalation making its spread global and leaving only limited areas untouched. Hitherto reports confirm that this virus crosses the species barriers and found to affect canines and few other animal species (cat and camel). EIV is continuously evolving with changes at the amino acid level wreaking the control program a tedious task. Until now, no natural EI origin infections have been reported explicitly in humans. Recent advances in the diagnostics have led to efficient surveillance and rapid detection of EIV infections at the onset of outbreaks. Incessant surveillance programs will aid in opting a better control strategy for this virus by updating the circulating vaccine strains. Recurrent vaccination failures against this virus due to antigenic drift and shift have been disappointing, however better understanding of the virus pathogenesis would make it easier to design effective vaccines predominantly targeting the conserved epitopes (HA glycoprotein). Additionally, the cold adapted and canarypox vectored vaccines are proving effective in ceasing the severity of disease. Furthermore, better understanding of its genetics and molecular biology will help in estimating the rate of evolution and occurrence of pandemics in future. Here, we highlight the advances occurred in understanding the etiology, epidemiology and pathobiology of EIV and a special focus is on designing and developing effective diagnostics, vaccines and control strategies for mitigating the emerging menace by EIV.

Keywords: control; diagnosis; epidemiology; equine; influenza virus; pathogenesis; prevention; vaccine.

Figures

Figure 1
Figure 1
Structure of Equine Influenza Virus. EIV is a segmented RNA virus possessing eight (single) segmented negative sense RNA strands. Segmented genome encodes eight structural proteins and at least two non-structural proteins.
Figure 2
Figure 2
Phylogenetic analysis of hemagglutinin (HA) genes nucleotide sequences from 57 Equine Influenza Viruses (EIVs). The maximum likelihood tree was constructed using stringent T92 + G algorithm which was identified using the find best DNA/protein model tool available in MEGA 6. The reliability of the trees was assessed by bootstrap with 1,000 replications with cut off at 50 are shown in the tree. The phylogram depicts five major clusters of global EIVs. Phylogenetic group's viz., Florida sub-lineage clade 1, Florida sub-lineage clade 2, American, Eurasian and Pre-divergent, are mentioned by bars on the right. The major mutations (I179V and A144V) observed in the Clade 2 viruses of Florida sublineage in recent isolates have been denoted by solid dots.
Figure 3
Figure 3
Transmission of EIV. Droplet infection is an important mode of transmission. Transmission between animals includes crowded housing practices, non-vaccination, young horses of 1–5 years and international trade. Dog gets EIV by consuming infected dead horse meat.
Figure 4
Figure 4
Replication and pathogenesis of EIV. EIV damages the upper and lower respiratory tract's ciliated epithelial cells thereby causes inability to clear foreign substances. Spike glycoprotein HA fastens to the receptors present on the respiratory epithelial cells and it enters the cells by endocytosis. After endocytosis, EIV undergoes fusion and uncoating. Opening of M2 channel leads to proton entry and subsequent release of viral RNA followed by synthesis of viral structures leading to assembly of EIV. EIV is released from the infected cells by the process of budding.
Figure 5
Figure 5
Different vaccine platforms available for EIV. Platforms include killed vaccine, inactivated vaccine, subunit vaccine, DNA vaccine, subunit vaccine, vectored vaccine, reverse genetics-based vaccine.

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