EQUINE INFLUENZA - OVERVIEW

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Equine Influenza is highly contagious and is responsible for most upper respiratory tract disease in horses [1, 2, 3].  It is caused by members of the Influenza A genus of the Orthomyxoviridae [3, 4] (ortho = right or proper and myxo = snotty so orthomyxovirdae means right and properly snot producing) family of viruses.  Orthomyxoviridae are linear, negative-sense, single stranded RNA viruses. Outside of their hosts (horses for equine influenza) viruses exist as virions.  These are minute inert particles composed of genetic material embedded in a protein coat which are referred to as nucleocapsids.  In the case of equine influenza the nucleocapsid is additionally surrounded by a delicate lipid envelope [5].  

Influenza virions first attach to the surface of respiratory epithelial cells then use their lipid envelopes to fuse with the lipid outer membrane of the cell to gain entry to the cell where they are released into the cell interior.  At this point the virus comes to life, taking over the metabolic machinery of the host cell in order to replicate its genome, and produce its own proteins in order to create new nucleocapsids.  As a final insult the nucleocapsids remove a piece of the host cell membrane as they leave the cell becoming fully infective virions which may continue to infect other respiratory epithelial cells of the host or may pass out into the environment, particularly through coughing, to infect other horses.  Infected host epithelial cells are destroyed in this process, which in conjunction with the response of the horse’s immune system, creates the disease experienced by the horse [6].

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The incubation period of equine influenza is 1 to 3 days after infection at which point most horses develop fever, lose appetite, cough and may have discharge from their nostrils or eyes.  This phase usually lasts between one or two weeks and most horses resolve the infection on their own.  Young, old or immuno-compromised individuals are at risk of developing pneumonia due to secondary bacterial infections or rarely other complications such as edema, myocarditis or encephalitis.  Once recovered from infection by equine influenza virus, athletic horses may not be able to effectively return to work for several weeks [3, 7].
 
There are two important proteins embedded in the surface of the lipid envelope.  They are hemagglutinin (H or HA) which is used by the virion to attach to cells in the upper respiratory tract and neuraminidase (N or NA) which is required for release of newly manufactured virions from an infected cell.

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The genome of influenza virus is segmented into eight pieces.  Hemagglutinin and neuraminidase are coded on different segments which allows reassortment (mixing) of different types of proteins should different types of equine influenza virus infect the same individual.  In horses there are two types of hemagglutinin (HA3 and HA7) and two types of neuraminidase (N7 and N8).  These different types of hemagglutinin and neuraminidase are referred to as serotypes and are identified by the presence of different types of neutralizing antibodies in the horse’s blood [8].  

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Antibodies are specialized proteins produced by the bodies’ immune system that very precisely bind to specific proteins on the virion.  These proteins are referred to as antigens.  Antibodies against hemagglutinin protect from infection by equine influenza virus by preventing the virion from attaching to cells.  Antibodies against neuraminidase limit infection by preventing escape of virions from an infected cell.  This type of response by the immune system is referred to as humeral immunity.  There are other antigenic proteins in the equine influenza virion that stimulate cell mediated immunity (CMI) which appears to provide a more powerful and longer lasting defence on the part of the host [3, 9].
 
Selection pressure imposed against equine influenza virus by the immune system of horses favors virions that have subtle changes in their antigenic proteins that impair the ability of the immune system to recognize and neutralize the virions [10, 11].  This is particularly true of hemagglutinin and neuraminidase where extensive vaccination may have a role the selection pressure along with other factors which are not well understood but help maintain circulation within the equine population of a wide variety of equine influenza strains [12].  The main mechanism behind these alterations of virion proteins is point mutations in the viral genome caused by errors in genetic replication, which is a feature of RNA viruses [7].  These point mutations combined with selection pressure result in the emergence of new strains equine influenza virus in a process known as antigenic drift [13].  Antigenic drift is an important feature of equine influenza when considering vaccination [3, 4, 13].


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