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 .
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 .
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.
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
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 . 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 .
These point mutations combined with selection pressure result in the
emergence of new strains equine influenza virus in a process known as
antigenic drift . Antigenic drift is an important feature of
equine influenza when considering vaccination [3, 4, 13].