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Gonzalez-Obando, J.;  Forero, J.E.;  Zuluaga-Cabrera, A.M.;  Ruiz-Saenz, J. Equine Influenza Virus. Encyclopedia. Available online: (accessed on 09 December 2023).
Gonzalez-Obando J,  Forero JE,  Zuluaga-Cabrera AM,  Ruiz-Saenz J. Equine Influenza Virus. Encyclopedia. Available at: Accessed December 09, 2023.
Gonzalez-Obando, Juliana, Jorge Eduardo Forero, Angélica M Zuluaga-Cabrera, Julián Ruiz-Saenz. "Equine Influenza Virus" Encyclopedia, (accessed December 09, 2023).
Gonzalez-Obando, J.,  Forero, J.E.,  Zuluaga-Cabrera, A.M., & Ruiz-Saenz, J.(2022, October 26). Equine Influenza Virus. In Encyclopedia.
Gonzalez-Obando, Juliana, et al. "Equine Influenza Virus." Encyclopedia. Web. 26 October, 2022.
Equine Influenza Virus

Equine influenza is a highly contagious disease caused by the H3N8 equine influenza virus (EIV), which is endemically distributed throughout the world. It infects equids, and interspecies transmission to dogs has been reported. The H3N8 Florida lineage, which is divided into clades 1 and 2, is the most representative lineage in the Americas. The EIV infects the respiratory system, affecting the ciliated epithelial cells and preventing the elimination of foreign bodies and substances. Certain factors related to the disease, such as an outdated vaccination plan, age, training, and close contact with other animals, favor the presentation of equine influenza.

equine influenza vaccines H3N8 zoonosis

1. Introduction

Equine influenza is a highly contagious disease distributed worldwide that infects equids [1][2]. New Zealand, Australia, and Iceland are the only territories considered free of the diseases [3][4][5]. The equine influenza virus (EIV) belongs to the Orthomyxoviridae family with a segmented negative RNA genome, which can be subtyped based on two glycoproteins: hemagglutinin (HA) and neuraminidase (NA) [1][3].
This virus, with a diameter of 80–120 nm, is considered one of the most important respiratory viral pathogens in horses. It has been established that EIV evolved from a common ancestral progenitor in the influenza A virus (IAV), with a natural reservoir in aquatic birds sharing the same host cell surface receptors as avian influenza viruses [6][7]. Two different avian-origin interspecies transmission events originated the noncirculating H7N7 subtype in 1956 and H3N8 in 1963 [8][9]. H3N8 is the primary EIV subtype, and this subtype has been divided into two lineages since the 1980s: the American and Eurasian lineages. The American lineage is divided into the Kentucky, South America, and Florida sublineages, whereas the latter is divided into two subtypes: Florida Clade 1 (FC1) and Florida Clade 2 (FC2) [10]. More than 85 outbreaks in Africa, Asia, Europe, and Australia have been attributed to FC1; however, FC2 is predominant in America and Asia [3].

2. Virus Classification

The Orthomyxoviridae family is divided into the genera Alphainfluenzavirus, Betainfluenzavirus, Gammainfluenzavirus, and Deltainfluenzavirus, which are influenza A, B, C, and D, respectively, and are classified according to the antigenic differences in the NP (nucleoprotein of the nucleocapsid) and in the M (matrix protein) [11]. Influenza A subtypes have been classified according to the hemagglutinin (HA-18 subtypes) and neuraminidase (NA-11 subtypes) [12]. Type A viruses primarily infect horses, swine, and humans [13], and the emerging influenza D virus (IDV) can also affect farm animals, including horses, bovines, and swine [14][15]. Recently, in equine populations from the Midwestern United States, the cocirculation of two lineages of IDV was reported, supporting the need for further surveillance of IDV viruses in agricultural species [16].
Influenza A viruses are composed of eight 13.6 KB negative polarity segments [17]. There are ~500 projections in the envelope of the virus, 80% of which correspond to the hemagglutinin protein and the remaining 20% correspond to the neuraminidase protein [10][18] (Figure 1). The proteins encoded by the segmented genome include structural proteins (called HA and NA), nucleoprotein (NP), matrix proteins (M1 and M2), three polymerase proteins (PB1, PB2, and PA), one nuclear export protein (NEP) that is also called nonstructural NS2, and one nonstructural protein called NS1 [11]. HA is an envelope antigenic glycoprotein that can bind to red blood cells, leading to agglutination. It promotes the binding of the virion to cell surface receptors (neuraminic and sialic acid). NA is an envelope protein whose enzymatic activity results in the liquid formation of mucus, thus contributing to the spread of the virus [13][18].
Figure 1. Diagram of the equine influenza virus structure and its genome. The diagram of the virion shows multiple proteins. See text for references.
The H3N8 subtype was isolated in Florida (USA) in 1963 [19]. A phylogenetic analysis of HA determined that H3N8 evolved as a single lineage until the mid-1980s and then diverged into two different evolutionary lineages: an American lineage and a European lineage. Subsequently, the American lineage became a sublineage of South America, Kentucky, and Florida. The Florida sublineage is currently predominant and has diverged into FC1 and FC2 [20]. Currently, the H7N7 subtype is considered to be no longer circulating or extinct in horses, and no known circulation of this subtype has been recorded since the end of the 1970s [21].

3. Replication EIV

After inhaling the virus, most viral particles are captured by the mucosa of the respiratory system. EIV primarily damages the lower respiratory tract of ciliated epithelial cells, resulting in the inability to remove foreign bodies and substances. Early changes caused by the influenza virus in the epithelium of the upper airway are variable, including necrosis followed by desquamation of these cells into the luminal space; necrotic cells may also undergo phagocytosis by macrophages [22].
The HA glycoprotein binds to sialic acid receptors located on the surface of the host cell and subsequently generates the endocytosis of the viral particles, thus leading to an acidic pH [1]. The infection cycle begins when the viral particle binds to the sialic acids of the cell membrane. Endosomal acidification results in a three-dimensional modification of HA, which is crucial for the fusion of viral proteins with the endosomal membranes. Subsequently, the proton channels of the virion (M2) activate because of the dissociation of the vRNP complexes of the M1 matrix proteins that provide stability to the viral architecture by interacting with the viral envelope and nucleocapsid. VRNPs that are released into the cytoplasm are translocated to the nucleus for their transcription and replication. For this purpose, the viral genome uses the import-specific α/β nuclear import system that requires the presence of a nuclear localization signal. Furthermore, NP, M1, and the nuclear export protein (NEP) are also introduced into the nucleus of the host cell [17]. From the viral polymerase complex PB2, PB1, and PA, first, the positive sense copy is synthesized, that is, cRNA, from which copies of the viral RNA are produced. This activity begins when PB2 snatches the 5-cap structure of the host cell’s messenger RNAs, and this transcription stage continues until the polymerase complex is stopped in a polyadenylation signal [23] (Figure 2).
Figure 2. Schematic view of influenza A virus replication within an epithelial cell of the respiratory tract.
NEP (14 kDa, 121 aa) directly binds to the Chromosome Region Maintenance 1 (CRM1) export cells. NEP binds to the M1 protein using its C-terminal domain. Multiple studies have demonstrated that NEP assimilates an adapter between vRNPs and the nuclear export system via a specific signal (NES) [24][25]. NESs are binding sequences rich in hydrophobic amino acids, particularly leucine. The N-terminal domain of NEP mediates the dependent binding of RanGTP to CRM1 and translocates to the cytoplasm through the nucleoporins of the nuclear pore complex (NPC). The hydrolysis of RanGTP to RanGDP leads to the dissociation of the export complex and release of the vRNP viral load in the cytoplasm of the host cell. The virus is later released from the infected cells through budding. This viral replication lasts 6 h [17].
The assembly process of the eight segments is mediated by the M1 and M2 proteins; the latter mediates the incorporation of the vRNPs into the assembled particle, where HA and NA associate with the lipid rafts for subsequent packaging together with the other proteins [1][23].

4. EIV Risk Factors in the Americas

According to the different reported papers in the Americas, different risk factors have been highlighted as remarkably associated with EIV infection and transmission within and between herds.
Age. Younger animals used to have a lower level of EIV antibodies than older individuals, increasing their susceptibility to infection. In Brazil, Daly et al. reported a statistically significant difference (p = 0.001) for the presence of antibodies between horses under 5 years of age and horses between 5 and 14 years of age, who had higher levels of antibodies [20]. In the United States between 2010 and 2013, it was reported that the mean age of horses positive for EIV was 4.7 years: in the multivariate analysis, being between 1 and 5 years was a factor associated with the positive diagnosis for equine influenza with an OR (7.37) and a p value of 0.001, and being between 6 and 10 years old was a factor associated with an OR (8.94) and a p value of 0.001 [26]. In the equine influenza outbreak that occurred in 2012 in Argentina and Uruguay, the most affected animals were those between two and three years of age [27]. Additionally, in the 2018 outbreak in Argentina, the most affected individuals were between 1 and 6 years of age [28]. In Mexico, between 2010 and 2011, a greater presence of antibodies against influenza H3N8 was found in individuals older than 2 years, which indicates that young individuals were more susceptible to the presentation of the disease [29]. Although every age group appeared to be susceptible to EIV, age-dependent susceptibility may be an important feature for epidemiological control and may be related to increased contact and risk with other infected animals [30][31].
In foals, the onset of the adaptive immune response is delayed in comparison to the adult horse. The foal’s adaptive immune response seems to be immature for adaptive immune parameters, such as immunoglobin antibody production and adaptive T-cell responses [32]. Moreover, oxidative stress has been observed in young growing horses that have just started exercise training [33]. These findings could explain, at least in part, the increased susceptibility of young horses to infectious agents such as EIV and the reduced responsiveness of foals to the EIV vaccine. Colostrum maternal antibodies from EIV-vaccinated mares induce protection in the foal [6]; therefore, it is recommended to vaccinate pregnant mares four to six weeks before delivery, which prevents the presentation of severe equine influenza clinical signs in foals [6].
Equine movement and travel. National and international increases in horse movement, especially competition horses, have been related to the transmission and spread of EIV outbreaks and could potentially lead to an increased global spread of infectious equine diseases [34]. In Mexico in 2012, a higher presence of antibodies against equine influenza H3N8 was reported in those horses linked to sports activities such as horse riding (OR = 1.36) and jumping (OR = 1.32), which traveled more due to attendance at sporting events [29]. The relationship between the appearance of influenza outbreaks and the displacement of competing individuals was also reported in Argentina [27].
The 2012 EIV outbreak throughout South America was first reported in Chile in December 2011 and spread rapidly through Chile, Brazil, Uruguay, and Argentina [27][35]. Phylogenetic analysis of the EIV from different countries showed that South American isolates from 2012 were closely related to the 2011–12 isolates from the USA, suggesting that these viruses are likely to have originated from the USA and with a possible importation to Chile and a subsequent spread via travel through South America [35]. Additionally, in 2012, a group of endurance horses were transported from Uruguay to Dubai carrying EIV, highlighting the risk of EIV spread to multiple countries via international travel [36].
In Chile, in the 2018 outbreak, most of the EIV-positive horses were competitive, either from polo, jumping, or racing sports. The outbreak rapidly spread across Chile, facilitated by the rodeo season, which increases horse movement [37]. The analyzed phylogenetic relationship with international sequences showed that this new introduction of EIV to South America was related to concurrent outbreaks occurring globally in Europe, Asia, and North America and introduced to the country as a result of international horse movements [37], as has been previously reported for EIV and other equine infectious diseases [34].
Vaccination status. Despite the availability of EIV vaccines, multiple challenges remain to achieving effective immunization in horses and control of EIV, including the evolution of the virus, vaccine breakdown, vaccination-induced short-lived immunity, the inability of vaccines to induce sterilizing immunity, and, in young horses, interference with maternally derived immunity [6]. Antigenic differences between field strains and vaccine strains may affect vaccine efficacy due to a low specific immune response [38], with low to mild cases even in vaccinated animals but reducing severe disease. In Latin America, the use of outdated vaccine strains, incomplete EIV vaccination programs, or updated vaccines without sufficient antibody production may be a contributing factor to the presence of the disease [28][35][37].
The first outbreak in South America in which the presence of cases due to an ineffective vaccination program was evident was in Chile in 1963 with the introduction of H3N8 EIV strains into a population [27]. In 2015 in Brazil, 37.5% of infected horses were vaccinated with outdated strains (A/equine/Kentucky/97, A/equine/SouthAfrica/4/2003, A/equine/Kentucky/94) [39]. For the 2018 Argentinean outbreak, it was reported that 76% of affected horses had been vaccinated with outdated A/eq/Kentucky/1997 strains [1][28]. The situation was similar in Uruguay in 2018, for which the authors mention that many of the vaccines distributed in this country were outdated, associating them with the presentation of the outbreak [40].
Although infection has been reported in vaccinated animals, it is clear that most of the cases during an outbreak belong to EIV-unvaccinated animals [6][38]. As the rate of change in HA/NA leading to antigenic drift is slower in EIV than in human influenza viruses, it is accepted that relatively “old” vaccine strains could protect horses longer than is known for humans. However, those strains will be antigenically no longer representative of EIV circulating strains and will become obsolete as vaccine strains sooner or later [41][42]. In addition, EIV vaccine efficacy also depends on the vaccine adjuvant, which is included to stimulate the equine immune response to the target antigen either in the whole inactivated or subunit virus vaccines and modified viral vector vaccines [38].
Low herd immunity. To date, vaccination remains one of the most efficient methods of prevention against several major equine infectious diseases; however, the establishment of efficacious and long-lasting protective immunity at the herd level is a complex issue. Herd immunity reduces the size and frequency of epizooties at the population level and reduces virus shedding; however, sterilizing immunity is rarely observed, and vaccine breakdown may possibly occur [43]. High levels of vaccine coverage (80–90%) have been reported to be required to provide herd immunity against infection [43][44].
For the 2018 Chilean outbreak, it was concluded that one of the causes associated with the spread of EIV in the country was the low vaccine coverage, especially in thoroughbreds. In Chile, equine vaccination is not mandatory, and in the country, there is only an average of 58,000 doses available per year, that is, enough doses for 20% of the total equine population being too low to achieve a constant herd level of protection [45]. In Mexico, in 2015, 114 equine samples with clinical signs associated with influenza were investigated, and of those, 75% were positive for equine influenza: none of the equines were vaccinated against equine influenza [46]. Even in the United States, 85% of horses positive for H3N8 EIV (60/761) had no or undetermined vaccination status [26]. In Canada, in a study conducted on 23 respiratory outbreaks that occurred between 2003 and 2005, it was reported that only 36% of horses were vaccinated against equine influenza [47]. These results highlight the fact that there is not enough vaccine coverage in the Americas to avoid or prevent a possible vaccine breakthrough. Additionally, achieving a protective herd immunity level should be the most important factor associated with the presentation of EIV outbreaks in the Americas.
Some of these risk factors have been extensively reported for IAV infections in humans, which are mainly related to international travel and outbreaks appearing through contact with fomites or microdroplets from infected individuals [48].


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