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Equine influenza virus (EIV) remains one of the most economically devastating respiratory pathogens in the global equine industry. As the causative agent of a highly contagious acute respiratory disease, EIV is responsible for significant morbidity in immunologically naïve or improperly vaccinated equine populations. The pathogen spreads rapidly through aerosolized droplets, particularly in environments characterized by high animal density and frequent global movement, such as racetracks, equestrian competitions, and breeding facilities. An outbreak of equine flu can paralyze equestrian activities on a national scale, leading to the cancellation of major sporting events, profound veterinary costs, and severe financial losses due to training interruptions. In an era of unprecedented international horse transport, understanding the virology, pathogenesis, and evolutionary dynamics of EIV is a critical priority for veterinary surveillance networks, immunologists, and agricultural policymakers. This review explores the biological mechanisms of EIV, its current epidemiological landscape, and the ongoing challenges in vaccine development and diagnostic interventions.
Equine influenza is caused by an RNA virus belonging to the Orthomyxoviridae family, specifically classified as Influenza A. Historically, two distinct subtypes of Influenza A were known to infect horses: H7N7 (formerly equine-1) and H3N8 (formerly equine-2). However, the H7N7 subtype has not been isolated from horses since the late 1970s and is now presumed to be extinct in the equine population. Consequently, all contemporary global outbreaks of equine influenza are driven exclusively by the H3N8 subtype.
The viral particle is pleomorphic, featuring a host-derived lipid envelope studded with two critical major surface glycoproteins: Hemagglutinin (HA) and Neuraminidase (NA). The HA protein is the primary viral adhesin and the major target for the host's neutralizing antibodies. It initiates infection by binding with high affinity to sialic acid receptors linked to galactose via an α(2→3) linkage, which are abundantly expressed on the apical surface of the ciliated epithelial cells lining the equine respiratory tract. Following receptor binding and endocytosis, the acidic environment of the endosome triggers a profound conformational change in the HA protein, mediating the fusion of the viral envelope with the endosomal membrane and releasing the viral ribonucleoprotein (vRNP) complexes into the host cell cytoplasm for subsequent nuclear transport and replication.
Conversely, the NA protein functions as a receptor-destroying enzyme. Once new viral particles are assembled at the host cell membrane, NA cleaves the terminal sialic acid residues, releasing the nascent virions and preventing their aggregation, thereby allowing the virus to spread efficiently through the respiratory mucus to infect adjacent healthy cells.
Figure 1. Diagram of the equine influenza virus structure and its genome
(Source: Gonzalez-Obando J, et al. 2022)
The pathogenesis of EIV is characterized by rapid viral replication and severe, localized tissue damage. Following the inhalation of infectious aerosols, the virus predominantly targets the ciliated epithelial cells of the upper and lower respiratory tract, including the trachea and bronchi. The explosive replication cycle of the virus induces widespread cytopathology, leading to the rapid apoptosis and desquamation (shedding) of the respiratory epithelium.
This massive cellular destruction drastically impairs the mucociliary escalator—the lung's primary mechanical defense system. The loss of ciliated cells means that mucus, cellular debris, and inhaled environmental particulate matter can no longer be efficiently cleared from the lower airways. Clinically, this manifests within a short incubation period of 24 to 48 hours as a high, biphasic fever, profound lethargy, anorexia, and a characteristic harsh, dry, paroxysmal cough. Serous nasal discharge is common initially, which may become mucopurulent as the disease progresses.
Furthermore, the destruction of the epithelial barrier and the virus-induced suppression of localized immune responses render the horse highly susceptible to secondary bacterial infections. Opportunistic pathogens naturally residing in the equine upper respiratory tract, such as Streptococcus equi subspecies zooepidemicus, can easily invade the compromised lower airways, leading to severe bacterial pneumonia, pleuropneumonia, and potentially fatal outcomes, particularly in foals and geriatric animals. The recovery of the respiratory epithelium is a slow process, often requiring a minimum of three weeks, during which the animal must be strictly rested to prevent chronic respiratory disease.
Like all Influenza A viruses, EIV exhibits a high mutation rate due to the lack of proofreading activity in its RNA-dependent RNA polymerase. This continuous accumulation of point mutations within the HA and NA genes leads to a phenomenon known as "antigenic drift." As the structural conformation of the HA protein gradually changes, the virus becomes capable of evading pre-existing neutralizing antibodies generated by prior infections or outdated vaccines.
This evolutionary mechanism has led to the divergence of the H3N8 subtype into distinct phylogenetic lineages. In the late 1980s, the virus diverged into the "American" and "Eurasian" lineages. Subsequently, the American lineage further evolved into the "South American," "Kentucky," and "Florida" sublineages. Today, the Florida sublineage is the overwhelmingly dominant strain circulating globally, and it has further bifurcated into two distinct clades: Florida Clade 1 (FC1) and Florida Clade 2 (FC2).
Historically, FC1 was predominantly endemic to North and South America, while FC2 circulated primarily in Europe and Asia. However, the globalization of equestrian sports has thoroughly blurred these geographical boundaries. For instance, massive outbreaks in Europe and the United Kingdom in 2019 were driven by the incursion of highly virulent FC1 strains into populations that were primarily vaccinated against FC2, highlighting the rapid and unpredictable nature of global viral dissemination.
Figure 2. Recent evolution of H3N8 influenza virus.
(Source: Wasik BR, et al. 2023)
Given the rapid transmission rate of EIV, swift and accurate diagnostics are imperative for the implementation of effective quarantine and biosecurity protocols. Clinical suspicion based on a sudden onset of fever and coughing in a group of horses must be immediately confirmed through laboratory testing.
The current gold standard for EIV diagnosis is real-time reverse transcription-polymerase chain reaction (rRT-PCR). Conducted on deep nasopharyngeal swabs taken during the acute febrile phase of the illness, rRT-PCR offers exceptional sensitivity and specificity. It allows for the rapid detection of viral RNA and can be multiplexed to differentiate EIV from other pathogens in the equine respiratory disease complex, such as Equine Herpesvirus (EHV-1 and EHV-4) and Streptococcus equi.
For stall-side diagnostics, rapid antigen detection ELISAs targeting the conserved viral nucleoprotein are available. While these provide results within minutes and are highly useful in field outbreak scenarios, they generally exhibit lower sensitivity than PCR, meaning negative results in symptomatic horses should ideally be confirmed with molecular testing. Ongoing genomic surveillance, heavily coordinated by the World Organisation for Animal Health (WOAH, formerly OIE) Expert Surveillance Panel, relies on the continuous sequencing of viral isolates from global outbreaks to monitor antigenic drift and track clade movements.
Vaccination remains the cornerstone of EIV prevention and control. The primary goal of equine influenza vaccination is not necessarily to provide sterilizing immunity—as mucosal respiratory infections are notoriously difficult to completely block—but rather to reduce the severity of clinical signs, shorten the duration of illness, and critically, minimize the shedding of infectious virions into the environment to maintain herd immunity.
Various vaccine platforms are currently utilized in veterinary medicine, including whole-inactivated virus vaccines (often adjuvanted with immunostimulating complexes), live-attenuated intra-nasal vaccines, and recombinant viral vector technologies that express the specific HA glycoproteins of circulating strains. Despite high vaccination coverage in many elite equestrian sectors, "vaccine breakdown" remains a persistent challenge. This occurs when the viral strains circulating in the field have antigenically drifted too far from the seed strains included in commercial vaccines.
To combat this, the WOAH continuously reviews global surveillance data and issues formal recommendations regarding the composition of equine influenza vaccines, currently advising the inclusion of representative strains from both Florida Clade 1 and Clade 2. Looking toward the future, the rapid development platforms seen in human medicine, specifically mRNA technology, hold immense promise for veterinary applications. An mRNA-based equine influenza vaccine could hypothetically be updated within weeks to perfectly match a newly emerged drifted strain, bypassing the lengthy manufacturing processes associated with traditional egg-based or cell-culture vaccine production.
Until such novel therapeutics become widely available, stringent biosecurity remains the ultimate defense. The rigorous quarantine of new arrivals, the isolation of febrile animals, the utilization of dedicated equipment, and the maintenance of current vaccination status are non-negotiable practices for safeguarding the health and economic stability of the global equine industry.
References
| Target | Cat. No. | Product Name | Host | Isotype | Application | |
| IAV | CABT-ZB105 | Mouse Anti-EIV H3 hemagglutinin monoclonal antibody, clone D-3713 | Mouse | IgG1 | IA | Inquiry |
| IAV | CABT-ZB104 | Mouse Anti-EIV H7 hemagglutinin monoclonal antibody, clone D-6026 | Mouse | IgG1 | IA | Inquiry |
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