Equine Viral Arteritis

(Epizootic Cellulitis-Pinkeye, Equine Typhoid, Rotlaufseuche)

ByPeter J. Timoney, MVB, PhD, FRCVS
Reviewed/Revised Mar 2021

Equine viral arteritis (EVA) is an economically important, contagious, viral disease of equids caused by equine arteritis virus (EAV). Exposure to EAV may result in clinical or more frequently, asymptomatic infection, depending on the virus strain, host genetic factors, and various management and environmental factors. EAV infection can cause abortion, respiratory illness, establishment of a carrier state in stallions, and interstitial pneumonia and death in young foals. Diagnosis of EVA is based on virus detection in body secretions or fluids, whole blood, or tissues by virus isolation, RT-PCR and in situ hybridization; identification of viral antigen in tissues; and detection of viral-specific antibodies by serology. The treatment of EVA is general supportive care during the acute phase of infection. There is no treatment to eliminate persistent infection in stallions. Attenuated and inactivated vaccines are available in North America and Europe, respectively, for prevention and control.

Although equine arteritis virus (EAV) infection is restricted almost exclusively to equids (horses, donkeys, mules, and zebras), limited data suggest the host range may also extend to alpacas and llamas. EAV is known to be present in equine populations in many countries worldwide, with the notable exceptions of Japan, Iceland, and New Zealand, which successfully eradicated the disease. The prevalence of infection varies widely both between countries and among breeds in the same country. It is frequently highest in Standardbreds and Warmbloods. Despite the widespread global distribution of EAV, laboratory-confirmed outbreaks of equine viral arteritis (EVA) are relatively uncommon. However, this situation appears to be changing in more recent years, with an increase in the number of verified occurrences of the disease being reported. A major factor contributing to this change is the continued escalation in the volume of international horse movements and trade in equine germplasm.

Etiology and Pathogenesis of Equine Viral Arteritis

Equine arteritis virus is a small, enveloped, positive-sense, single-stranded RNA virus. EAV has been reclassified as a member of the subfamily Equarterivirinae, genus Alphaarterivirus, in the order Nidovirales, and renamed as Alphaarterivirus equid. The viral genome is approximately 12.7 kb and contains at least 10 open reading frames (ORFs). ORFs 1a and 1b encode two polyproteins that are processed into 13 nonstructural proteins. The remaining ORFs 2a, 2b, 3, 4, 5a, 5b, 6, and 7 encode seven envelope structural proteins (E, GP2, GP3, GP4, ORF5a protein, GP5, and M) and the nucleocapsid N protein. The major neutralization determinants of the virus are located in the N-terminal ectodomain of GP5.  Phylogenetic analysis based on partial ORF5 sequences segregates EAV isolates from around the world into North American (NA) and European (EU) lineages, with each of these lineages further subdivided into two North American (NA-1 and NA-2) and European (EU-1 and EU-2) clades. Although, there is only one known serotype of EAV, the prototype Bucyrus strain, genomic and antigenic variation exists among temporally and geographically different strains of the virus. EAV field strains have been shown to differ in their virulence, pathogenicity and neutralization phenotypes. Thus, some field strains of EAV are capable of causing moderate to severe clinical signs whereas others only induce mild clinical disease.

EAV is readily inactivated by lipid solvents and by common disinfectants and detergents. The virus survives 75 days at 4°C, 2–3 days at 37°C, and 20–30 minutes at 56°C. EAV can maintain infectivity in tissues and various body fluids, including semen, for years when stored at -70°C or below.

After respiratory exposure, EAV invades the upper and lower respiratory tract and multiplies in nasopharyngeal epithelium and tonsillar tissue and in bronchial and alveolar macrophages. Infected CD14+ monocytes and a small subpopulation of CD3+ T lymphocytes transport EAV to the regional lymph nodes (eg, bronchial lymph node), where it undergoes a further cycle of replication before being released into the bloodstream.

The cell-associated viremia that follows ensures dissemination of EAV throughout the body. By day 6–8, the virus localizes in the vascular endothelium and medial myocytes of the smaller blood vessels, especially the arterioles, and causes a panvasculitis. It can also be found in the epithelium of certain tissues, particularly the adrenals, seminiferous tubules, thyroid, and liver. Vascular lesions include endothelial swelling and degeneration, neutrophilic infiltration, and necrosis of the tunica media of affected vessels. These lesions give rise to edema and hemorrhage, which are believed to result from activation of the proinflammatory cytokines IL-1 beta, IL-6, IL-8, and possibly TNF-alpha. Maximal vascular injury occurs by about day 10, after which lesions begin to resolve. Except in certain infected stallions that become carriers of the virus, EAV is no longer detectable in tissues and body fluids beyond day 28 after primary infection.

The virus causes abortion in pregnant mares, and abortion rates during natural outbreaks of EVA can vary from < 10%–71%. EAV-induced abortions can occur at any time between 2 and 10 months of gestation without premonitory signs. However, the pathogenesis of fetal infection and the mechanism responsible for abortion is poorly characterized. EAV is vertically transmitted to the fetus as evidenced by the high viral titers and abundance of viral antigen in fetal membranes and diverse fetal tissues. It is speculated that abortion occurs as a consequence of vasculitis of myometrial blood vessels and myometrial necrosis, which leads to placental dysfunction and chorionic detachment.

Following natural EAV infection, 10%–70% of stallions become persistently infected and continuously shed virus in their semen for either a short (ranging from several weeks to < 1 year, defined as short-term shedders [STS] or short-term carriers) or a long period of time (> 1year to lifelong; defined as longterm persistently infected [LTPI] shedders or carriers) without adverse effects on semen quality or reproductive capacity. The carrier state has been confirmed in sexually mature intact males, specifically postpubertal colts and stallions, but not in mares, geldings, sexually immature colts, or fillies. The establishment and LTPI of EAV in the reproductive tract of stallions is testosterone-dependent and, therefore, does not cause persistent infection in mares, foals, and sexually immature colts. The virus persists exclusively in the male reproductive tract despite the presence of high levels of neutralizing and mucosal antibodies, and a moderate to severe inflammatory response. The analysis of multiple tissues from the reproductive tract of EAV carrier stallions unequivocally confirmed the ampullae as the primary site of EAV persistence. EAV infects vimentin-positive fibrocytes and mononuclear cells (T and B lymphocytes and macrophages) but not in the ampullae's glandular epithelium.

It has been demonstrated that the establishment of EAV LTPI correlates with the in vitro susceptibility of a subpopulation of CD3+ T lymphocytes to EAV infection and, consequently, stallions with the CD3+ T lymphocyte susceptibility phenotype are at higher risk of becoming LTPI carriers compared to those that lack this phenotype. Thus, variation in the frequency of the carrier state in certain horse breeds has been shown to be related to the distribution of CD3+ T lymphocyte cell populations susceptible or resistant to infection with EAV. A genome-wide association study demonstrated that these phenotypes are associated with the CXCL16 gene located on equine chromosome 11. Subsequently, studies have identified two allelic variants of CXCL16 (CXCL16S and CXCL16R) that differ by four nonsynonymous nucleotide substitutions in exon 1. Of the two encoded proteins, the CXCL16S isoform has EAV receptor activity and is associated with the CD3+ T lymphocyte susceptible phenotype and establishment of LTPI in stallions; whereas the CXCL16R isoform lacks receptor activity and results in a CD3+ T lymphocyte resistant phenotype and early viral clearance in stallions (short-term carriers of the virus).

Carrier stallions also serve as the principal means by which genetic diversification of EAV can occur, with potential emergence of novel viral variants. It has been shown that persistent infection is characterized by extensive genome-wide purifying selection mediated by intrahost selective pressures; nucleotide substitutions occurring in nonstructural protein-2 encoding region of ORF1a, ORF3, and ORF5 have been found to be important in the evolution of EAV in carrier stallions over time. 

Epidemiology and Transmission of Equine Viral Arteritis

The epidemiology of equine viral arteritis involves virus-, host-, and environment-related factors that include variability in pathogenicity among naturally occurring strains of the virus, modes of transmission, occurrence of the carrier state in stallions, and the nature of acquired immunity to infection. Outbreaks of EVA are most often linked to the movement of infected animals or the shipment of virus-contaminated semen (chilled or frozen) and frozen embryos.

Transmission of EAV can occur by respiratory, venereal, and congenital routes or by indirect means. Spread by the respiratory route is the principal mode of dissemination of the virus during the acute phase of infection. It is primarily responsible for transmission of EAV among susceptible equids kept in close contact (eg, at racetracks, shows, sales, veterinary hospitals, and under conditions of intensive management on breeding farms). It can also occur through contact with placenta, placental fluids, and tissues of EAV abortions. EAV can also be transmitted venereally during natural or artificial insemination with infective semen from acutely and persistently infected stallions. Mares can be readily infected by the venereal route after breeding to a carrier stallion either by live cover or artificial insemination with fresh-cooled or cryopreserved semen. There is limited evidence that EAV can be spread through embryo transfer. It is important to emphasize that infection can also be spread through indirect contact with virus-contaminated fomites (eg, breeding shed equipment, buckets, shanks, or twitches) or on the hands, apparel, or footwear of animal handlers.

The carrier stallion is the natural reservoir of EAV and is responsible for its dissemination and persistence in equine populations. Persistently infected stallions shed EAV constantly in the sperm-rich fraction of the semen but not in any other secretions or excretions. Persistent EAV infection clears spontaneously in a variable percentage of stallions, with no evidence of subsequent reversion to a shedding state. Whereas acutely infected stallions may experience a period of subfertility that can last for up to 4 months, existence of the carrier state does not appear to impair the fertility of infected stallions nor otherwise adversely affect their health.

Compared with other equine respiratory viruses, EAV stimulates a stronger, longer-lasting immunity that is protective against development of clinical disease, including abortion and establishment of the carrier state in stallions. High levels of neutralizing antibodies that frequently persist for at least 2–3 years can be stimulated by natural exposure to the virus and by vaccination.

Clinical Findings of Equine Viral Arteritis

Clinical signs of equine viral arteritis vary considerably among individual horses and among outbreaks. Exposure to equine arteritis virus may result in clinical or asymptomatic infection, depending on the relative virulence of the strain involved, viral dose, age and physical condition of the animal, and various environmental factors. Most cases of primary infection are asymptomatic. Onset of the acute phase of EAV infection, whether associated with clinical signs or not, is preceded by an incubation period of 2–14 days, which varies mainly with the route of exposure. The interval can be 2–3 days after respiratory exposure and is usually 6–8 days after venereal transmission of the virus.

Clinical signs can differ in range and severity between outbreaks and between individuals in the same outbreak. Any combination of the following clinical signs may be observed:  

  • fever (up to 41°C)

  • depression

  • anorexia

  • leukopenia

  • dependent edema (limbs, ventrum, scrotum, prepuce, mammary glands, peri- or supraorbital region)

  • conjunctivitis, with or without lacrimation

  • photophobia

  • serous to mucoid nasal discharge

  • stiffness of gait

  • petechial hemorrhages on oral mucous membranes

  • urticaria or hives (localized on face, neck, pectoral region, or generalized)

  • diarrhea

  • icterus

  • ataxia

  • abortion

  • fatal pneumonitis or pneumoenteritis in neonatal and young foals

  • temporary subfertility in stallions

Strains of EAV can cause abortion throughout much of pregnancy (2 months to more than 10 months). Abortion may occur late in the acute phase or early in the convalescent phase of infection, with or without prior clinical signs of EVA. In natural outbreaks, abortion rates can vary from < 10% to as high as 60%. There is no evidence confirming that mares bred with EAV-infective semen will abort later in gestation. Mares that abort from the virus are already pregnant at time of exposure; this occurs primarily by the respiratory route through direct proximity with an acutely infected animal, frequently sharing the same pasture or having across-the-fence contact. Abortion occurs 1–4 weeks later. Mares exposed very late in gestation may not abort but give birth to a foal congenitally infected with the virus. There is no evidence to indicate that mares that abort from EAV infection are subsequently less fertile.

Aborted fetuses may be delivered autolyzed or nonautolyzed and may exhibit interlobular pulmonary edema, pleural and pericardial effusion, and petechial and ecchymotic hemorrhages on the serosal and mucosal surfaces of the small intestine.

Stallions with EVA may undergo a period of short-term subfertility during acute infection. This has been observed in individuals that develop a high and/or prolonged fever and significant scrotal edema. Affected stallions may exhibit reduced libido associated with decreases in total and progressively motile sperm, curvilinear velocity, percentage of live spermatozoa, and percentage of morphologically normal spermatozoa. The changes in semen quality are believed to result from increased intratesticular temperature and not from the direct effect of EAV on spermatogenesis and testicular function. There is strong evidence that fever and scrotal edema can exert independent effects on semen quality. Semen changes can last for 14–16 weeks before returning to normal. No longterm adverse effects on fertility have been seen in fully recovered stallions.

The frequency and severity of clinical illness associated with EAV infection tend to be greater in very young, old, or debilitated individuals and under adverse climatic conditions. Regardless of severity of clinical signs, affected horses invariably make complete recoveries, even in the absence of symptomatic treatment. Mortality in older horses is very rarely encountered in natural outbreaks. However, it can occur in neonatal and in young foals up to a few months of age that succumb from a fulminating pneumonia or pneumoenteritis.


The gross and microscopic lesions observed in fatal cases of EVA reflect the extensive and considerable vascular damage caused by the virus; these descriptions are primarily based on experimental infection with the horse-adapted highly pathogenic Bucyrus strain of EAV.

The most significant gross findings include edema, congestion, and hemorrhages, especially in the subcutis of the limbs and abdomen; excess peritoneal, pleural, and pericardial fluid; and edema and hemorrhage of the intra-abdominal and thoracic lymph nodes and of the small and large intestine, especially the cecum and colon.

Gross lesions are usually absent in aborted fetuses; if present, they are limited to an excess of fluid in body cavities and a variable degree of interlobular pulmonary edema.

Pulmonary edema, emphysema and interstitial pneumonia, enteritis, and infarcts in the spleen have been reported in naturally acquired fatal cases of the disease in foals.

The characteristic microscopic lesion seen in cases of EAV infection is a vasculitis, involving primarily smaller arterioles and venules. Histologically, changes can range from vascular and perivascular edema, with occasional lymphocytic infiltration and endothelial cell hypertrophy in mild cases, to fibrinoid necrosis of the tunica media, extensive lymphocytic infiltration, necrosis and loss of endothelium, and thrombus formation in severe cases.

There are no characteristic histologic features of EAV infection in the fetus, but severe necrotizing panvasculitis of small vessels has been observed. Affected muscular arteries show foci of intimal, subintimal, and medial necrosis, with edema and infiltration of lymphocytes and neutrophils. Prominent vascular lesions are also seen in the placenta, brain, liver, and spleen of the aborted fetuses. Lungs of affected neonatal foals have severe interstitial pneumonia.

Fatal cases of EAV infection in young foals are characterized by interstitial pneumonia, emphysema, interlobular edema, congestion and mononuclear cell infiltration in the lungs, and lymphoid depletion and hemorrhage in lymphoreticular tissues. Focal hemorrhages and necrosis of the intestinal mucosa have been described in cases with an associated enteritis.

Diagnosis of Equine Viral Arteritis

  • Viral isolation, serology, RT-PCR, or demonstration of viral antigens in tissue

The signs of equine viral arteritis can mimic that of a range of other respiratory and nonrespiratory equine diseases. Thus, the differential diagnosis of EVA includes other viral respiratory tract infections such as equine herpesvirus 1 and 4, equine influenza virus, equine rhinitis A and B viruses, and equine adenovirus. It may also include equine infectious anemia, purpura hemorrhagica, allergy-induced urticaria, and toxicosis due to hoary alyssum (Berteroa incana). Furthermore, several foreign animal diseases that should be considered in a differential diagnosis of EVA include Getah virus infection, dourine, and African horse sickness. Thus, confirmation of a provisional clinical diagnosis of EVA should be pursued without delay in suspected outbreaks of the disease.

Abortion caused by EAV must be differentiated from that due to equine herpesvirus 1 or 4. A helpful but not always reliable distinguishing feature is that mares that abort because of EAV may display prior clinical signs of EVA, whereas mares that abort because of equine herpesvirus 1 or 4 seldom exhibit any premonitory clinical evidence of infection. Furthermore, EAV-infected fetuses not infrequently are somewhat autolyzed at time of expulsion and very often, are devoid of any gross and even microscopic lesions. In contrast, herpesvirus-infected fetuses are invariably fresh and usually display characteristic gross and microscopic lesions.

Laboratory confirmation of EVA can be based on virus isolation, detection of viral nucleic acid by standard RT-PCR, real-time RT-qPCR or RT-insulated isothermal PCR (RT-iiPCR), and in situ hybridization (conventional or RNAscope), visualization of viral antigen by immunohistochemical examination, or demonstration of a humoral antibody response by testing paired (acute and convalescent) sera collected 3–4 weeks apart.

Of the serologic assays evaluated for detection of antibodies to EAV, the complement-enhanced virus neutralization test continues to be regarded as the most reliable for the diagnosis of acute EAV infection and for seroprevalence studies. A number of ELISAs have been developed, only one or two of which approximate the sensitivity and specificity of the virus neutralization test. None of the available serologic tests can differentiate antibody titers resulting from natural infection from those due to vaccination.

The most appropriate samples for virus isolation and/or detection of viral nucleic acid by RT-PCR are nasopharyngeal swabs or washings and unclotted (citrated or EDTA) blood samples. To optimize the chances of isolation or detection of virus, samples should be collected as early as possible upon onset of clinical signs or suspicion of EAV infection. After collection, swabs should be transferred directly into viral transport medium and shipped refrigerated or frozen in an insulated container via an overnight delivery service to a laboratory with expertise and experience in testing for this infection. Unclotted blood samples should be transported refrigerated but not frozen.

In suspect cases of EAV-related abortion, virus detection should be attempted from placental tissues and fluids and from fetal lung, liver, lymphoreticular tissues (especially thymus), and peritoneal or pleural fluid. Chorioallantoic membrane and fetal lung are the tissues of choice for recovery of virus. When EAV is suspected in deaths of young foals or older horses, a wide range of tissue specimens, especially the lymphatic glands in the thoracic and abdominal cavities and related organs, should be collected and submitted for laboratory examination, including viral nucleic acid detection by RT-PCR or virus isolation, together with histologic and immunohistochemical testing.

Investigation of the putative carrier status of a stallion is based initially on determining whether the individual is seropositive or negative for antibodies to EAV. In the absence of a certified history of vaccination, stallions with a virus neutralizing antibody titer ≥1:4 are considered seropositive and should be regarded as potential carriers of the virus until proven otherwise, based on absence of detectable EAV in their semen. Confirmation of the carrier state is based on demonstration of virus in a semen sample containing the sperm-rich fraction of the ejaculate either by isolation of virus in cell culture or its detection by RT-qPCR. The carrier state can also be determined by test breeding a stallion to two seronegative mares and checking the mares for seroconversion to EAV 28 days after breeding.

Treatment of Equine Viral Arteritis

  • Supportive care

There is no specific antiviral treatment currently available for equine viral arteritis. Aside from young foals, virtually all horses naturally infected with EAV make complete clinical recoveries, even in the absence of symptomatic treatment.

Supportive treatment is indicated, however, in moderate to severely affected horses, especially stallions. This supportive treatment should include:

  • antipyretics

  • anti-inflammatory drugs

  • diuretics

  • adequate rest

  • good nursing care

  • gradual return to breeding activity

Prompt symptomatic treatment of stallions with a high or prolonged fever and significant scrotal and preputial edema can reduce the likelihood of short-term subfertility.

There is no effective treatment for EVA-related cases of pneumonia or pneumoenteritis in foals. Because congenitally infected foals are very productive sources of EAV by the respiratory route and their chances of survival are essentially nil, early euthanasia is warranted to minimize the risk of further spread of the virus to any susceptible contacts, especially pregnant mares and young foals.

There is some evidence that temporary downregulation of circulating testosterone by GnRH immunization or through the use of a GnRH antagonist promotes clearance of EAV from the reproductive tract of some but not all treated carrier stallions. Neither strategy has yet been proven to be free from possible adverse effects on the reproductive behavior of treated individuals. The carrier state can be permanently eliminated from a stallion by surgical castration.

Prevention and Control of Equine Viral Arteritis

  • Vaccination and sound management of breeding populations

The primary focus of current control programs is to restrict the spread of equine viral arteritis in breeding populations and to reduce the risk of outbreaks of virus-related abortion, death in young foals, and establishment of the carrier state in stallions and postpubertal colts. Although EAV has occasionally been responsible for extensive outbreaks of disease at racetracks, shows, sales, and veterinary hospitals, these have been so sporadic that no specific control programs have been developed to prevent such occurrences.

EVA is a manageable and preventable disease that can be controlled by observance of sound management practices together with a targeted vaccination program. Attenuated live and inactivated vaccines are available in North America and Europe, respectively, for prevention and control.

The attenuated modified-live vaccine available in North America protects against development of EVA, including abortion, and establishment of the carrier state in stallions. Annual revaccination of vaccinated horses is recommended to boost the level of protective immunity. Although the vaccine is safe and immunogenic for stallions and nonpregnant mares, the manufacturers do not recommend its use in pregnant mares, especially in the final 2 months of gestation or in foals < 6 weeks of age, unless there is a high risk of exposure to natural infection. Experimental and field studies have shown that there are no adverse consequences to vaccinating pregnant mares up to 3 months before foaling and during the immediate postpartum period. However, there is a low risk of abortion in mares vaccinated during the last 2–3 months of pregnancy. All seronegative mares being bred to a persistently infected stallion should be vaccinated 21 days prior to natural breeding or artificial insemination. Those previously vaccinated should be given a booster immunization. Minimizing or eliminating direct or indirect contact of unprotected horses with infected animals or with virus-infective semen is critical to the success of any prevention program.

Control programs are predicated on observance of sound management practices similar to those recommended for other respiratory infections. These include isolation of new arrivals on a premises for 3–4 weeks before allowing them to co-mingle with the resident equine population, maintenance of pregnant mares in small isolated groups, identification of carrier stallions, annual immunization of noncarrier breeding stallion populations, and vaccination of colts at 6–12 months of age to minimize their risk of becoming carriers later in life.

Carrier stallions should be managed separately and bred only to naturally seropositive mares or mares vaccinated against EVA. Personnel need to take all appropriate precautions during the breeding or collection of semen from such stallions to ensure that EAV is not accidentally spread to other horses on the premises by indirect means through the use of virus-contaminated fomites.

Because fresh-cooled or frozen semen can be an important source of EAV, it should be tested by a laboratory with appropriate diagnostic expertise to confirm its negative EAV status, especially if imported. When breeding a mare artificially with virus-infective semen, the same precautions apply as if breeding by live cover to a carrier stallion.

Specific measures to prevent or control EVA on breeding farms include:

  • identifying any carrier stallions

  • separately managing any carrier stallions

  • vaccinating noncarrier stallions annually

  • restricting breeding carrier stallions to EVA-vaccinated mares or mares naturally seropositive for antibodies to EAV

  • isolating mares bred with infective semen for the first time from EAV seronegative horses for 3 weeks

  • screening semen intended for AI use for virus, particularly if imported

  • observing sound management practices, especially of pregnant mares

  • vaccinating colt (male) foals between 6 and 12 months of age to prevent possible development of a carrier state later in life

  • under circumstances of intensive management and limited facilities, considering vaccination of all at-risk animals

In the event of a suspected outbreak of EVA, relevant animal health authorities, federal, state, or other officials should be promptly notified, with affected and in-contact horses isolated and with restrictions immediately imposed on movement of horses onto and off the affected premises. Appropriate specimens should be collected as soon as possible after onset of clinical signs and submitted for laboratory confirmation of a diagnosis of EVA. Breeding activity should be suspended on breeding farms to minimize risk of further spread of the infection. Stalls and equipment that might have come in contact with infected animals should be thoroughly sanitized. In consultation with a veterinarian, vaccination of the at-risk equine population on a premises should be seriously considered as a means of restricting further transmission of EAV and of expediting control and resolution of an outbreak. Movement restrictions should not be lifted until at least 3 weeks after the last clinical or suspected case of EVA or laboratory-confirmed case of EAV infection.

There is no evidence that equine arteritis virus is a zoonotic agent and transmissible to humans.

Key Points

  • Equine viral arteritis is an economically important, contagious respiratory, systemic, and reproductive disease of equids.

  • Carrier stallions are the primary reservoir of equine arteritis virus. 

  • Diagnosis is by virus or virus nucleic acid detection in body fluids or tissues, viral antigen visualization in infected tissues, and serology.

  • Symptomatic treatment (eg, antipyretic, anti-inflammatory, and diuretic drugs) is indicated, especially in severely affected stallions.

  • Available vaccines can protect against clinical disease, including abortion and establishment of the carrier state in stallions.

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