Equine picornavirus infection

Previous authors: R J GERAGHTY AND J A MUMFORD

Current authors:
C A HARTLEY - Senior Lecturer in Veterinary Virology, BSc (Hons), PhD, Faculty of Veterinary and Agricultural Science, The University of Melbourne, Building 400, Corner of Flemington Road and Park Drive, Parkville, Victoria, 3010, Australia
J R GILKERSON - Professor of Veterinary Microbiology, BVSc, BSc (Vet), PhD, Centre of Equine Infectious Diseases, The University of Melbourne, Building 400, Corner of Flemington Road and Park Drive, Parkville, Victoria, 3010, Australia

GENERAL INTRODUCTION: PICORNAVIRIDAE

Introduction and aetiology

The equine rhinitis viruses cause upper respiratory tract infections in horses and have the potential for long term shedding in urine and faeces. While these viruses have long been detected in horses with respiratory disease, their role, especially the erboviruses, as the main driver of widespread respiratory disease remains to be unequivocally defined. Four types of equine rhinitis viruses have been identified within 2 genera of the family Picornaviridae.  With a publication history more than 50 years long, the names and classifications of these viruses have evolved along with the transformations in virus taxonomy that have occurred over this time. Equine rhinitis A virus (ERAV, formerly equine rhinovirus-1) contains a single serotype and is classified within the Aphthovirus genus together with foot-and-mouth disease virus (FMDV) and bovine rhinitis A and B viruses.  The newly named species erbovirus A is the only member of the Erbovirus genus and contains the 3 known serotypes of this species, known as equine rhinitis B virus (ERBV)-1 (formerly equine rhinovirus-2), ERBV2 (formerly equine rhinovirus-3) and ERBV3 (formerly acid stable equine picornavirus).⁴⁴

Equine picornaviruses have single stranded positive sense RNA genomes from ~7600 nucleotides for ERAV²⁷ to ~8800 bp for ERBV⁴³ that are enclosed in small (~30 nm) non enveloped capsids.  The icosahedral capsid contains 60 copies of each of the capsid proteins (VP1, VP2, VP3 and VP4) where the sequence and three-dimensional structure of these capsid proteins determines the antigenic sites, serotype, and the physical properties of the capsid.  These proteins also mediate cell binding and entry and are important molecular determinants of virulence.⁴⁴ Picornaviruses are resistant to ether and chloroform, but equine picornaviruses have variable acid stability; whereas most are labile below pH 5.5, ERBV3 only loses infectivity below pH 3.3.²¹

Most of the available studies that describe these viruses focus on ERAV and ERBV1, and the information presented in this chapter will reflect this focus, and provide information about ERBV2 and ERBV3 where available.

Epidemiology and pathogenesis

In all of regions of the world where studies have been performed, ERAV and ERBV have either been detected directly by virus isolation or RT-PCR or by antibody detection in seroprevalence surveys.^{2, 7, 9, 11, 16, 19, 21, 25, 31, 33, 35, 37, 39, 40, 42, 43} These studies suggest that these viruses occur endemically worldwide, or at least that their distribution aligns with the presence of significant horse populations, although their existence in the isolated Icelandic horse population has not been documented.

Infection by ERAV is widespread, where seroprevalence studies show that close to 100 per cent of older horses are seropositive.^{19, 31} Primary infection with ERAV is most likely to occur at a time after maternal antibody is waning (3- 9 months) prior to increased opportunity for contact with other horses, such as entry into training stables.^{2, 19} Infection occurs via the upper respiratory tract, where infectious virus can be detected in the nasopharynx and in oral secretions before the systemic phase of infection characterized by transient viraemia and virus dissemination to distant sites.^{18, 39}  Viraemia ceases concomitant with the development of neutralizing antibody, at approximately Day 7 post- infection in experimental infection studies.  After the development of neutralizing antibodies, ERAV genome can still be detected in the nasopharynx by RT-PCR at least at 35 days post- infection.³⁰ More strikingly, experimental infection studies show that the highest load of ERAV is shed in the urine of infected animals. Prolonged urinary shedding of ERAV is a feature of this virus in the natural host, with the viral load shed from this site significantly higher than that shed from the respiratory tract, both by volume and titre. Long-term urinary shedding can be detected for up to 143 days in both experimental and field studies.^{30, 31} This finding suggests that while ERAV may be transmitted to new hosts via respiratory aerosols, direct or in direct contact with urine-contaminated fomites or aerosols created by urine splash onto hard floor surfaces are also likely an important mechanism of spread.

The seroprevalence of the erboviruses is also very high. Up to 100 per cent of older horses have antibody to the ERBVs in most of the populations studied in the USA, European countries, New Zealand and Australia.^{2, 7, 9, 11, 12, 19, 23, 31, 37, 38, 41, 43} Primary infection occurs at four to six months of age, and there is some evidence to suggest that recrudescence or reinfection may continue to occur over time.^{3, 20, 33, 38} A study of sequential samples from 50 weanlings between four and 13 months of age over a...