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Sapelovirus (SPV), an emerging virus in the family Picornaviridae, is detected in several animal and bird species irrespective of their age. Amid all SPVs, porcine sapeloviruses (PSVs) are more ubiquitously present all over the world in porcine population. These viruses are highly stable in different environmental conditions and spread easily within the susceptible animals mainly through faeco-oral route. Usually, PSVs cause asymptomatic infections but are also clinically associated with encephalomyelitis, respiratory distress, fertility disorders and skin lesions. PSV-associated outbreaks have been reported where death occurs due to polioencephalitis and respiratory paralysis. Till date, PSVs have been detected from several European and Asian countries with moderate-to-high prevalence and clinical course. Viral capsid proteins are immunogenic and mutations in these proteins are responsible for the diverse nature of the viruses. Further, genomic analysis shows the varied evolutionary patterns and the presence of recombination within PSV strains. These viruses also exist as concurrent infections with several enteric bacterial, viral and parasitic pathogens. Classical to modern biotechnological assays are in use to detect PSV involving virus isolation in cell culture, immunohistochemistry, conventional nucleic acid amplification techniques, quantitative real-time amplification assays and isothermal amplification molecular techniques. Till date, there is no vaccine available against PSVs.
KeywordsSapelovirus Picornaviridae Porcine Encephalomyelitis Mutation Diversity Recombination Diagnosis Epidemiology
Sapeloviruses, formerly known as porcine enterovirus (PEV)-8, are ubiquitous and most commonly responsible for causing asymptomatic infection of the gastrointestinal tract of animals. The genetic analysis revealed unique markers based on which PEV-8 viruses were reclassified under a new genus named Sapelovirus (Krumbholz et al. 2002). As on date, these viruses have been found to infect porcine, avian and simian species. Porcine sapelovirus (PSV)-associated clinical symptoms include pneumonia, reproductive defects, skin lesions, enteritis and encephalomyelitis. As the information available on avian sapelovirus (ASV) and simian sapelovirus (SSV) is limited, this chapter comprehends the information on PSV only.
14.2 Virus Characteristics
PSVs belong to the genus Sapelovirus under the family Picornaviridae. The size of virion particles is small (~35 nm) and they are non-enveloped possessing icosahedral symmetry with a distinct surface morphology visible under the electron microscope (Bai et al. 2018). Mature infectious virions are stable in the environment and could resist acidic pH. Furthermore, virions are not destabilised at elevated temperature (60 °C for 10 min), lipid solvents and some disinfectants. Sodium chlorite or 70% ethanol is effective to inactivate PSV (Horak et al. 2016).The Sapelovirus exhibits buoyant density in CsCl of 1.32–1.34 g/cm3.
14.3 Virus Taxonomy
The current Sapelovirus taxonomy is the result of efforts from the picorna study group and the International Committee on Taxonomy of Viruses (ICTV) Executive Committee (www.picornastudygroup.com) that are contributing their expertise to provide a classification scheme that is supported by verifiable data and expert consensus. The genus Sapelovirus contains three species, namely Avian sapelovirus (ASV), Sapelovirus A (SV-A, porcine) and Sapelovirus B (SV-B, simian) (ICTV 10th report, https://talk.ictvonline.org/ictv-reports/ictv_online_report/positive-sense-rnaviruses/picornavirales/w/picornaviridae/701/genus-sapelovirus). ASV and SV-A consist of only a single antigenically heterogenous serotype, respectively, known as ASV-1 and PSV-1. However, SSVs are highly divergent and are classified into three genetically defined Sapelovirus types as SSV-1 to SSV-3. PSV (strain csh) was first isolated from China in 2011 (Lan et al. 2011). As on date, 50 complete genomic sequences of PSV strains have been published from China, South Korea, Japan, Germany, France, India and the United Kingdom (Lan et al. 2011; Chen et al. 2012; Schock et al. 2014; Son et al. 2014; Ray et al. 2018; Piorkowski et al. 2018; Bai et al. 2018). Different virus strains exhibit affinity towards different target organs, as the PSV-csh strain (China, Shanghai) and PSV-G5 (the United Kingdom) affect mostly nervous system (Lan et al. 2011; Schock et al. 2014), whereas strains like KS0515, KS04105 and KS0552179 and Chinese PSV strain YC2011 are associated with diarrhoea. Notably, PSV-csh is a diarrhoeagenic strain that leads to respiratory distress before the onset of polioencephalomyelitis in infected animals (Lan et al. 2011).
14.4 Viral Genome
14.5.1 Species Affected
Sapeloviruses have been isolated from pigs, wild boars, monkeys and ducks whereas sapelovirus-like-specific genome has been detected in a variety of species like bats (several species), cats, cattle, dogs, pigeons, quails‚ and sea lions (Li et al. 2011). Notably, these viruses to date are not known to cause any zoonotic transmission to human.
14.5.2 Geographic Distribution and Strain Variability
14.6 Transmission and Pathogenesis
The most common route of transmission of the virus is faecal-oral; however, due to its high stability the infectious virions spread through fomites also (Huang et al. 1980; Lan et al. 2011). Several intestinal epithelial cell lines are commonly used for the pathogenicity and virulence studies of PSVs (Lan et al. 2013).
After ingestion through the oral route, PSVs primarily replicate in the intestinal tract. Receptor used by the PSV is unknown, but one recent study shows that a 2,3-linked terminal sialic acid (SA) on the cell surface GD1a ganglioside could be used for PSV binding and infection as a receptor (Kim et al. 2016). Experimental data shows that PSV utilises caveolae-dependent endocytosis pathway for PK-15 cell internalisation and depends upon lower pH, dynamin, Rab7 and Rab11 (Zhao et al. 2019). PSV strains are known to cause viremia through which they access the central nervous system (CNS). The incubation periods vary from 5 to 14 days.
14.7 Clinical Signs
PSVs can cause both symptomatic and asymptomatic infections in the natural field cases and experimentally infected piglets. Commonly, co-infections of PSV with other enteric pathogens like porcine kobuvirus (PKV), porcine enterovirus (PEV), porcine teschovirus (PTV), group A-C rotaviruses (RVA-C), porcine sapovirus (PSaV), porcine norovirus (PNoV), transmissible gastroenteritis coronavirus (TGEV), porcine epidemic diarrhoea coronavirus (PEDV), Escherichia coli and Salmonella spp., Lawsonia intracellularis, Brachyspira hyodysenteriae, Brachyspira pilosicoli, Brachyspira intermedia and Clostridium perfringens. Symptomatic manifestations are mainly neurological, which include spinal cord damage, ataxia, mental dullness, paresis, paralysis and a decreased response to environmental stimuli. Polioencephalitis in grower pigs is characterised by ataxia and paraparesis. Experimental infection of polioencephalitis has been documented in 50–60-day-old grower pigs. A novel PSV isolate from the United States was found to be associated with typical polioencephalomyelitis (Arruda et al. 2016). Gastroenteritis and respiratory distress may also be seen with PSV-induced polioencephalomyelitis (Lan et al. 2011). Intravaginal inoculation at day 15 of gestation causes early embryonic death and foetal resorption, but when inoculated at day 30, it results in a significant increase in foetal death (Huang et al. 1980). PSV is also detected from intestinal contents of stillbirth animals from Indian pig population, which suggests the transplacental transmission of the virus (Kumari et al. 2019).
14.8 Morbidity and Mortality
No specific data is available on the mortality and morbidity associated with PSV infection. Experimental infection through intravaginal and intrauterine route in gilts with PSV on day 30 of gestation results in a 94.4% foetal mortality (Huang et al. 1980). An outbreak reported in the United States in 2016 stated 20% morbidity and 30% case fatality rate (Arruda et al. 2016).
14.8.1 Post-mortem and Histopathology
Lesions are mainly seen in the central nervous system (CNS), consistent with the other neurotropic viral infection, characterised as subacute, multifocal and non-suppurative polioencephalomyelitis, accompanied with punctate haemorrhage and hyperaemia in the dura mater (Lan et al. 2011; Schock et al. 2014). Neuronal vacuolisation and perivascular cuffing are also commonly observed (Lan et al. 2011). Congestion is the most common gross lesion seen in the small intestine along with pronounced loss of villi with haemorrhage in the lamina propria histologically (Lan et al. 2011). In the case of clinical pneumonia, consolidation and multifocal haemorrhage are commonly seen in the lung lobes, where erythrocytes infiltrate throughout the interstitium and alveoli with alveolar wall thinning (Lan et al. 2011). Pathological lesions from naturally infected Indian pig show severe clouding, thickening and congestion of meninges, pleural thickening, frothy exudates in the trachea, congested mesenteric lymph nodes, yellowish discolouration of liver, intestinal (ileum) corrugation and thickening of the intestinal mucosal fold (Kumari et al. 2019)
14.9.1 Clinical History
A neurological disorder characterised by ataxia and limb paralysis, with or without other clinical symptoms (diarrhoea or pneumonia), is suggestive of PSV infection (Lan et al. 2011). The PSV-induced reproductive disorder can be suspected in litters with a few to several stillborn or mummified foetuses (Huang et al. 1980).
Samples from live animal include faeces and blood (serum). In the case of the faecal sample, direct collection from the anus is preferred to avoid sample contamination. Spinal cord and brain are the most common preferred samples from the dead animal for PSV-induced CNS infection diagnosis. Other than these, liver, spleen, trachea, lung and intestine samples are also useful in diagnosing PSV infections. Though PSV has not been successfully isolated from the tissues of stillborn or mummified foetuses, molecular detection has been reported from stillbirth cases (Huang et al. 1980; Kumari et al. 2019).
14.9.3 Detection of Virus, Nucleic Acid or Antigens
RT-PCR assays used for detection of PSVs
Primer sequence (5′–3′)
Zell et al. (2000)
Duplex PCR for PTV and PSV
Palmquist et al. (2002)
Son et al. (2014)
Wang et al. (2014)
Chen et al. (2014)
Minor groove-binding Taqman probe—CGATAGCCATGTTAGTG
Kumari et al. (2018)
There is little information available on the immune response to PSVs. The humoral response is primarily based on the IgA. A study done on porcine intestinal epithelial cells (IPEC-J2) reveals the role of PSV infection in changing the innate immune response pathway (Lan et al. 2013). The study shows both upregulation (e.g. TLR3) and downregulations (e.g. TLR4) of several innate immune system molecules (Lan et al. 2013). Maternal antibodies proved not to be protective in the case of transplacental infection (Huang et al. 1980). Seropositive gilts when inoculated intrauterinely and intravaginally resulted in embryonic and foetal infection (Huang et al. 1980). Though maternal antibody in the colostrums is believed to be protective infections are found in post-weaning animals (Schock et al. 2014). As of now, there is no vaccine available for PSVs.
14.11 Conclusion and Prospects
Although PSV is widely distributed all over the world among the porcine population, detailed information is lacking about their evolutionary pattern and mechanisms driving their divergence. However, precise data about the prevalence of PSV infections and the genetic diversity of this virus in pigs and wild boars have been reported only in a limited number of countries. Moreover, the association of co-infections with other enteric pathogens is exactly not known which raises ambiguity in the pathogenic potential of PSVs. Several recent findings on recombination events between PSV strains emphasise to study genetic variability among PSVs.
All the authors of the manuscript thank and acknowledge their respective universities and institutes.
Conflict of interest: There is no conflict of interest.
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