An Electron Microscopic Study of Experimentally-induced HEV Encephalitis

Meyvisch, C; Hoorens, J.

doi:10.1177/030098587801500112

Cited by 11 publications

(9 citation statements)

References 10 publications

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“…In the present study, PRV infected nerve cells and nonneuronal cells, but HEV antigen was found only in nerve cells. These in vitro findings were consistent with previous in vivo studies in which PRV antigens were found in astrocytes and nerve cells [3,9], whereas HEV particles could be found in nerve cells but were not detected in glial cells and infiltrating cells [11,12,23]. Based on these in vivo and in vitro findings, infectivity of HEV may be more strictly restricted to nerve cells than PRV and rabies virus, for which non-neuronal cells may support viral entry and replication [19].…”

Section: Discussionsupporting

confidence: 90%

“…HEV antigens localized to the periphery of nerve cells in the early stage of infection and then spread to the entire cytoplasm and axon terminals. In general, coronaviruses bind to specific cell surface receptors via the surface projectional glycoproteins and then replicative cycles occur in the cytoplasm [21][22][23][24]. Complete virions assemble to the rough endoplasmic reticulum or Golgi apparatus [15,24,29].…”

Section: Discussionmentioning

confidence: 99%

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Propagation of Swine Hemagglutinating Encephalomyelitis Virus and Pseudorabies Virus in Dorsal Root Ganglia Cells

et al. 2009

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ABSTRACT. Swine hemagglutinating encephalomyelitis virus (HEV) causes encephalomyelitis or vomiting and wasting disease in suckling piglets. Neurotoropism of the virus has been demonstrated in previous in vivo studies. In the present study, we investigated the infectivity and propagation of HEV in comparison with those of pseudorabies virus (PRV), another neurotropic virus, using dorsal root ganglia cells of newborn mice containing nerve cells and non-neuronal cells. HEV infected nerve cells but did not infect non-neuronal cells, whereas PRV infected both cell types. By using cytoskeletal inhibitors, it was suggested that propagation of HEV and PRV within and among nerve cells depended on microtubules and intermediate filaments of nerve cells, indicating that the viruses may be transported between the cell body and axonal terminals of neurons by fast axonal flow.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Propagation of Swine Hemagglutinating Encephalomyelitis Virus and Pseudorabies Virus in Dorsal Root Ganglia Cells

et al. 2009

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“…Subsequent studies demonstrated that HEV first oronasally infects the epithelial cells lining the respiratory tract and small intestine and thereafter is delivered retrogradely via peripheral nerves to the central neurons in charge of peristaltic function of the digestive tract, resulting in the so-called vomiting diseases (Andries and Pensaert, 1980). Early electron microscopic (EM) and virological analysis showed that glial cells were not infected by HEV in primarily cultivated astrocytes (Yagami et al, 1993) or in the brains of infected piglets or mice (Meyvisch and Hoorens, 1978;Yagami et al, 1986), indicating that Grant sponsor: RIKEN Brain Science Institute; Grant number: G29 (to T.Has. ); Grant sponsor: MEXT Japan; Grant number: 15650066 (to K.T., T.Has.).…”

Section: Indexing Terms: Coronavirus; Virus Replication; Transsynaptimentioning

confidence: 99%

Neurotropic virus tracing suggests a membranous‐coating‐mediated mechanism for transsynaptic communication

Li¹,

Bai²,

Hirano³

et al. 2012

J of Comparative Neurology

148

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Swine hemagglutinating encephalomyelitis virus (HEV) has been shown to have a capability to propagate via neural circuits to the central nervous system after peripheral inoculation, resulting in acute deadly encephalomyelitis in natural host piglets as well as in experimental younger rodents. This study has systematically examined the assembly and dissemination of HEV 67N in the primary motor cortex of infected rats and provides additional evidence indicating that membranous‐coating‐mediated endo‐/exocytosis can be used by HEV for its transsynaptic transfer. In addition, our results suggested that this transsynaptic pathway could adapted for larger granular materials, such as viruses. These findings should help in understanding the mechanisms underlying coronavirus infections as well as the intercellular exchanges occurring at the synaptic junctions. J. Comp. Neurol. 521:203–212, 2013. © 2012 Wiley Periodicals, Inc.

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“…The virus can also spread peripherally from the intestinal myenteric plexuses to the local sensory ganglia of the spinal cord. Electron microscopy yielded the discovery of viral particles within nerve cells, moving from the periphery through the cell cytoplasm to reach the axon (85). However, viral particles could not be found in surrounding glial or in inflammatory cells (85).…”

Section: Pathogenesis and Gross And Histological Lesionsmentioning

confidence: 99%

Porcine Hemagglutinating Encephalomyelitis Virus: A Review

et al. 2019

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The porcine hemagglutinating encephalomyelitis virus (PHEV) is classified as a member of genus Betacoronavirus , family Coronaviridae , sub-family Cornavirinae , and order Nidovirales . PHEV shares the same genomic organization, replication strategy, and expression of viral proteins as other nidoviruses. PHEV produces vomiting and wasting disease (VWD) and/or encephalomyelitis, being the only known neurotropic coronavirus affecting pigs. First clinical outbreak was reported in 1957 in Ontario, Canada. Although pigs are the only species susceptible to natural PHEV infections, the virus displays neurotropism in mice and Wistar rats. Clinical disease, morbidity, and mortality is age-dependent and generally reported only in piglets under 4 weeks old. The primary site of replication of PHEV in pigs is the respiratory tract, and it can be further spread to the central nervous system through the peripheral nervous system via different pathways. The diagnosis of PHEV can be made using a combination of direct and indirect detection methods. The virus can be isolated from different tissues within the acute phase of the clinical signs using primary and secondary pig-derived cell lines. PHEV agglutinates the erythrocytes of mice, rats, chickens, and several other animals. PCR-based methods are useful to identify and subsequently isolate animals that are actively shedding the virus. The ability to detect antibodies allows producers to know the status of first-litter gilts and evaluate their risk of tier offspring to infection. PHEV is highly prevalent and circulates subclinically in most swine herds worldwide. PHEV-related disease is not clinically relevant in most of the swine-producing countries, most likely because of dams are immune to PHEV which may confer passive immunity to their offspring. However, PHEV should be considered a major source of economic loss because of the high mortality on farms with high gilt replacement rates, specific pathogen-free animals, and gnotobiotic swine herds. Thus, in the absence of current PHEV vaccines, promoting virus circulation on farms with early exposure to gilts and young sows could induce maternal immunity and prevent disease in piglets.

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An Electron Microscopic Study of Experimentally-induced HEV Encephalitis

Cited by 11 publications

References 10 publications

Propagation of Swine Hemagglutinating Encephalomyelitis Virus and Pseudorabies Virus in Dorsal Root Ganglia Cells

Propagation of Swine Hemagglutinating Encephalomyelitis Virus and Pseudorabies Virus in Dorsal Root Ganglia Cells

Neurotropic virus tracing suggests a membranous‐coating‐mediated mechanism for transsynaptic communication

Porcine Hemagglutinating Encephalomyelitis Virus: A Review

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