Swine hemagglutinating encephalomyelitis virus (HEV) has been shown to have a capability to gain access to the cell bodies of sensory neurons after peripheral inoculation, resulting in ganglionic infection. It is not clearly understood how this virus is replicated within and released from the sensory neurons, and it remains to know how satellite cells response to the HEV invasion. By ultrastructurally examining HEV-infected rat dorsal root ganglia, we found that HEV in the cell bodies of infected neurons budded from endoplasmic reticulum-Golgi intermediate compartments, and were assembled either individually within small vesicles or in groups within large vesicles. The progeny virions were released from the sensory neurons mainly by smooth-surfaced vesicle-mediated secretory pathway, which occurred predominantly at the perikaryal projections and infoldings of sensory neurons. Released HEV particles were subsequently taken up by the adjacent satellite cells. Almost all virus particles in the cytoplasm of satellite cells were contained in groups within vesicles and lysosome-like structures, suggesting that these glial cells may restrict the local diffusion of HEV. These observations give some insights into the pathogenesis of coronavirus infection and are thought to help understand the interactions between sensory neurons and their satellite cells.

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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.

The genomic RNA and intracellular RNA of mouse hepatitis virus, strain JHM (MHV-JHM) and two plaque mutants (1a and 2c), which have been isolated from a persistently infected culture (JHM-CC), have been analyzed by T1-resistant oligonucleotide finger-printing. The genomic RNA of the virus population (JHM-CC virus) released from different passage levels of the same persistent infection has also been analyzed. The analysis shows the locations within the genomic and intracellular RNAs of more than 45 T1-resistant oligonucleotides and confirm earlier studies (J. L. Leibowitz, K. C. Wilhelmsen, and C. W. Bond (1981), Virology 114, 39-51), showing that the six subgenomic RNAs of MHV-JHM form a 3' coterminal nested set which extends for different lengths in a 5' direction. The analysis also identifies in each subgenomic RNA those large T1 oligonucleotides derived from noncontiguous regions of the genome during mRNA synthesis. Two important conclusions can be reached from analysis of the mutant viruses. First, the virus population released from the persistent infection represents a fairly constant mixture of viruses, and the fluctuating emergence of variants as predominant species in the culture does not occur. Second, the data indicate that for particular intracellular RNAs of mutant viruses the sequence rearrangements occurring during subgenomic mRNA synthesis are different from those in the corresponding intracellular RNA of wild-type virus. The result may indicate a potential flexibility in the leader/body fusion process that has not been previously recognized.

SUMMARYThe rabbit-adapted Borna disease~(BD) virus strain V was passaged by intracerebral infection of 1-day-old Wistar rats. Infectivity titres reached l08 infectious units per gram of brain 4 weeks after infection. No clinical signs were evident. The persistent infection could be induced with adapted or field strains of BD virus. Strains were identified by neutralization tests. The virulence of the rabbit-adapted BD virus for the rat increased with rat passages. The 5th passage induced clinical symptoms in animals infected at 1 week of age or older. Between 20% and 50% of diseased rats died. Virusspecific antigen was detectable immunohistologically in neurons of rats infected at all ages. Animals inoculated at 1 or 2 months of age, but not the neonatal rats, showed signs of inflammation in the brain. Infected rats produced specific antibodies. In the older groups (infected at ages of 1 or 2 months), and especially in surviving animals, occasionally, neutralizing antibodies with high titres were found. Transfer of primed spleen cells resulted in subacute disease. These findings demonstrate that neonatal rats can acquire a persistent, tolerant infection and that expression of disease is mediated by immunological factors.

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SummaryThe pathogenicity for mice of nine strains of mouse hepatitis virus was studied in mice free from the virus by the intracerebral, intraperitoneal, intravenous and intranasal routes of inoculation.

We describe an outbreak of vomiting, wasting, and encephalomyelitis syndrome in piglets in Argentina, caused by porcine hemagglutinating encephalomyelitis coronavirus (PHE-CoV) infection. Diagnosis was made by epidemiologic factors, pathologic features, immunohistochemistry, reverse transcription-PCR, and genomic sequencing. This study documents PHE-CoV infection in South America.