[Virus infections--disease pictures and laboratory diagnosis. Part 8: Slow viruses, rabies virus, varicella zoster virus and cytomegalovirus].
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Pathogenesis of skunk rabies virus: rabies inhibiting substance as related to rabies diagnosis.
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The effect of anti-lymphocytic serum of infection by congo virus (Crimean haemorrhagic fever virus related) and Mokola virus (rabies virus related).
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Absorption↗
The distribution of Challenge virus standard rabies virus versus skunk street rabies virus in the brains of experimentally infected rabid skunks.
The proposal that the bizarre behavioral changes which occur during rabies infection are due to selective infection of limbic system neurons was further studied in skunks (a species important in naturally occurring disease). A detailed immunohistochemical study of brains of skunks experimentally infected with either Challenge virus standard (CVS) or street rabies virus revealed only trace amounts of viral antigen in many limbic system neurons and marked differences in viral distribution between street and CVS virus. These data were collected during early stage rabies when behavioral changes occur. Areas which contained heavy accumulations of street rabies virus but low amounts of CVS rabies virus were the neuronal perikarya and processes of the dorsal motor nucleus of the vagus, midbrain raphe, hypoglossal and red nuclei. In contrast, large accumulations of CVS virus were found in the Purkinje cells of the cerebellum, the habenular nuclei and in pyramidal cells throughout the cerebral cortex, while corresponding areas in all street virus-infected skunks contained minimal antigen. These findings were very consistent for animals of the same experimental group and between skunks inoculated both intramuscularly and intranasally with skunk street virus. Skunks inoculated intramuscularly with CVS rabies virus failed to develop rabies. Since, in this model, street virus infection generally produces furious rabies and CVS infection results in dumb rabies, we speculate that the behavioral changes which occur in these two different clinical syndromes are due to the heavy and specific accumulation of virus in different regions of the CNS. These results show that regions other than those of the limbic system may also be involved in the pathogenesis of behavior changes in rabid animals.
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Infection of Bergmann glia in the cerebellum of a skunk experimentally infected with street rabies virus.
Rabies virus is a highly neuronotropic virus and glial cell infection is not prominent in the central nervous system (CNS). Paraffin-embedded tissues from the cerebella of skunks experimentally infected with either a skunk salivary gland isolate of street rabies virus or the challenge virus standard (CVS) strain of fixed rabies virus were examined with immunoperoxidase staining for rabies virus antigen by using an anti-rabies virus nucleocapsid protein monoclonal antibody. A skunk infected with street rabies virus showed prominent infection of Bergmann glia. Although infected Purkinje cells were observed, they usually demonstrated a relatively small amount of antigen in their perikarya. A CVS-infected skunk showed many intensely labeled Purkinje cells and a relatively small number of infected Bergmann glia. These findings indicate that although rabies virus is a highly neuronotropic virus, street rabies virus strains do not always demonstrate strict neuronotropism in the central nervous system.
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Infection of cultured rat myotubes and neurons from the spinal cord by rabies virus.
Rabies virus multiplication was investigated in cultured primary rat myotubes and neurons. The susceptibility of these two cell types to fixed rabies challenge virus strain (CVS) was monitored by fluorescence and virus titration. Differentiated rat myotubes were susceptible to rabies virus infection, and showed an increasing accumulation of viral material from day one to day four. However, these cells did not release infective viral particles, nor did they accumulate infectious virions in the cytoplasm. In contrast, infected neurons released large amounts of infectious particles. Electron microscopy observation of infected myotubes showed minor alterations and the presence of typical viral inclusions in the cytoplasm without mature virions assembling viral membranes. Competition binding experiments show that alpha-bungarotoxin inhibits rabies virus infection from 10(-5) to 10(-7) M, whereas lower toxin concentrations failed to have any effect. These data do not confirm the hypothesis of a fixed rabies virus amplification step at the site of the viral entry. On the other hand, the high susceptibility of peripheral neurons to rabies virus infection is an argument for the direct uptake of virions by these cells. The restrictive viral multiplication in the myotubes is an alternative explanation for the local persistence of rabies virus at the site of inoculation.
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Biological characterization of human monoclonal antibodies to rabies virus.
Rabies virus antigen-specific human monoclonal antibodies (MAbs) that recognized either viral glycoprotein, ribonucleoprotein, or matrix proteins were generated. Only glycoprotein-specific MAb neutralized a variety of rabies viruses and protected laboratory rodents against lethal rabies virus infection. The determinant recognized by this MAb does not appear to reside in previously defined antigenic sites of the viral glycoprotein.
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Preparation and mass spectrometric study of egg yolk antibody (IgY) against rabies virus.
Rabies virus was used as the antigen to immunize laying chickens. Anti-rabies virus immunoglobulin Y(IgY) was isolated from yolks of the eggs laid by these chickens using a two-step salt precipitation and one-step gel filtration protocol. The purified IgY was reduced with dithiothreitol, and heavy chains (HC) and light chains (LC) were obtained. In addition, the purified IgY was digested with pepsin and the fragment with specific antigen binding properties (Fab) was produced. Using matrix-assisted laser desorption/ionization mass spectrometry (MALDI-TOFMS), the average molecular weights of IgY, HC, LC, and Fab were determined as 167 250, 65 105, 18 660, and 45,359 Da, respectively. IgY has two structural differences compared with mammalian IgGs. First, the molecular weight of the heavy chain of IgY is larger than that of its mammalian counterpart, while the molecular weight of the light chain of IgY is smaller. Second, upon pepsin digestion, anti-rabies virus IgY is degraded into Fab, in contrast to mammalian IgG, which has been reported to be degraded into F(ab')(2) under the same conditions.
Alkylation↗
[Studies on morphological superstructure of inactivated rabies virus and uninactivated rabies virus].
Rabies is widely epidemic in human and animals. It is a very dangerous disease at present. In 1919, semple has shown that antigenicity was not destroyed by chemicals. After that inactivated rabies vaccine was widely used in human being up to more than seventy years. But the afferration of morphological superstructure between inactivation and uninactivated, we have not see any report on the world.
Formaldehyde↗
Immunization of dogs with a DNA vaccine induces protection against rabies virus.
Rabies is a fatal encephalomyelitis which is transmitted to man, mostly by dogs in developing countries. This zoonosis can be prevented by vaccination of humans before or after exposure. However, a more radical approach is possible, involving the elimination of the principal vector/reservoir by vaccinating dogs. The vaccine must be effective, safe and inexpensive. Mass production of plasmids is possible and DNA-based immunization with a plasmid encoding the antigen responsible for inducing protection seems to be more cost-effective than classical techniques involving cell culture. Beagles were immunized by intramuscular (i.m.) injection with a plasmid encoding the rabies virus (PV strain) glycoprotein. Neutralizing antibodies against both wild-type rabies virus and European Bat Lyssaviruses (EBL1 and EBL2) were detected after a single injection and a boost, but levels of neutralizing antibodies against EBL1 were low. Moreover, all vaccinated dogs were protected against a lethal challenge with a wild-type dog rabies strain. This is one of the first studies to demonstrate that dogs can be protected by DNA vaccines, and opens important perspectives for rabies control.
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Sickness and recovery of dogs challenged with a street rabies virus after vaccination with a vaccinia virus recombinant expressing rabies virus N protein.
Dogs were vaccinated intradermally with vaccinia virus recombinants expressing the rabies virus glycoprotein (G protein) or nucleoprotein (N protein) or a combination of both proteins. The dogs vaccinated with either the G or G plus N proteins developed virus-neutralizing antibody titers, whereas those vaccinated with only the N protein did not. All dogs were then challenged with a lethal dose of a street rabies virus, which killed all control dogs. Dogs vaccinated with the G or G plus N proteins were protected. Five (71%) of seven dogs vaccinated with the N protein sickened, with incubation periods 3 to 7 days shorter than that of the control dogs; however, three (60%) of the five rabid dogs recovered without supportive treatment. Thus, five (71%) of seven vaccinated with the rabies N protein were protected against a street rabies challenge. Our data indicate that rabies virus N protein may be involved in reducing the incubation period in dogs primed with rabies virus N protein and then challenged with a street rabies virus and, of more importance, in subsequent sickness and recovery.
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Generation and characterization of P gene-deficient rabies virus.
Rabies virus (RV) deficient in the P gene was generated by reverse genetics from cDNA of HEP-Flury strain lacking the entire P gene. The defective virus was propagated and amplified by rescue of virus, using a cell line that complemented the functions of the deficient gene. The P gene-deficient (def-P) virus replicated its genome and produced progeny viruses in the cell lines that constitutively expressed the P protein, although it grew at a slightly retarded rate compared to the parental strain. In contrast, no progeny virus was produced in the infected host when the def-P virus-infected cells that did not express the P protein. However, we found that the def-P virus had the ability to perform primary transcription (by the virion-associated polymerase) in the infected host without de novo P protein synthesis. The def-P virus was apathogenic in adult and suckling mice, even when inoculated intracranially. Inoculation of def-P virus in mice induced high levels of virus-neutralizing antibody (VNA) and conferred protective immunity against a lethal rabies infection. These results demonstrate the potential utility of gene-deficient virus as a novel live attenuated rabies vaccine.
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Subversive neuroinvasive strategy of rabies virus.
Rabies virus (RABV) is a pathogen well-adapted to the nervous system, where it infects the neurons. RABV is transmitted by the bite of an infected animal. It enters the nervous system via a motor neuron through the neuromuscular junction, or via a sensory nerve through nerve spindles. It then travels from one neuron to the next, along the spinal cord to the brain and the salivary glands. The virions are then excreted in the saliva of the animal and can be transmitted to another host by bite. Thus, preservation of the neuronal network integrity is crucial for the virus to be transmitted. Successful invasion of the nervous system by RABV seems to be the result of a subversive strategy based on the survival of infected neurons including protection against virus-mediated apoptosis and destruction of T cells that invade the CNS in response to infection.
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Replication strategies of rabies virus.
Rabies virus (RV) is a prototype neurotropic virus that causes fatal disease in human and animals. RV infects hosts at the periphery, enters motoneurons or sensory nerves and moves to the central nervous system (CNS) via retrograde axonal transport. At later stages, there is also centrifugal spread to major exit portals, such as the salivary glands. Transmission to other hosts is facilitated by behavioral changes related to the CNS infection. Successful accomplishment of the RV infectious cycle depends on multiple functions of the virus, and of individual virus proteins, all together defining the typical pathogenicity and virulence, i.e. the biological fitness of this virus. In particular, it appears important for RV to sneak into the host without causing pronounced host responses and to preserve, at least for some time, the integrity of infected cells and of the neuronal network. The availability of reverse genetics systems that allow generation of engineered recombinant RV has provided tools for a more detailed analysis of viral functions relevant to the typical RV pathogenesis. Novel developments such as tracking of live fluorescent RV are further increasing the opportunities to decipher RV pathogenicity factors. In this review, we describe different aspects of the molecular biology of RV that are relevant to pathogenesis, with a particular emphasis on the accurate control of RV transcription, gene expression, and replication. In addition, the role of individual virus proteins in maintaining host cell integrity and supporting retrograde transport is discussed. The potential of recombinant RVs with single or multiple pathogenicity factors eliminated is being discussed in terms of vaccine and virus vector development.
Amino Acid Sequence↗
Modulation of the immune response in the nervous system by rabies virus.
Rabies virus (RABV) is a pathogen well-adapted to the nervous system, where it infects neurons. RABV is transmitted by the bite of an infected animal. It enters the nervous system via a motor neuron through the neuromuscular junction, or via a sensory nerve through nerve spindles. It then travels from one neuron to the next, along the spinal cord to the brain and the salivary glands. The virions are then excreted in the saliva of the animal and can be transmitted to another host by bite. Thus preservation of neuronal network integrity is crucial for the virus to be transmitted. Successful invasion of the nervous system by RABV seems to be the result of a subversive strategy based on the survival of infected neurons. This strategy includes protection against virus-mediated apoptosis and destruction of T cells that invade the CNS in response to infection.
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Multigenic relation to the attenuation of rabies virus.
Rabies virus Nishigahara strain causes lethal infection in adult mice after intracerebral inoculation. On the other hand, the RC-HL strain, derived from the Nishigahara strain, does not cause lethal infection in adult mice. We previously demonstrated that a chimeric virus, R(G), with the open reading frame of the G gene (G-ORF) from the Nishigahara strain in the background of the RC-HL genome, is virulent. Reversely, in order to demonstrate that the G gene of the RC-HL strain is related to the attenuated phenotype, we established a reverse genetics system of the Nishigahara strain and generated a chimeric virus, Ni(G), with the G-ORF from RC-HL in the background of the Nishigahara genome. Contrary to our prediction, Ni(G) killed adult mice after intracerebral inoculation with neuropathic symptoms like those of Nishigahara strain infection. Therefore, the G-ORF of the RC-HL strain is not the sole determinant of the attenuated phenotype. In additional investigation, we examined other genes, including N, P, M and L genes, and generated chimeric viruses exhaustively. We found that chimeric viruses with a single gene from the RC-HL were not attenuated and that chimeric viruses with the G-ORF and at least one other ORF from the RC-HL were attenuated. In conclusion, attenuation from the Nishigahara to RC-HL strain is multigenic.
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Characterization of nucleoprotein gene sequence of an Indian isolate of rabies virus.
Rabies occurs in all parts of Indian sub-continent except Andaman and Nicobar and Lakshadweep group of islands. The full-length nucleoprotein (N) gene sequence of a rabies virus isolate from India is reported for the first time and the same has been compared with available N gene sequences from the database. A central domain of 230 amino acids (aa) from aa 141 to aa 370 exhibited more than 95% similarity. There were 8 amino acid positions (aa 29, 32, 38, 84, 119, 379, 438, and 439) at which substitution was unique for Indian isolates but common for laboratory strains. In antigenic epitopes, except for a single amino acid difference at the antigenic site IV, the amino acids were conserved. The Indian isolate also possessed two Bam HI sites (aa 247 and 278), while the other Asian isolates had only one site at aa 278 or were not digested with Bam HI at all. Phylogenetic analysis also demonstrated that the Indian isolate was closely related to the Sri Lankan isolate and grouped in the cluster that comprised of the isolates from other Asian countries namely China and Pakistan.
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The evolutionary history and dynamics of bat rabies virus.
Rabies virus (RABV) is endemic in terrestrial mammals throughout the world and in bats on the American continent. We performed the most extensive phylogenetic analyses of bat RABV sequences undertaken to date using a variety of genes. Our study supported previous suggestions that viral sequences are grouped according to the behaviour of the host species. However, there was more genetic and geographical diversity within each phylogenetic group than previously recognised, including evidence for new groups. Furthermore, three clades of Latin American bat RABV that were distinct from the previously identified "group IV" bat RABV clade and more closely related to North American bat RABV clades, were identified. Strikingly, phylogenetic trees for the G (glycoprotein) gene had a significantly different evolutionary history to those inferred for the N (nucleoprotein) and P (phosphoprotein) genes, and an analysis of these competing topologies revealed that it is not possible on current data to resolve whether bat RABV arose from terrestrial mammal RABV, or vice-versa. Finally, using coalescent approaches, we estimated that RABV had similar rates of population growth and nucleotide substitution (approximately 2.5-4x10(-4) substitutions per site, per year) in both bats and terrestrial mammals, despite underlying differences in epidemiology.
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