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Identification of aviadenovirus and dependoparvovirus in an Adélie penguin fecal sample from Cape Royds (Ross Island, Antarctica).
Adenoviruses (Adenoviridae) and their associated replication-deficient dependoparvoviruses (Parvoviridae) are recognized as significant components of the avian virome. While well-studied in domestic birds, these viruses remain underexplored in wild Antarctic birds. Information is limited on viruses circulating in penguins, particularly outside of the Antarctic Peninsula Region. Here we leverage a fecal sample collected for diet analyses to identify an aviadenovirus (37,731 nt) and two distinct dependoparvoviruses. The Adélie penguin (Pygoscelis adeliae) feces-derived adenovirus exhibits a genome organization consistent with members of the genus Aviadenovirus but shares only ~64% amino acid identity in the DNA polymerase protein with its closest known relative and thus represents a new species of aviadenovirus identified in penguins. Additionally, we identified two new dependoparvoviruses, one in length of 4,869 nt and a second of 4,162 nt. These two dependoparvoviruses are diverse, sharing <61% Rep amino acid identity with those of other dependoparvoviruses. Penguin dependoparvovirus 1 represents a new species. The co-detection of these viruses in a single seasonal sample could suggest a potential helper-satellite relationship in Adélie penguins. This study provides the first evidence of aviadenoviruses in Adélie penguin feces. These findings highlight the importance of surveillance to understand pathogen dynamics in isolated Antarctic populations.
Histopathologic evidence for parvovirus infection in dogs.
Two dogs kenneled at a commercial establishment died of a disease manifested as severe hemorrhagic diarrhea. Histopathologic findings in both dogs bore a striking resemblance to those typical of feline infectious enteritis. Viral particles resembling members of the Parvoviridae family were observed in the contents of the small intestine of one of the dogs. The disease was similar to the recently recognized canine gastroenteritis associated with a parvovirus-like agent.
Uncovering viral protein acquisition events and human-specific folds with pairwise comparisons of predicted protein structures.
Pairwise sequence comparisons are at the center of molecular evolutionary analyses. However, viral pairwise comparisons are challenging because extreme mutation rates and evolutionary pressure cause genomes to diverge rapidly, limiting detectable sequence similarity to fewer than 3% of virus pairs. To overcome these limitations, we compared viruses based on structural similarity, using predicted protein structures from ColabFold and Foldseek to define protein fold clusters. We represented each virus genome by its protein structural content. Pairwise similarities between viruses were then quantified using the Jaccard index based on the presence or absence of protein fold clusters. Using a recently established viral protein fold database, we compared all pairs of eukaryotic viruses in RefSeq. This approach increased the proportion of comparable viral genome pairs from 2.4% to 16.5%. Using this protein-fold representation of viruses, we were able to accurately predict viral families with an average sensitivity of 85.9%. Investigation of viral families showing limited sensitivity with this approach uncovered a laterally transferred structural cluster (Rep/NS1) broadly shared across diverse viral families and found in the avian lineage of adenoviruses. Sequence homology suggests that this Rep was acquired from Parvoviridae, but the protein is mutant in the ATPase active site, indicating possible exaptation toward a purely DNA-binding function. In Gammapapillomaviruses, several E4 clusters were associated with human tropism. In summary, by representing viruses with structural protein clusters, we can classify highly divergent viruses, trace lateral gene transfer, and uncover features associated with viral host range.
[Morphological virus diagnosis--electron microscopy study of animal viruses with negative contrast procedure].
Reported in this paper are results obtained in morphological virus diagnosis by using the negative contrast technique on the basis of electron microscopy. The availability of high-efficiency electron microscopy as well as of perfectly improved techniques of preparation, knowledge of the latest virus model concepts, and indivudual skills in diagnosis are essential conditions for the above approach. Parvoviridae, picornaviridae, and togaviridae are identifiable only in high particle concentrations and by group representation. Papovaviridae, adenoviridae, herpetoviridae, poxviridae, and reoviridae, on the other hand, can be safely identified even as single particles. The diagnosis of orthomyxoviridae, paramyxoviridae, rhabdoviridae, and retroviridae is facilitated by their own dimensions and their characteristic helico-symmmetrical nucleocapside. Coronaviridae are of highly conspicuous morphology but, nevertheless, pose problems in differential diagnosis. Substantive improvement of morphological virus diagnosis, in terms of minute details, may be achieved by means of the negative contrast method on the basis of immune electron microscopy. Advantages implied in that morphological method include less time-consuming and quite uninvolved practicability and good dependability of diagnosis for more efficient decision-making in research and practice.
Myocarditis of probable viral origin in chickens.
Severe nonsuppurative myocarditis with Feulgen-positive intranuclear inclusions in six adult White Leghorn chickens is described. Livers of three birds had mild to moderate centrilobular coagulative necrosis, with no inclusions. The myocardial intranuclear inclusions contained a large number of 18-to-20-nm particles; these are compared with members of the family Parvoviridae.
Hydrocephalus produced by the 6/94 virus; A parainfluenza type 1 isolate from multiple sclerosis brain tissue.
The 6/94 virus, parainfluenza type 1 isolate from multiple sclerosis brain tissue, produced hydrocephalus in newborn Syrian hamsters. All animals developed clinical disease and died within a week. Ependymal cells lining the aqueduct of Sylvius became necrotic and fused, resulting in obstructive hydrocephalus. The 6/94 virus antigen was seen in ependyma and meninges. Paramyxovirus nucleocapsids were seen within cytoplasm of ependymal cells. Virus was recovered from hamster brains for only two days. Infectious virus could be recovered from brains grown in vitro as explants for 21 days. No evidence of rising hemagglutination-inhibiting antibody was noted for up to one month after infection. Intraperitoneal or subcutaneous injection of 6/94 virus did not produce hydrocephalus. HA2 virus and the temperature sensitive mutant of HA2 virus failed to produce hydrocephalus, while Sendai virus caused lesions similar to those of 6/94 virus.
Viruses associated with acute gastroenteritis in young children.
Conventional virologic investigations generally failed to implicate viruses as a cause of acute gastroenteritis in young children. When negative-contrast stain electron microscopy was used for the examination of stool samples from affected patients, several candidate etiologic agents were discovered. Rotavirus (otherwise known as orbivirus, reo-like agent, and infantile gastroenteritis virus) emerged as an important causative agent. In a considerable number of patients, however, no causative agent was identified. Several other candidate etiologic viruses now "stand in the wings" awaiting additional evidence as to their role in the pathogenesis of acute gastroenteritis. In a study period of 12 months, 669 patients were found to be shedding virus in association with symptoms of diarrhea, vomiting, and temperature elevation. Approximately one third of these patients acquired their infection in hospital.
The pathogenesis of parvovirus-induced cerebellar hypoplasia in the Syrian hamster, Mesocricetus auratus. Fluorescent antibody, foliation, cytoarchitectonic, Golgi and electron microscopic studies.
Cerebellar histogenesis was studied in hamsters infected at birth with a parvovirus, rat virus strain PRE 308. Cerebellar granule cell precursors in these animals were selectively infected and lysed in the external germinal layer before their migration to form the internal granular layer. The effects of the absence of granule cells on cerebellar development and especially on the development of the Purkinje cells and their dendrites was analyzed using fluorescent antibody. Golgi, conventional paraffin, and electron microscopic methods. This study represents the first Golgi and ultrastructural study of the pathogenesis of rat virus infections in the cerebellum. The destruction of the granule cell precursors resulted in a dysplastic cerebellar hypoplasia with total disruption of normal cerebellar stratification and cytoarchitectonics. The Purkinje cells developed misshapen, progressively disoriented dendritic stems lacking tertiary dendrites and studded with numerous spines, devoid of afferent synaptic contacts (naked spines) and encased by glial processes. These developmental studies, together with the mouse mutant studies, demonstrated that the spines of the Purkinje cells were elaborated in the absence of both tertiary dendrites and afferent parallel fiber contacts. Such data suggested that spine formation, once triggered, was intrinsically programmed rather than being dependent on the development of parallel fiber contacts. Despite the loss of a major interneuronal component and disintegration of normal cytoarchitectonic relationships, synapses in the cerebellar cortex developed normally as long as both the pre- and post-synaptic elements were present. Thus synaptic specificity is maintained in the face of gross disruption of cytoarchitectonic relationships. If either the pre- or post-synaptic portion of a contact was absent, then glial processes isolated the persisting element or aberrant contacts formed. In addition to glial encasement of naked spines, there were dendrodendritic articulations between Purkinje cell dendrites, some of which were joined by septate, plaque-like junctions. Aberrant synaptic contacts between mossy and climbing fiber glomeruli and the smooth surface of the Purkinje cell somata were found rarely. In addition to these contacts which also occur in the hypoplastic cerebella produced by other methods, previously undescribed non-synaptic spine-articulations between Purkinje cell dendrites were seen. The role played by granule cells and their axons in Purkinje cell development appeared to be two-fold. First, the development of the orderly array of parallel fibers in the normal animal played a role in orienting and flattening the dendritic trees of Purkinje cells. Second, the formation of tertiary dendritic branches appeared to depend primarily upon the presence of an external germinal layer throughout this stage of Purkinje cell development. By contrast, dendritic spines developed and persisted in the absence of granule cells.
Embryonal carcinoma cells (and their somatic cell hybrids) are resistant to infection by the murine parvovirus MVM, which does infect other teratocarcinoma-derived cell lines.
Minute virus of mice (MVM), a non-defective parvovirus, has been shown to infect cultures of non-pluripotent differentiated teratocarcinoma-derived cells, but pluripotent (and "nullipotent") embryonal carcinoma cells derived from the same teratocarcinoma resist MVN infection. Somatic cell hybrids between an embryonal carcinoma line and Friend erythroblastic leukemia cells are also resistant to MVM, even though Friend cells are susceptible. Among three blastocyst-derived lines tested, only one, a parietal yolk sac cell line, resists MVM infection. These results suggest that teratocarcinoma cultures may provide useful systems in which to study the cellular factors which mediate susceptibility to this teratogenic and oncolytic virus.
Multiple buoyant densities of hepatitis A virus in cesium chloride gradients.
Hepatitis A virus (HAV) recovered from stools of human cases of hepatitis A and from stools of chimpanzees experimentally infected with HAV was shown to possess multiple buoyant densities in CsCl gradients. The greatest proportion of HAV was most frequently found at a buoyant density of 1.32-1.34 g/cm3, however, large proportions of HAV were also frequently found at higher densities, including 1.36-1.37, 1.40-1.42, and 1.45-1.48 g/cm3. These findings are consistent with the notion that HAV may be a parvovirus.
Antigenic relationship of the feline infectious peritonitis virus to coronaviruses of other species.
Utilizing the direct and indirect fluorescent antibody procedure, the antigenic relationship of the feline infectious peritonitis virus (FIPV) to 7 other human and animal coronaviruses was studied. FIPV was found to be closely related to transmissible gastroenteritis virus (TGEV) of swine. Transmissible gastroenteritis virus and FIPV were in turn antigenically related to human coronavirus 229E (HCV-229E) and canine coronavirus (CCV). An interesting finding in the study was that the 8 coronaviruses selected for this study fell into one of two antigenically distinct groups. Viruses in each group were antigenically related to each other to varying degrees, but were antigenically unrelated to coronaviruses of the second group. The first antigenically related group was comprised of mouse hepatitis virus, type 3 (MHV-3), hemeagglutinating encephalomyelitis virus 67N (HEV-67N) of swine, calf diarrhea coronavirus (CDCV), and human coronavirus 0C43 (HCV-OC43). The second antigenically related group was comprised of FIPV, TGEV, HCV-229E and CCV.
Growth of an autonomously replicating parvovirus (feline panleukopenia): kinetics and morphogenesis.
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Observations on the pathogenesis of porcine parvovirus infection.
Differences in the pathogenesis of porcine parvovirus (PPV) were shown when pregnant gilts were infected by the oral and intramuscular (i.m.) routes. By the oral route, PPV took 23-32 days to cross the placenta following infection of the dam, as compared to 15 days by the i.m. route, Successful transplacental infection occurred following oral infection of dams only in the second third of gestation, whilst i.m. infection resulted in infection of foetuses in both first and second thirds of gestation. Foetal infection resulted in death and mummification only where infection of foetuses occurred before onset of immune competence--estimated at 70 days gestation. Infected foetuses either died before onset of immune competence, or survived to mount an immune response with subsequent death or survival to farrowing. It is suggested in discussion that reproductive failure due to PPV, characterised by mummification or occasional stillbirth, is associated in nature with oral infection, and occurs only when dams are infected in the first part of the midthird of gestation.
Interaction in replication between goose parvovirus strain B and duck plague herpesvirus.
The goose parvovirus strain B was found to replicate only in cells with DNA synthesis. Cells in the stationary phase of DNA synthesis or maintained under 2 mM thymidine (TdR) in excess were refractive to the parvovirus infection. However, stationary phase cells could be rendered to produce progeny paroviruses by herpesvirus superinfection. In reverse, the replication of the herpesvirus was significantly inhibited by parvovirus preinfection of cells.
Infection of newborn and fetal hamsters induced by inoculation of LuIII parvovirus.
The LuIII parvovirus was adapted to the newborn hamster and produced a systemic infection with massive intestinal hemorrhage. Inoculation of pregnant hamsters lead to transplacental infection of the fetuses and abortion. Most fetal deaths were observed in animals inoculated on days 8 and 10 of gestation. Virus was recovered from dead fetuses, placentas, and viable fetuses. Histological lesions were found in the heart, liver, kidney and CNS of infected fetuses.