The M2 Gene Is a Determinant of Reovirus-Induced Myocarditis.

Although a broad range of viruses cause myocarditis, the mechanisms that underlie viral myocarditis are poorly understood. Here, we report that the M2 gene is a determinant of reovirus myocarditis. The M2 gene encodes outer capsid protein µ1, which mediates host membrane penetration during reovirus entry. We infected newborn C57BL/6 mice with reovirus strain type 1 Lang (T1L) or a reassortant reovirus in which the M2 gene from strain type 3 Dearing (T3D) was substituted into the T1L genetic background (T1L/T3DM2). T1L was nonlethal in wild-type mice, whereas more than 90% of mice succumbed to T1L/T3DM2 infection. T1L/T3DM2 produced higher viral loads than T1L at the site of inoculation. In secondary organs, T1L/T3DM2 was detected with more rapid kinetics and reached higher peak titers than T1L. We found that hearts from T1L/T3DM2-infected mice were grossly abnormal, with large lesions indicative of substantial inflammatory infiltrate. Lesions in T1L/T3DM2-infected mice contained necrotic cardiomyocytes with pyknotic debris, as well as extensive lymphocyte and histiocyte infiltration. In contrast, T1L induced the formation of small purulent lesions in a small subset of animals, consistent with T1L being mildly myocarditic. Finally, more activated caspase-3-positive cells were observed in hearts from animals infected with T1L/T3DM2 than T1L. Together, our findings indicate that substitution of the T3D M2 allele into an otherwise T1L genetic background is sufficient to change a nonlethal infection into a lethal infection. Our results further indicate that T3D M2 enhances T1L replication and dissemination in vivo, which potentiates the capacity of reovirus to cause myocarditis. IMPORTANCE Reovirus is a nonenveloped virus with a segmented double-stranded RNA genome that serves as a model for studying viral myocarditis. The mechanisms by which reovirus drives myocarditis development are not fully elucidated. We found that substituting the M2 gene from strain type 3 Dearing (T3D) into an otherwise type 1 Lang (T1L) genetic background (T1L/T3DM2) was sufficient to convert the nonlethal T1L strain into a lethal infection in neonatal C57BL/6 mice. T1L/T3DM2 disseminated more efficiently and reached higher maximum titers than T1L in all organs tested, including the heart. T1L is mildly myocarditic and induced small areas of cardiac inflammation in a subset of mice. In contrast, hearts from mice infected with T1L/T3DM2 contained extensive cardiac inflammatory infiltration and more activated caspase-3-positive cells, which is indicative of apoptosis. Together, our findings identify the reovirus M2 gene as a new determinant of reovirus-induced myocarditis.

Establishment of a rare minnow (Gobiocypris rarus) model for evaluation of experimental vaccines against a disease induced by grass carp reovirus genotype II.

Vaccination is the most effective way to control the grass carp haemorrhagic disease (GCHD) with the primary pathogen grass carp reovirus genotype II (GCRV-II). However, due to the large difference in breeding conditions and unclear genetic background of grass carp, the results of the experiment were not reliable, which further hinders the effective prevention and control of GCHD. The rare minnow (Gobiocypris rarus) is highly sensitive to GCRV. Its small size, easy feeding, transparent egg membrane, and annual spawning are in line with the necessary conditions for an experimental aquatic animals culture object. In this study, immunogenicity and protective effects of attenuated and inactivated viruses for grass carp and rare minnow were evaluated in parallel. The expression of immune-related genes increased statistically significant after immunization. With the rise of specific serum antibody titers, the results of rare minnow and grass carp were consistent. In addition, there was no significant residue of adjuvant observed in both fish species injected with an adjuvanted and inactivated virus. Challenge of immunized grass carp and rare minnow with the isolate HuNan1307 resulted in protection rates of 95.8% and 92.6% for attenuated virus, 81.4% and 77.7% for inactivated virus, respectively, as well as the viral load changed consistently. The results indicated that rare minnow can be used as a model for evaluation of experimental vaccines against GCHD.

Global and Complement Gene-Specific DNA Methylation in Grass Carp after Grass Carp Reovirus (GCRV) Infection.

Grass carp reovirus (GCRV) causes huge economic loss to the grass carp cultivation industry but the mechanism remains largely unknown. In this study, we investigated the global and complement gene-specific DNA methylation in grass carp after GCRV infection aimed to uncover the mechanism underlying GCRV infection. The global DNA methylation level was increased after GCRV infection. Expression levels of enzymes involved in DNA methylation including DNA methyltransferase (DNMT), ten-eleven translocation proteins (TETs), and glycine N-methyltransferase (GNMT) were significantly altered after GCRV infection. In order to investigate the relationship between the gene expression level and DNA methylation level, two representative complement genes, complement component 3 (C3) and kininogen-1 (KNG1), were selected for further analysis. mRNA expression levels of the two genes were significantly increased at 5 and 7 days after GCRV infection, whereas the DNA methylation level at the 5' flanking regions of the two genes were down-regulated at the same time-points. Moreover, a negative correlation was detected between gene expression levels and DNA methylation levels of the two genes. Therefore, the current data revealed a global and complement gene-specific DNA methylation profile after GCRV infection. Our study would provide new insights into understanding the mechanism underlying GCRV infection.

Novel reovirus associated with epidemic mortality in wild largemouth bass (Micropterus salmoides).

Reoviruses (family Reoviridae) infect vertebrate and invertebrate hosts with clinical effects ranging from inapparent to lethal. Here, we describe the discovery and characterization of Largemouth bass reovirus (LMBRV), found during investigation of a mortality event in wild largemouth bass (Micropterus salmoides) in 2015 in WI, USA. LMBRV has spherical virions of approximately 80 nm diameter containing 10 segments of linear dsRNA, aligning it with members of the genus Orthoreovirus, which infect mammals and birds, rather than members of the genus Aquareovirus, which contain 11 segments and infect teleost fishes. LMBRV is only between 24 % and 68 % similar at the amino acid level to its closest relative, Piscine reovirus (PRV), the putative cause of heart and skeletal muscle inflammation of farmed salmon. LMBRV expands the known diversity and host range of its lineage, which suggests that an undiscovered diversity of related pathogenic reoviruses may exist in wild fishes.

A new aquareovirus causing high mortality in farmed Atlantic halibut fry in Norway.

A new aquareovirus was isolated from cultured Atlantic halibut (Hippoglossus hippoglossus) fry at a facility where massive mortalities had occurred during the start-feeding phase. The same virus was also detected in juveniles (about 10 grams) of the 2013 generation at two other production sites, but not in larger fish from generations 2007-2012. The virus replicated in BF-2 and CHSE-214 cell cultures and produced syncytia and plaque-like cytopathic effects. This Atlantic halibut reovirus (AHRV) was associated with necrosis of the liver and pancreas, syncytium formation in these tissues, and distinct viroplasm areas within the syncytium in halibut fry. Transmission electron microscopy revealed that the viroplasm contained virions, non-enveloped, icosahedral particles approximately 70 nm in diameter with a double capsid layer, amorphous material, and tubular structures. The RNA-dependent RNA polymerase (RdRp) gene from the AHRV isolates showed the highest amino acid sequence identity (80 %) to an isolate belonging to the species Aquareovirus A, Atlantic salmon reovirus TS (ASRV-TS). A partial sequence from the putative fusion-associated small transmembrane (FAST) protein of AHRV was obtained, and this sequence showed the highest amino acid sequence identity (46.8 %) to Green River Chinook virus which is an unassigned member of the genus Aquareovirus, while a comparison with isolates belonging to the species Aquareovirus A showed <33 % identity. A proper assessment of the relationship of AHRV to all members of the genus Aquareovirus, however, is hampered by the absence of genetic data from members of several Aquareovirus species. AHRV is the first aquareovirus isolated from a marine coldwater fish species and the second reovirus detected in farmed fish in Norway. A similar disease of halibut fry, as described in this paper, has also been described in halibut production facilities in Canada and Scotland.

The role of avian reoviruses in turkey tenosynovitis/arthritis.

Turkey arthritis reovirus (TARV) has been isolated from the gastrocnemius tendons and tibiotarsal joint fluid of lame male turkeys >12 weeks old in the Midwest. Two experiments were conducted to compare the pathogenicity in turkeys of three TARVs (TARV-MN2, TARV-MN4 and TARV-O'Neil), one turkey enteric reovirus (TERV strain MN1) and one chicken arthritis reovirus (CARV strain MN1). Two hundred microlitres of virus were inoculated by the oral, intratracheal, or footpad route into 6-day-old poults placed in isolator units. Poults were necropsied at 1 and 4 weeks post infection in Experiment 1, and at 2 and 4 weeks post infection in Experiment 2. Reovirus was detected by reverse transcription-polymerase chain reaction and virus isolation in tendons of TARV-inoculated poults at 1, 2 and 4 weeks post infection. TARV-O'Neil and TARV-MN2 were detected in tendons of sentinal birds at 1 and 4 weeks and 1 week p.i., respectively. In general, TARVs produced lymphocytic tenosynovitis of the gastrocnemius and digital flexor tendon sheaths without inflammation of the tendons proper. In Experiment 1, poults inoculated with TARV-MN2 and TARV-O'Neil had significantly higher gastrocnemius tendon inflammation scores, as determined by histology, than those inoculated with TERV-MN1 or CARV-MN1. In Experiment 2, poults inoculated with TARV-MN2 and TARV-O'Neil had significantly higher gastrocnemius tendon inflammation scores than those inoculated with TARV-MN4 and virus-free medium (negative control group). Koch's postulates was fulfilled when TARV-MN2 and TARV-O'Neil were re-isolated from tendons of poults that had originally been challenged with either of these viruses. Results of these experiments indicate that TARVs have a unique ability to induce gastrocnemius tenosynovitis in turkeys and that administration of TARV-O'Neil through the oral or intratracheal route is a reproducible model to study pathogenesis of TARV infection.

Patterns of Hemorrhagic Disease in White-Tailed Deer (Odocoileus virginianus) in the Great Plains of the USA, 1982-2020.

Hemorrhagic disease (HD) of deer is caused by epizootic hemorrhagic disease virus (EHDV) or bluetongue virus (BTV) and is considered one of the most important viral diseases of white-tailed deer (Odocoileus virginianus). Despite evidence of changing patterns of HD in the northeastern and upper midwestern US, the historical and current patterns of HD in the Great Plains remain poorly described. We used results from an annual survey documenting HD mortality to characterize historic and current patterns of HD in the northern and central Great Plains (North Dakota, South Dakota, Nebraska, Kansas, and Oklahoma), US, between 1982 and 2020. Further, we assessed temporal change using linear regression to determine change in annual reporting intensity (percentage of counties in a state with reported HD) and change in reporting frequency (the number of years a county or state reported HD) during each decade between 1982 and 2020. Across the 38-yr study period, HD reports expanded northeast across latitude and longitude. Intensity of HD reports significantly increased during this period for three (North Dakota, South Dakota, Kansas) of five states examined. Frequency of reports also increased for all five states. Such changes in northern latitudes might lead to increased deer mortality in regions where HD epizootics have been historically less frequent. Understanding how patterns of HD are changing on the landscape is important when considering future deer management in the face of other mortality factors.

A 15 nucleotide deletion mutation in coding region of the RIG-I lowers grass carp (Ctenopharyngodon idella) resistance to grass carp reovirus.

RIG-I (Retinoic acid-inducible gene I) is a pivotal receptor that detects numerous RNA and DNA viruses and plays crucial roles in the induction of type I interferons. In the present study, a deletion mutation in CiRIG-I (Ctenopharyngodon idella RIG-I) coding region was detected, its association with resistance/susceptibility to grass carp reovirus (GCRV) was examined, and possible mechanism was analyzed. A 15-bp deletion mutation was found, and the mutation results in a deletion of five amino acids. To investigate the genotypes and alleles, the relevant PCR products were electrophoresed on 2.5% agarose gel. Three genotypes and two alleles were discovered. The general allele was named as A and the deletion mutation allele was named as B. The deletion mutation cancels a predicted phosphorylation site and changes the secondary structure and the probability of peroxisomal targeting signal 1 in CiRIG-I. To explore the correlation between these genotypes and the resistance of grass carp to GCRV, a challenge experiment was carried out. The cumulative mortality in genotype AA (40.70%) and AB (52.73%) was significantly lower than that in genotype BB (71.43%) (P = 0.032). The result demonstrated that genotype AA and AB were resistant to GCRV, while genotype BB was susceptible. The 15-bp deletion mutation lowers the resistance of grass carp to GCRV. This result might provide a potential genetic marker for further investigation of selective breeding of resistant grass carp to GCRV.

Type I interferon signaling limits reoviral tropism within the brain and prevents lethal systemic infection.

In vivo and ex vivo models of reoviral encephalitis were utilized to delineate the contribution of type I interferon (IFN) to the host's defense against local central nervous system (CNS) viral infection and systemic viral spread. Following intracranial (i.c.) inoculation with either serotype 3 (T3) or serotype 1 (T1) reovirus, increased expression of IFN-α, IFN-ß, and myxovirus-resistance protein (Mx1; a prototypical IFN stimulated gene) was observed in mouse brain tissue. Type I IFN receptor deficient mice (IFNAR(-/-)) had accelerated lethality, compared to wildtype (B6wt) controls, following i.c. T1 or T3 challenge. Although viral titers in the brain and eyes of reovirus infected IFNAR(-/-) mice were significantly increased, these mice did not develop neurologic signs or brain injury. In contrast, increased reovirus titers in peripheral tissues (liver, spleen, kidney, heart, and blood) of IFNAR(-/-) mice were associated with severe intestinal and liver injury. These results suggest that reovirus-infected IFNAR(-/-) mice succumb to peripheral disease rather than encephalitis per se. To investigate the potential role of type I IFN in brain tissue, brain slice cultures (BSCs) were prepared from IFNAR(-/-) mice and B6wt controls for ex vivo T3 reovirus infection. Compared to B6wt controls, reoviral replication and virus-induced apoptosis were enhanced in IFNAR(-/-) BSCs indicating that a type I IFN response, initiated by resident CNS cells, mediates innate viral immunity within the brain. T3 reovirus tropism was extended in IFNAR(-/-) brains to include dentate neurons, ependymal cells, and meningeal cells indicating that reovirus tropism within the CNS is dependent upon type I interferon signaling.

A Mortality-Based Description of EHDV and BTV Prevalence in Farmed White-Tailed Deer (Odocoileus virginianus) in Florida, USA.

Hemorrhagic disease (HD) caused by bluetongue virus (BTV) and epizootic hemorrhagic disease virus (EHDV) is the most important viral disease of farmed and wild white-tailed deer (WTD; Odocoileus virginianus) and can cause substantial mortality in susceptible hosts. Captive cervid farming is an emerging industry in Florida, an HD-enzootic region. Morbidity and mortality due to HD are major concerns among deer farmers, but the impact of HD on Florida's cervid farming industry is unknown. Our primary objective was to determine the prevalence of epizootic hemorrhagic disease virus (EHDV) and bluetongue virus (BTV) among WTD submitted to the University of Florida Institute of Food and Agricultural Sciences Cervidae Health Research Initiative (CHeRI) for post-mortem diagnostics. Our secondary objectives were to identify the predominant circulating EHDV serotypes during each sampling year and to determine the age class with the greatest proportion of EHDV- and BTV-positive post-mortem specimens. From 2016 to 2020, spleen samples from 539 farmed WTD with unexplained mortality were tested for the presence of EHDV and BTV by RT-qPCR. Overall, the prevalence of EHDV, BTV, or EHDV/BTV coinfection was 26%, 16%, and 10%, respectively, and 44% of deer (237/539) were diagnosed with HD by RT-qPCR. The predominant circulating EHDV serotype varied by year. Overall, EHDV-2 was the most commonly identified serotype (55% of PCR-positive cases), and EHDV-1 was the least frequently identified serotype (16% of PCR-positive cases). The greatest proportion of EHDV/BTV positives among mortality cases was observed in young WTD aged 3-6 months (50%-82% positive). There was a significant difference in the prevalence of EHDV/BTV by age when comparing specimens from WTD over 1 year old (p = 0.029, n = 527). Among these samples, the number of reported mortalities and the prevalence of EHDV/BTV were highest in yearling animals (56%). These data provide the first estimate of EHDV and BTV prevalence and virus serotypes among farmed WTD in Florida, identify the WTD age groups with the greatest proportions of EHDV- and BTV-positive specimens, and suggest that HD caused by these two viruses may be a major source of mortality challenging the captive cervid farming industry in Florida.

Survival of white-tailed deer fawns in central Iowa.

Understanding demographic parameters such as survival is important for scientifically sound wildlife management. Survival can vary by region, sex, age-class, habitat, and other factors. White-tailed deer fawn survival is highly variable across the species' range. While recent studies have investigated fawn survival in several Midwestern states, there have been no published estimates from Iowa for 30 years. We radio-collared 48 fawns in central Iowa from 2015-2017 to estimate survival, home range size, and habitat composition and identity causes of mortality. Estimated fawn survival (± SE) was similar to other Midwest studies at 30 (0.78 ± 0.07)) and 60 days (0.69 ± 0.08), but considerably lower at 7 months (0.31 ± 0.02). Survival was positively associated with woodland habitat through 30 and 60 days, but not related to habitat at 7 months. Female fawns avoided agricultural habitat in their home ranges. Fawn 95% kernel density home ranges were smaller than in other studies in the Midwest (21.22 ± 2.74 ha at 30 days, 25.47 ± 2.87 ha at 60 days, and 30.59 ± 2.37 ha at 7 months). The large amount of woodland and grassland (>90%) in our study area meant that fawns did not have to travel far to find suitable cover, which may explain their small home ranges. We recorded 21 mortalities, the leading cause of which was disease (n = 9; 56% epizootic hemorrhagic disease [EHD]) followed by suspected predation (4) and harvest (3). The mortality associated with an outbreak of EHD in 2016, all of which occurred after 60 days post-capture, is the most likely explanation for our low survival estimate at 7 months. While predation, usually early in life, is the leading cause of mortality in most studies, sporadic diseases like EHD can be a major source of mortality in older fawns in some years.

Effect of beta-glucan on activity of antioxidant enzymes and Mx gene expression in virus infected grass carp.

The effects of beta-glucan, an immunostimulatory agent, on the superoxide dismutase (SOD) and catalase (CAT) activities of erythrocytes and Mx gene expression were studied from grass carp that were challenged with grass carp hemorrhage virus (GCHV). The SOD and CAT activities in erythrocytes and Mx gene expression in spleen from the fish were detected by spectrophotometry and RT-PCR, respectively. Negative control fish were injected with PBS; positive control groups were injected with either beta-glucan or GCHV only; and the experimental groups were pre-injected with beta-glucan 15 days prior to injection with GCHV. The results show that the SOD and CAT activities were higher in fish injected with beta-glucan for 15 days than the negative control group injected with PBS. The SOD and CAT activities significantly decreased when the fish were challenged with GCHV, but it was higher in the group pre-treated with beta-glucan than in infected fish not pre-treated, 15 days after GCHV infection. Mx gene expression levels increased during the early stages (at 12 h and 36 h) of GCHV infection, and it remained at higher levels from the 6th till the 10th day in the beta-glucan pre-treated group, but it was falling from the 6th day in the beta-glucan untreated group. The GCHV-infected group pre-treated with beta-glucan had a higher survival rate (60%) than the group not pre-treated with beta-glucan (20%), suggesting that beta-glucan possesses or enhances anti-viral responses.

Lethal murine infection model for human respiratory disease-associated Pteropine orthoreovirus.

Pteropine orthoreovirus (PRV) is an emerging bat-borne human pathogen causing severe respiratory illness. To date, however, the evaluation of PRV virulence has largely depended on the limited numbers of clinical cases owing to the lack of animal models. To develop an in vivo model of PRV infection, an inbred C3H mouse strain was infected intranasally with pathogenic PRV strain Miyazaki-Bali/2007. C3H mice suffered severe lung infection with significant body weight reduction and died within 7 days after intranasal infection. Infectious viruses were isolated mainly from the lungs and trachea. Histopathological examination revealed interstitial pneumonia with monocytes infiltration. Following repeated intranasal infection, mice developed antibodies to particular structural and non-structural proteins of PRV. The results of these immunological assays will help to develop laboratory protocols for sero-epidemiological studies. Our small rodent model of lethal respiratory infection will further allow investigation of the molecular mechanisms underlying the high pathogenicity of PRV.

Plasmid pcDNA3.1-s11 constructed based on the S11 segment of grass carp reovirus as DNA vaccine provides immune protection.

Although some commercial vaccines against grass carp reovirus (GCRV) are available, given the many varieties of GCRV and limited types of vaccines, the disease caused by GCRV remains a major problem, which leads to economic losses in grass carp aquaculture. A reovirus strain (GCRV-HN14) was recently isolated from local diseased fish in our laboratory. The S11 segment of GCRV-HN14 was speculated to encode the virus capsid protein VP35. In our study, the S11 segment was cloned into the eukaryotic expression vector pcDNA3.1(+) to construct the recombinant plasmid pcDNA3.1-s11, which was then transfected into CIK cells, and the VP35 protein was successfully expressed. Grass carp was immunized with pcDNA3.1-s11, and the in vivo distribution and expression of the pcDNA3.1-s11 plasmids were analyzed by PCR and Western blot. Recombinant plasmids were detected in the blood, liver, spleen, kidney, and muscle. However, protein expression could only be detected in the muscle. The immune protection of the pcDNA3.1-s11 plasmid in grass carp was evaluated using a series of experiments. Results showed that the population of white blood cells significantly increased at 1, 7, and 14 days post-immunization (dpi) and reached a peak with (9.58 ±â€¯0.72) × 107/ml at 7 dpi (P < 0.01 or P < 0.05). The percentage of neutrophils reached a peak with (24.13 ±â€¯2.38)% at 7 dpi (P < 0.01), whereas the lymphocytes peaked with (93.30 ±â€¯4.71)% at 14 dpi (P < 0.05). Serum antibody levels were significantly enhanced in immunized fish at 14, 21, and 28 dpi (P < 0.01). The mRNA expression levels of type I interferon, immunoglobulin M, Toll-like receptor 22, and major histocompatibility complex class I were significantly up-regulated in the head kidney and spleen of immunized fish (P < 0.05). Grass carp immunized with pcDNA3.1-s11 exhibited a higher survival percentage (70.4%-73.3%) than the controls (5%-13%). Overall, as a DNA vaccine, the pcDNA3.1-s11 plasmid could induce immune protection against GCRV.

Central nervous system signs in chickens caused by a new avian reovirus strain: a pathogenesis study.

The present study describes the pathogenesis of infection of chicks with a new avian reovirus strain, belonging to the so-called enteric reovirus strains (ERS) that is capable of causing central nervous system signs in SPF white leghorns. After intramuscular (IM) or oral inoculation birds were either observed for clinical signs or sacrificed for macroscopic, histological and virological examination for 21 days. Virus isolation was performed on the brain, leg muscle, hock joint, liver and spleen. For the detection of viral antigen the immunohistochemistry (IHC) technique was performed on the caudal part of the cerebrum, spinal cord including spinal ganglia and right N. Ischiadicus. High mortality (79% in 7 days) was seen in birds that were inoculated IM. Survivors were depressed and stayed small until the end of the experiment. One bird had tremor and showed torticollis at 9 days after IM inoculation. Birds that were inoculated orally were depressed from day 4 and stayed small until the end of the experiment. One bird showed a torticollis at 10 days after inoculation. After both IM and oral inoculation ERS was isolated from the brain between 3 and 10 days after inoculation. Other examined organs were positive for virus isolation from day 1 or 5 until day 21. IHC revealed viral antigen positive cells in the Plexus chorioideus (plexus epithelial cells or cells within the underlying connective tissue) and in a spinal ganglion. The results indicate that the pathogenesis of ERS infection in chickens bears some resemblance with that of the mammalian reoviruses serotype 1 in mice.

Isolation and pathogenicity of the mammalian orthoreovirus MPC/04 from masked civet cats.

Mammalian reoviruses (MRVs) are associated with pulmonary infections and have been isolated from humans and various animals experiencing respiratory illness. We report here the first case of an MRV detected in the masked palm civet, which showed the highest similarity to the serotype 3 MRV. Reovirus particles were identified by electron microscopic examination of both negative-stain and thin-section. Genomic pattern analysis on SDS-PAGE showed that MPC/04 had 10-segmented double-strand RNA genome. Intranasal infection of four-week-old female BALB/c mice resulted in fatal respiratory distress but not other routes. Infections caused tissue damage and inflammation. MPC/04 grew to higher titers in the lungs than in other tissues. This research strongly suggests a need for additional experimentation to understand the pathogenic mechanisms of mammalian orthoreoviruses in infected animals and humans.

Anti-interleukin-3 and anti-nerve growth factor increase neonatal mice survival to reovirus type 3 clone 9 per oral challenge.

Reovirus type 3 clone 9 (T3C9) induces lethal encephalitis in neonatal, but not adult mice. Whether host factors that promote the development and/or functioning of nervous and gastrointestinal tissues could modulate the pathogenesis of this enteric virus was examined. The results showed that antibody specific for interleukin-3 or nerve growth factor antiserum, but not anti-interleukin-6 or anti-tumor necrosis factor-alpha/beta increased mice survival to T3C9 and decreased viral titers in nervous tissues early after infection. These data suggest that IL-3 and NGF are involved in the pathogenesis of T3C9 infection in neonatal mice.

Reovirus associated with excessive mortality in young bobwhite quail.

Multiple submissions of bobwhite quail (Colinus virginianus) were received for diagnosis from a commercial-size quail operation. The history and clinical signs included respiratory distress, lethargy, and substantial mortality. Reovirus was recovered from quail in the first submission, and both reovirus and adenovirus were isolated from later submissions. To determine the pathogenicity of the isolated reovirus, the initial isolate was inoculated into young quail from a different source. Those inoculated by the subcutaneous route became lethargic, and more than half died during the 2 weeks of the trial. Reovirus was recovered from a high percentage of those inoculated by this route. To the authors' knowledge, the isolation of reovirus from quail has rarely been reported, and reovirus has never before been suggested as a pathogen in this species.

American woodcock (Scolopax minor) mortality associated with a reovirus.

A virus isolate associated with a 1989-90 die-off in American woodcock (Scolopax minor) was identified as a reovirus. Emaciation was a consistent necropsy finding in the woodcock involved in this die-off. This reovirus infection appeared to be systemic, had the potential for fecal oral virus transmission, and was associated with deterioration of body condition. To our knowledge this is the first report of a virus isolate from wild American woodcock. A survey conducted in 1990-92 indicated that this virus was not present at detectable levels in the woodcock breeding and wintering population.