Tissue Distribution Of Virus Research Articles

Camelids as a host of bovine viral diarrhoea virus infection — what we have learned to date

Bovine viral diarrhoea virus (BVDV) has been associated with reproductive loss, diarrhoea, immune-suppression with increased susceptibility to opportunistic infection (such as parasitism and pneumonia), wastage and death in South American Camelids (SAC). Unidentified BVDV infection thus poses a significant threat to herd health. BVDV type 1b strains predominate in alpacas and are able to establish transplacental infection, potentially leading to persistently infected (PI) offspring in >80% of naive, pregnant alpacas naturally exposed to BVDV type Ib during early gestation. PI alpaca crias experience a high degree of morbidity and mortality in the first 6 months of life, associated with a variety of clinical disease manifestations. Peripartum phenotypic and haematological characteristics of PI crias may be clinically indistinguishable from those of chronically infected crias with extended viraemia. Low birth weight, stunted growth, anaemia, relative and absolute monocytosis are commonly observed in affected animals. PI crias may have host defense deficits similar to PI calves and experience widespread viral tissue distribution. Both clinical and epidemiological studies underscore the importance of routine BVDV-specific diagnostic testing in order to identify persistently (lifelong) and chronically infected camelids, which serve as an important source of viral spread within and between farms.

Highly (H5N1) and Low (H7N2) Pathogenic Avian Influenza Virus Infection in Falcons Via Nasochoanal Route and Ingestion of Experimentally Infected Prey

An experimental infection with highly pathogenic avian influenza (HPAI) and low pathogenic avian influenza (LPAI) viruses was carried out on falcons in order to examine the effects of these viruses in terms of pathogenesis, viral distribution in tissues and viral shedding. The distribution pattern of influenza virus receptors was also assessed. Captive-reared gyr-saker (Falco rusticolus x Falco cherrug) hybrid falcons were challenged with a HPAI H5N1 virus (A/Great crested grebe/Basque Country/06.03249/2006) or a LPAI H7N2 virus (A/Anas plathyrhynchos/Spain/1877/2009), both via the nasochoanal route and by ingestion of previously infected specific pathogen free chicks. Infected falcons exhibited similar infection dynamics despite the different routes of exposure, demonstrating the effectiveness of in vivo feeding route. H5N1 infected falcons died, or were euthanized, between 5–7 days post-infection (dpi) after showing acute severe neurological signs. Presence of viral antigen in several tissues was confirmed by immunohistochemistry and real time RT-PCR (RRT-PCR), which were generally associated with significant microscopical lesions, mostly in the brain. Neither clinical signs, nor histopathological findings were observed in any of the H7N2 LPAI infected falcons, although all of them had seroconverted by 11 dpi. Avian receptors were strongly present in the upper respiratory tract of the falcons, in accordance with the consistent oral viral shedding detected by RRT-PCR in both H5N1 HPAI and H7N2 LPAI infected falcons. The present study demonstrates that gyr-saker hybrid falcons are highly susceptible to H5N1 HPAI virus infection, as previously observed, and that they may play a major role in the spreading of both HPAI and LPAI viruses. For the first time in raptors, natural infection by feeding on infected prey was successfully reproduced. The use of avian prey species in falconry husbandry and wildlife rehabilitation facilities could put valuable birds of prey and humans at risk and, therefore, this practice should be closely monitored.

Pathogenesis and transmissibility of highly (H7N1) and low (H7N9) pathogenic avian influenza virus infection in red-legged partridge (Alectoris rufa)

An experimental infection with highly pathogenic avian influenza virus (HPAIV) and low pathogenic avian influenza virus (LPAIV) was carried out in red-legged partridges (Alectoris rufa) in order to study clinical signs, gross and microscopic lesions, and viral distribution in tissues and viral shedding. Birds were infected with a HPAIV subtype H7N1 (A/Chicken/Italy/5093/1999) and a LPAIV subtype H7N9 (A/Anas crecca/Spain/1460/2008). Uninoculated birds were included as contacts in both groups. In HPAIV infected birds, the first clinical signs were observed at 3 dpi, and mortality started at 4 dpi, reaching 100% at 8 dpi. The presence of viral antigen in tissues and viral shedding were confirmed by immunohistochemistry and quantitative real time RT-PCR (qRRT-PCR), respectively, in all birds infected with HPAIV. However, neither clinical signs nor histopathological findings were observed in LPAIV infected partridges. In addition, only short-term viral shedding together with seroconversion was detected in some LPAIV inoculated animals. The present study demonstrates that the red-legged partridge is highly susceptible to the H7N1 HPAIV strain, causing severe disease, mortality and abundant viral shedding and thus contributing to the spread of a potential local outbreak of this virus. In contrast, our results concerning H7N9 LPAIV suggest that the red-legged partridge is not a reservoir species for this virus.

Plasmid containing CpG oligodeoxynucleotides can augment the immune responses of pigs immunized with porcine reproductive and respiratory syndrome killed virus vaccine

Porcine reproductive and respiratory syndrome virus (PRRSV), the causative agent of porcine reproductive and respiratory syndrome (PRRS), causes serious health problems in swine, resulting in great economic losses to the swine industry worldwide. The porcine reproductive and respiratory syndrome (PRRS) killed virus (KV) vaccine has been widely used in China but has been linked with side effects in pigs and only partial protection. A few studies have demonstrated the immunostimulatory adjuvant effects of the synthetic CpG oligodeoxynucleotide (ODN) motifs in humans and animals. In this study, the adjuvant efficacy and the protective effects of recombinant plasmid containing CpG ODN, in combination with PRRS KV vaccine against PRRSV were evaluated. The concentration of PRRSV-specific antibodies and cytokines and the clinical parameters (body temperature, weight gain and behavior) on the challenge and post-challenge virological profiles (virus distribution in tissues and virus titers in serum at autopsy) were investigated to define the immune responses of pigs. Our findings indicated that the immune responses of the pigs immunized with plasmid containing CpG ODN and PRRS KV vaccine were stronger than those induced by PRRS KV vaccine or PBS alone. Furthermore, the protection ratios, PRRSV titers in serum samples and virus tissue distribution, all demonstrated that the plasmid containing CpG ODN could augment the immune responses and improve the protective effect of PRRSV vaccination.

Characterization of Virus Distribution in Rock Bream ( Oplegnathus fasciatus; Temminck and Schlegel) Infected with Megalocytivirus

The distribution of virus-infected cells in the organs of Rock Bream naturally infected with megalocytivirus is reported. Examination of sections of liver, spleen and kidney stained by haematoxylin and eosin (HE) and periodic acid Schiff (PAS) revealed the presence of swollen and degenerate cells having morphology consistent with leucocytes. Many of these cells were shown to contain viral DNA by in-situ hybridization (ISH). Cells containing viral DNA were also found in the connective tissue of other organs in which there was no prominent infiltrate of degenerate leucocytes. Viral DNA was also found in the cytoplasm of leucocytes in blood smears. Transmission electron microscopy (TEM) confirmed the presence of viral particles in the cells within tissue and free within blood. The tissue distribution of virus in this infection is suggested to reflect the infiltration of virus-infected leucocytes.

Pathogenicity and growth characteristics of selected infectious laryngotracheitis virus strains from the United States

In a recent study, several US infectious laryngotracheitis virus (ILTV) strains and field isolates were genotyped by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) into nine different genotypes. All of the commercial poultry isolates were identified within genotypes IV, V, and VI. Based on the PCR-RFLP, Group IV isolates were characterized as genetically identical to the chicken embryo origin (CEO) vaccines, Group V as genetically closely related to the CEO vaccines, and Group VI as genetically different to the vaccine strains. The objective of this study was to determine the pathogenicity and growth characteristics of six ILTV commercial poultry isolates as compared with the CEO vaccine. Two isolates representative of PCR-RFLP Groups IV, V, and VI were selected. Differences in disease severity, viral tissue distribution in chickens, and plaque formation ability in cell culture were observed among viral genotypes IV, V, and VI, and between V-A and V-B isolates. Mild respiratory clinical signs were produced by IV-A, IV-B and the CEO vaccine, while VI-A and VI-B isolates produced severe respiratory signs and severe depression, and during the peak of clinical signs both isolates were re-isolated from the conjunctiva, sinus, trachea and thymus. Similarly to Group VI isolates, V-A and V-B produced severe respiratory signs, depression, and were re-isolated from conjunctiva, sinus, and trachea; on cell culture, both isolates produced significant larger plaques than any of the other isolates analysed. Overall, differences in pathogenicity and growth characteristics were observed among genetically closely related US ILTV isolates; however, complete genomes will be necessary to identify molecular determinants linked to the pathogenic viral phenotypes.

Antibody response and virus tissue distribution in chickens inoculated with wild-type and recombinant fowl adenoviruses

We demonstrated that the long tandemly repeated region (TR-2) is dispensable for in vitro replication of fowl adenovirus 9 (FAdV-9). The TR-2-deleted recombinant FAdV-9 expressing the enhanced green fluorescence protein was further characterized for in vivo effects. Groups of chickens were exposed to recombinant or wild-type FAdV-9 by intramuscular injection, through the feed or drinking water and one group served as a negative control. The antibody (Ab) response, evaluated by ELISA and a plaque reduction test depended on the virus, dosage and the route of inoculation. Although the highest levels of anti-viral Ab were detected in chickens inoculated intramuscularly (i.m.) with wild-type FAdV-9, the deletion of TR-2 did not have a significant effect on the immune response. The tissue distribution of the virus was examined by the polymerase chain reaction (PCR) and was similar for both wild-type and recombinant viruses. Based on these results the TR-2 was dispensable for viral replication in vivo and did not influence virus distribution, and the recombinant FAdV-9 induced the same immune response as the wild-type virus.

Immunohistochemical analysis of two strains of lion (Panthera leo)-adapted canine distemper virus in ferrets (Mustela putorius furo).

Canine distemper virus (CDV) caused epizootics in lions (Panthera leo) in Tanzania's Serengeti National Park in 1994 and in captive lions and other Panthera spp. in the USA in 1991-1992. In this study, immunohistochemistry was used to compare viral distribution in tissues collected from ferrets (Mustela putorius furo) inoculated with one of the two lion-derived CDV isolates, either from Serengeti (A94-11/13) or from California (A92-27/20). The California isolate resulted in severe morbidity in all nine ferrets, whereas the Serengeti isolate resulted in severe morbidity in five of the nine ferrets. A slightly higher proportion of infected cells was found in many tissues in the Serengeti isolate-inoculated ferrets. These findings indicate that the pathogenicity of the California isolate is not directly related to the number of infected cells.

Susceptibility of Three Genetic Lines of Chicks to Infection with a Nephropathogenic T Strain of Avian Infectious Bronchitis Virus

Mortality rates were compared in three genetic lines of specific pathogen-free chicks inoculated with one of two doses of a nephropathogenic strain of avian infectious bronchitis (IB) virus. The mortality rates were influenced primarily by the chick strain, but also by age and dose of virus. Chicks of the inbred S line were highly susceptible. After inoculation with a low dose of virus at 2 and 4 weeks of age, mortality was 90 and 45%, respectively. Chicks of the HWL non-inbred line were also susceptible, with mortality rates after inoculation at 2 and 4 weeks of age of 70 and 25%, respectively. Chicks of the inbred W line were resistant and non-significant mortality of 10% occurred only in 2-week-old chicks inoculated with a high dose of virus. Viral distribution in tissues of susceptible S and resistant W chicks did not differ, and virus was present in the trachea, lung and kidney of chicks from both lines throughout the acute phase (between days 3 and 7) of infection. Viral titres in the trachea and kidney in susceptible S chicks were slightly but not significantly higher than in the other chicks during the acute phase of infection. Histopathological assessment indicated an earlier onset of a regenerative phase in the trachea of W chicks than in S chicks. S chicks, in contrast to W chicks, showed no signs of renal regeneration. Additionally, the kidneys of S chicks differed from those of W chicks in showing more severe nephritis, more tubular necrosis and less heterophil infiltration and lymphocytic response throughout the acute phase of infection. The results indicate that chicken lines may differ greatly in their susceptibility to fatal IB nephritis and that resistance is likely to be under the control of immune responses to viral infection.

Replication and Pathogenicity after Intranasal and Intracranial Inoculation of Swine with a Recombinant Pseudorabies Virus Containing a Deletion at the UL/IR Junction

Pseudorabies virus (PRV) is a neurotropic herpesvirus of swine. Previously, we described construction of a recombinant strain of PRV (LLTβΔ2) which contains a 3.0-kb deletion spanning the junction of the unique long and internal repeat sequences. Compared to the parental strain, Indiana-Funkhauser, and a virus rescued for the deleted sequences (LLTβres), LLTβΔ2 replicated efficiently at the site of inoculation, yet exhibited significantly reduced virulence when inoculated intranasally in pigs. In this report, we investigated the effect of the deletion on PRV replication and virulence after intracranial inoculation of swine, in comparison to replication and virulence after intranasal inoculation, in order to more precisely locate the defect in LLTβΔ2. Four-day-old pigs were infected intranasally with LLTβΔ2 or LLTβres and necropsied at various times postinfection. Compared to LLTβres-infected pigs, tissue distribution of virus, PRV antigen, and lesions of LLTβΔ2-infected pigs were comparable in all peripheral tissues examined, including trigeminal ganglia, but were reduced in tissues from the central nervous system (CNS). LLTβΔ2 was able to replicate in the CNS after intracranial inoculation into the cerebral cortex of 2-day-old piglets and to spread from CNS to peripheral tissues. Neurovirulence of LLTβΔ2 was somewhat reduced, as demonstrated by delayed onset of neurological signs and death in intracranially inoculated pigs. These results indicate that decreased neurovirulence after intranasal inoculation is not due to inability of LLTβΔ2 to replicate in CNS tissues. The difference in the amount of antigen detected in CNS tissues after intracranial inoculation compared to intranasal inoculation suggests that one defect in LLTβΔ2 is reduced ability to spread from peripheral neurons to the CNS after intranasal inoculation.

Effect of T-Lymphocyte Depletion on the Pathogenesis of Marble Spleen Disease Virus Infection in Ring-Necked Pheasants

The purpose of this study was to determine the effect of cyclosporine (CSP)-mediated T-lymphocyte depletion on the pathogenesis of marble spleen disease virus (MSDV) infection in ring-necked pheasants. Seventy-two 6-week-old pheasants were divided into three groups; one group of 18 birds was inoculated with MSDV, a second group of 18 birds was treated with CSP, and a third group of 36 birds was both treated with CSP and inoculated with MSDV. Two birds each from both of the smaller groups and four birds from the largest study group were necropsied periodically over a 14-day period. T-lymphoblastogenesis assays documented significant T-cell depression in the CSP-treated groups. Routine histology and immunohistochemical staining for MSDV antigen demonstrated that the CSP-treated MSDV-inoculated birds had higher lesion incidence, had wider tissue distribution of virus, and retained virus in tissues longer than did the MSDV-inoculated-only birds. These results indicate that T-lymphocytes play a role in the host response to infection with MSDV.

Effect of concurrent graft-versus-host reaction on tissue distribution and infectious titer of murine cytomegalovirus.

Infection with cytomegalovirus is a major concern following bone marrow transplantation. Previously, we have described a model whereby infection by MCMV concurrent with the injection of parental strain lymphoid cells into F1 recipient mice results in a severe graft-versus-host reaction (GvHR) when the donor and host differ at the class I MHC locus (i.e., class I MHC disparate GvHR). The present studies were performed to determine whether one consequence of this severe GvHR is the alteration of the tissue distribution and/or levels of infectious virus as compared to mice not undergoing GvHR. Using PCR to detect MCMV DNA, it was observed that the tissue distribution of virus 3 days after injection was identical in recipients of virus alone and of GvHR plus virus inocula. At two weeks post injection, virus was recovered from the salivary gland and pancreas in both groups. In contrast to recipients of MCMV alone, lung tissue from GvHR plus virus mice also contained viral DNA. Notably, these results were corroborated by the plaque assay. Moreover, salivary gland and pancreas from recipients of GvHR plus virus were found to contain higher titers of infectious virus. In total, the data demonstrate that, with the notable exception of the lung, the distribution of virus was not changed in the animals despite the presence of a concurrent severe GvHR. However, viral replication in infected tissues appeared less restricted in these recipients.

Temporal replication of the Pullman strain of Aleutian disease virus in royal pastel mink.

Information was sought on the temporal replication of Aleutian disease virus in 27 royal pastel mink. Groups of three were examined 8 to 126 days after they were inoculated subcutaneously with 10(3) 50% lethal doses of the Pullman strain. Much individual variation was noted in the onset of infection, occurrence of viremia, and extent of virus replication in the tissues. Thus, virus was detected in lymph nodes regional to the site of inoculation in only some mink during the first 14 days after inoculation. During this period, virus was often present as well in the mesenteric lymph node and spleen. First detected on day 10, viremia was present in all mink examined on day 28 but occurred irregularly thereafter, even when virus was widespread in the tissues. Except in five mink succumbing to the disease, the tissue distribution of virus after day 28 tended to be more limited, and the titers were generally lower than they had been earlier. Even though present in the lymph nodes and spleen, virus was often absent from the kidney, liver, and intestine after day 28. Specific antibody was detected on day 28 and was present in all mink thereafter, ostensibly without any adverse effect on virus replication. In most mink, the infection was considered subclinical, for it was usually not accompanied by a rise in serum gamma globulin or by morphologic evidence of the disease. The virologic findings in this study have a bearing on the relationship of subclinical infections to both horizontal and vertical transmission of the virus.

Fate of Betanodaviruses in the Experimentally Infected Natural and Non-Natural Host

To investigate the fate of betanodavirus, the causative agent of viral nervous necrosis (VNN) in cultured fish, the tissue distribution of virus in experimentally infected fish was investigated. Two genetically different betanodaviruses, striped jack nervous necrosis virus (SJNNV; SJNNV-genotype) and kelp grouper nervous necrosis virus (KGNNV) belonging to red spotted grouper nervous necrosis virus (RGNNV)-genotype, were intramuscularly cross-injected with a dose of 106 TCID50/fish/200 μl in striped jack Pseudocaranx dentex or kelp grouper Epinephelus moara and sacrificed at scheduled to titre the virus in the spinal cord, brain, eye, kidney and blood at day 0, 1, 3, 5, 14 and 21. As a result, intramuscularly inoculated virus was recovered at high titres from the brain, spinal cord, and eye of their natural host species, i.e., striped jack for SJNNV and kelp grouper for KGNNV during 3-week experimental period, while the virus titres were relatively low in the organs of non-natural hosts, particularly in kelp grouper injected with SJNNV. In every case, no virus was detected in blood samples, suggesting that infection did not develop to be systemic. Keywords: Betanodavirus, Viral nervous necrosis, Fate, Tissue distribution, Pseudocaranx dentex, Epinephelus moara, 50% tissue culture infectious dose (TCID50)DOI: http://dx.doi.org/10.3329/bjm.v24i2.1252 Bangladesh J Microbiol, Volume 24, Number 2, December 2007, pp 100-104

Human rabies; a case report with necropsy studies wherein brain and salivary gland yielded virus: notes on the viral tissue distribution.

Journal Article Human Rabies: A Case Report with Necropsy Studies wherein Brain and Salivary Gland Yielded Virus: Notes on the Viral Tissue Distribution Get access Carl A. Berntsen, Jr., M.D., Carl A. Berntsen, Jr., M.D. New York, N. Y. Search for other works by this author on: Oxford Academic PubMed Google Scholar Lewis D. Stevenson, M.D. Lewis D. Stevenson, M.D. New York, N. Y. Search for other works by this author on: Oxford Academic PubMed Google Scholar Journal of Neuropathology & Experimental Neurology, Volume 12, Issue 2, April 1953, Pages 169–185, https://doi.org/10.1097/00005072-195304000-00004 Published: 01 April 1953