Neurological disorders,virus persistence and hypomyelination in calves due to intra‐uterine infections with bovine virus diarrhoea virus

The clinical and pathological findings after a natural intra‐uterine infection with BVD‐virus in a Friesian dairy herd are described. The virological and serological aspects will be discussed in a separate paper (30).

In a period of 4 years, 11 calves were hum with the following nervous symptoms: more or less serious incoördination, tremor, oscillating nystagmus, and a negative blinking reflex. The pupillary and sucking reflexe's were normal. No ocular defects, such as lenticular opacity or retinal atrophy were observed.

The first calf was born in 1979. Within 6 months the symptoms disappeared. After a normal conception and pregnancy this animal gave bⁱrth to 2 clinically normal calves in 1981 and 1982. The second calf died at the age of 2 months, due to an ulcerating enteritis.

In 1980, again 8 calves with the same nervous symptoms were born within a period of 3 months. Two calves died at the age of 3 days and 5 weeks respectively; 2 calves were sold when 10 days and 3 weeks old; one calf did not improve and was necropsied at the age of 17 days. The remaining 3 calves showed only a slight hypermetria when examined after 6 months. At that time nystagmus was only visible with ophthalmoscopy. Two calves were slaughtered when 10 months old. The last one, a bull, proved to be sterile and was necropsied at the age of 1 ½> year.

A calf, born in 1981, recovered within a week and was necropsied at the age of 15 days. The last calf, born in 1982, did not improve at all and was necropsied at the age of 14 days.

During these 4 years none of the other animals in the herd showed any symptoms due to an acute or chronic BVD‐virus infection.

At post mortem examination of 6 animals no macroscopically visible malformations were found. Hypomyelination and abnormal glial cells were evident in 5 cases, especially in the two youngest calves which did not show any improvement. One of them had an obvious thymic hypoplasia. The calf which recovered within a week showed only very slight changes. In one of the calves slaughtered at 10 months, inflammatory lesions were found in the brain. The diagnosis was confirmed by virological investigations.

Clinically as well as pathologically there was a close resemblance to Border disease in lambs and congenital tremor in piglets after prenatal exposure to Hog cholera virus.     

仙台病毒(sendai virus)

仙台病毒(sendai-virus),又名(hemagglutinatingvirus of Japan,HVJ)是实验啮齿类动物的最难控制的疾病之一.其影响和干扰实验,当仙台病毒和绿脓杆菌存在时,如把动物用于放射或使用免疫抑制剂实验可引起发病死亡.     

Is feline foamy virus really apathogenic?

Feline foamy virus (FFV) is a retrovirus commonly found in cats. It is generally thought to be apathogenic, making it a suitable candidate as a gene therapy vector. However, there have been reports of association of FFV with chronic progressive arthritis and a cofactor effect with feline immunodeficiency virus. This study investigated experimental FFV infection and whether this was associated with signs of disease.

Eight young specific pathogen free cats were inoculated intramuscularly with FFV. The cats were examined twice weekly and blood and pharyngeal samples were taken. Haematology, biochemistry and FFV quantitative polymerase chain reaction (qPCR) were performed. Tissue samples were also collected throughout the six month period.

FFV was initially detected by qPCR in the blood within the first two weeks of infection and viraemia persisted throughout the study. Two peaks of viraemia were observed, at day 20 (80–170 FFU/ml blood) and day 155 (332–415 FFU/ml blood). FFV was also consistently detected in oropharyngeal samples after day 36. Anti-FFV IgG was detected in all cats by ELISA; antibody levels had an early peak around day 35 and then increased again following the second rise in circulating viral load. All cats remained clinically normal, except for one cat with an unrelated gingivitis. None of the cats developed pyrexia. The biochemical profile and blood cell counts remained within normal limits except for one cat with a persistent eosinophilia. Initial fluctuations in white cell counts settled within three weeks and did not deviate outside of the normal ranges. All tissue samples contained FFV DNA; lymphoreticular tissues, salivary gland and lung had the highest viral loads. Although there were no gross pathological lesions on post mortem examination, histologically a mild glomerulonephritis and a moderate interstitial pneumonia were observed in all cats.

We conclude that during the six month period of infection, although cats appeared clinically normal, histopathological changes were observed in the lungs and kidneys. Further investigation of the significance of these changes is warranted before FFV is developed as a vector for gene delivery.     

Does porcine reproductive and respiratory syndrome virus potentiate classical swine fever virus infection in weaner pigs?

Fifteen 6-week-old crossbred weaners weighing about 12 kg each were randomly divided into three groups of five animals each. One group of pigs was inoculated first with porcine reproductive and respiratory syndrome (PRRS) virus and then 3 days later with CSF virus. The second group received classical swine fever (CSF) virus, while the third group was inoculated with PRRS virus only. The aim of the experiment was to determine whether a primary PRRS virus infection influences the clinical outcome of experimentally induced CSF in young pigs. The PRRS virus infected weaners developed mild respiratory symptoms and recovered completely. All five weaners which were inoculated with CSF virus only showed severe clinical signs typical of the acute form of CSF. One pig had to be killed 15 days post-inoculation (p.i.); the remaining four died between the 18th and 22nd day p.i. The clinical course of the animals inoculated with both viruses was slightly different from that of the pigs that received only CSF virus. Four out of five pigs from the PRRS/CSF group became febrile and viraemic earlier than the animals which received CSF virus only. These pigs had to be killed 15-17 days post CSF virus inoculation. One animal in this group survived the acute phase of CSF and recovered completely. It was concluded that the observed divergences of the clinical courses would not have been noticed under field conditions. Therefore these findings cast doubt on the relevance of PRRS virus infection potentiating significantly the clinical outcome of CSF in young pigs.     

Marek’s disease virus and skin interactions

Marek’s disease virus (MDV) is a highly contagious herpesvirus which induces T-cell lymphoma in the chicken. This virus is still spreading in flocks despite forty years of vaccination, with important economical losses worldwide. The feather follicles, which anchor feathers into the skin and allow their morphogenesis, are considered as the unique source of MDV excretion, causing environmental contamination and disease transmission. Epithelial cells from the feather follicles are the only known cells in which high levels of infectious mature virions have been observed by transmission electron microscopy and from which cell-free infectious virions have been purified. Finally, feathers harvested on animals and dust are today considered excellent materials to monitor vaccination, spread of pathogenic viruses, and environmental contamination. This article reviews the current knowledge on MDV-skin interactions and discusses new approaches that could solve important issues in the future.     

Swine reproductive and respiratory syndrome in Québec: Isolation of an enveloped virus serologically-related to Lelystad virus

Sera were collected from convalescent sows and sick piglets from six pig farms in southern Quebec that have experienced outbreaks of the so-called porcine reproductive and respiratory syndrome. By indirect immunoperoxidase, a few of these sera (4 of 14) (28.6%) were found to be positive for antibody to the Lelystad virus, whereas by indirect immunofluorescence 30 of 36 (83.3%) were positive for antibody to the antigenically-related American isolate ATCC-VR2332. Pregnant sows inoculated intranasally with filtered homogenates prepared from the lungs of necropsied piglets obtained from a seropositive farm developed fever, inappetence, and reproductive failure characterized by stillbirths and various stages of mummification. Lesions of interstitial pneumonia were induced in experimentally-infected specific pathogen-free piglets. A virus, having morphological and biological characteristics of viruses assigned to the family Togaviridae, was isolated from lung tissues of experimentally-infected animals; it could only be propagated in primary cultures of porcine alveolar macrophages. Identification of the virus was confirmed by indirect immunofluorescence using a monoclonal antibody directed against the nucleocapsid protein of the ATCC-VR2332 isolate and porcine sera that were found positive for antibody to both the Lelystad and ATCC-VR2332 isolates.     

The Marek��s disease virus (MDV) protein encoded by the UL17 ortholog is essential for virus growth

Marek’s disease virus type 1 (MDV-1) shows a strict dependency on the direct cell-to-cell spread for its propagation in cell culture. As MDV-1 shows an impaired nuclear egress in cell culture, we wished to address the characterization of capsid/tegument genes which may intervene in the maturation of intranuclear capsids. Orthologs of UL17 are present in all herpesviruses and, in all reported case, were shown to be essential for viral growth, playing a role in capsid maturation and DNA packaging. As only HSV-1 and PrV UL17 proteins have been characterized so far, we wished to examine the role of MDV-1 pUL17 in virus replication. To analyze MDV-1 UL17 gene function, we created deletion mutants or point mutated the open reading frame (ORF) to interrupt its coding phase. We established that a functional ORF UL17 is indispensable for MDV-1 growth. We chose to characterize the virally encoded protein by tagging the 729 amino-acid long protein with a repeat of the HA peptide that was fused to its C-terminus. Protein pUL17 was identified in infected cell extracts as an 82 kDa protein which localized to the nucleus, colocalizing with VP5, the major capsid protein, and VP13/14, a major tegument protein. By using green fluorescent protein fusion and HA tagged proteins expressed under the cytomegalovirus IE gene enhancer/promoter (P_{CMV IE}), we showed that MDV-1 pUL17 nuclear distribution in infected cells is not an intrinsic property. Although our results strongly suggest that another viral protein retains (or relocate) pUL17 to the nucleus, we report that none of the tegument protein tested so far were able to mediate pUL17 relocation to the nucleus.     

The Schmallenberg virus epidemic in Europe—2011–2013

During the Schmallenberg virus (SBV) epidemic, the European Food Safety Authority (EFSA) collected data on SBV occurrence across Europe in order to provide an assessment of spread and impact. By May 2013, twenty-nine countries were reporting to EFSA and twenty-two countries had reported cases of SBV. The total number of SBV herds reported was 13,846 and the number of SBV laboratory confirmed herds was 8730. The surveillance activities were based on the detection of SBV clinical cases (either adults or newborns). Malformation in newborns was the most commonly reported clinical sign of SBV-infection. All countries were able to provide the date when the first suspicion of SBV in the herd was reported and nineteen could report the location of the herd at a regional level. This allowed the spread of SBV in Europe to be measured both temporally and spatially. The number of SBV confirmed herds started to increase in December 2011 and two peaks were observed in 2012 (February and May). Confirmed herds continued to be reported in 2012 and into 2013. An increase during winter 2012 and spring 2013 was again observed, but the number of confirmed herds was lower than in the previous year. SBV spread rapidly throughout Europe from the initial area of detection. SBV was detected above the latitude of 60° North, which exceeds the northern expansion observed during the bluetongue virus serotype 8 epidemic in 2006–2009. The impact of SBV was calculated as ratio of the number of herds with at least one malformed SBV positive foetus and the total number of herds in this region. The 75th percentile of the malformations ratio in the various affected countries for the whole reporting period was below 1% and 3% for cattle and sheep herds, respectively. International data collection on emerging diseases represents a challenge as the nature of available data, data quality and the proportion of reported cases may vary widely between affected countries. Surveillance activities on emerging animal diseases are often structured only for case detection making the estimation of infection/diseases prevalence and the investigation of risk factors difficult. The impact of the disease must be determined to allow risk managers to take appropriate decisions. Simple within-herd impact indicators suitable for emerging disease outbreaks should be defined that could be measured as part of routine animal health surveillance programmes and allow for rapid and reliable impact assessment of emerging animal health diseases.     

Pseudorabies virus eradication by area‐wide vaccination is feasible

Summary

This article reviews the rationale for using marker vaccines and companion diagnostic tests in the eradication of pseudorabies virus (PRV). Recent advances in vaccinology and epidemiology indicate that, despite the inability to induce complete immunity, vaccination is a useful tool in the battle against PRV. This review focuses on the effectiveness of vaccination under field conditions and on herd, management and regional factors that are associated with PRV introduction or transmission.     

21世纪不容忽视的人畜共患病-Nipah virus disease

马来西亚卫生部长蔡锐明先生1999年4月13日宣布:最近数月内造成92人死亡的新病毒,正式被命名为Nipah病毒.这是以最先出现这种新病毒的地区-森美兰州的双溪Nipah命名的.     

Antiviral activity of rChIFN-α against vesicular stomatitis virus and Newcastle disease virus: a novel recombinant chicken interferon-α showed high antiviral activity

The sequences of 27 chicken interferon-alpha (ChIFN-α) genes were obtained from GenBank. The gene sequences were compared and homology between them was determined by using a bio-software. On the basis of these results, a new rChIFN-α peptide sequence with 194 amino acids was assembled. Thereafter, on the basis of the new amino acid sequences and by using the most frequently occurring codes of Pichia pastoris, and a 582 bp gene sequence was formed. In order to amplify this non-templated gene, 16 primers were designed, and their gene sequences were synthesized, and amplified. This amplified gene sequence was cloned into the expression vector pPICZα-A to construct a recombination plasmid named pPICZ-rChIFN-α. Then, the recombination plasmid was induced to express the rChIFN-α protein. The results demonstrated that the recombinant plasmid pPICZ-rChIFN-α was successfully expressed in P. pastoris. Furthermore, rChIFN-α had a considerable antiviral activity against both Newcastle disease virus (NDV) and vesicular stomatitis virus (VSV). Therefore, this method of gene engineering could give direction to research on the key amino acids in the interferon or analogous proteins and enable the construction of proteins with high antiviral activity, which can be used both for research and industrial purposes.