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At least 19 recordsLinked to original sources
PubMed1979

[Chronic progressive interstitial pneumonia in sheep (adenovirus pneumonia)].

Adenoviral infection was established in imported specialized meat strains of sheep Ile de France and Romni marsh. The disease followed a course typical of chronic interstitial progressive pneumonia with reduced tonus, loss of body weight, and high lethality. The disease was serologically proven by the discovery of specific complement binding antibodies in dynamics against the adenovirus. Titers varied from 1 : 2 to 1 : 32. The infestation was reproduced on sheep and lambs by tracheal infection with ultrafiltrate of changed lung tissue and bronchial lymph nodes. Morphologically the infection manifests itself by considerable hypeplastic processes in the lungs and less pronounced ones in the liver and kidneys. The typical changes indicated are accumulation of lymphoid cells and histocytes in the interstitial tissue, as well as adenomatous expansion of alveolar and bronchial epithelium. Considerable cell polymorphism is observed in the alveoles along with presence of gigantic cells and cell syncytia of desquamous epithelial cells, alveolar macrophages and intranuclear inclusions in some of these cells. Complications of Past. Haemolytica with developing catharalsuppurative pneumonia were observed in some cases.

Adenoviridae Infections↗
PubMed1975

Zwoegerziekte virus, the causative agent for progressive interstitial pneumonia (maedi) and meningo-leucoencephalitis (visna) in sheep.

The final results of experimental infections with virus recovered from the lungs of sheep suffering from progressive interstitial pneumonia (=zwoegerziekte=maedi) are reported. The virus could be reisolated from blood samples of all experimentally infected sheep. Every animal produced antibodies against the virus. The neutralising, complement-fixing and precipitating antibodies remained present in the blood for six years. Fourteen out of 21 intrapulmonarily infected sheep developed clinical and/or histopathological lung lesions and in three a meningo-leucoencephalitis was detected in addition. One of these three developed the clinical and pathological signs of 'visna' 14 months after inoculation. Signs of visna were seen in eight of 10 sheep that had been inoculated intracerebrally. Furthermore, nine of these sheep suffered from progressive interstitial pneumonia. Hence the name maedi-visna virus is proposed for the agent which causes both disease entities. Three sheep that yielded virus after infection and in which antibodies were detected, did not develop histopathological lesions.

Animals↗
PubMed1979

Lesions of ovine progressive pneumonia: interstitial pneumonitis and encephalitis.

Lesions in sheep with ovine progressive pneumonia are described. Lungs were mottled grayish-pink, firm, and large (two to three times normal weight). There was chronic diffuse interstitial pneumonitis characterized by extensive hyperplasia of lymphoid cells around airways and blood vessels and by accumulation of mononuclear cells in the interstitium. In some lungs, this reaction was accompanied by excessive fibrous tissue and smooth muscle and less frequently by hyperplastic epithelium of terminal bronchioles and alveoli. Secondary bronchopneumonia was common. Lymphocytic meningitis, choroiditis, and leukoencephalitis were seen in a few sheep. Meninges and choroid plexuses were infiltrated with lymphoid cells, and subependymal blood vessels were cuffed with lymphoid cells. Much subependymal white matter was demyelinated and had foci of necrosis and gliosis.

Animals↗
PubMed1980

[Maedi and maedi control (author's transl)].

Maedi/visna is a chronic progressive interstitial pneumonia of sheep caused by a persistent infection with a retrovirus. Approximately thirty per cent of the sheep population in the Netherlands carries antibodies to maedi virus. An experimental eradication scheme based upon serological testing with ELISA and culling of reactors every six months was started, recently. Initially, 353 (25.4 per cent) reactors were identified among 1391 sheep in sixteen flocks, whereas the second test, six months later, showed 130/1111(11.7 per cent) reactors. On 11 other farms with high infection level 382 lambs were separated from their dams immediately after birth, ovine colostrum deprived and artificially reared. The lambs were serotested at 6 months of age and 2/382 (0.5 per cent) were found positive, while naturally reared lambs on the same farms scored 39 per cent positive.

Animals↗
PubMed1993

Evaluation of an ELISA for detection of ovine progressive pneumonia antibodies using a recombinant transmembrane envelope protein.

An enzyme-linked immunosorbent assay (ELISA) was developed using a recombinant protein corresponding to the N'-terminal hydrophilic region of transmembrane glycoprotein (TM) of ovine lentivirus. This assay reproducibly detected antibodies in sera from 207 of 212 ovine progressive pneumonia (OPP) virus-infected sheep, and the recombinant TM ELISA accurately identified 26% (35 vs. 9) more seropositive samples than did the agar gel immunodiffusion test when applied to 100 sera from an infected flock. This assay also yielded no false-positive results in 14 true negative sera. Results of these experiments were further confirmed by the recombinant TM and recombinant p25 Western blot assay. A single recombinant TM antigen, as the coating antigen in ELISA, can be used successfully for the detection of OPP virus-infected animals and can improve the sensitivity and specificity for OPP diagnosis.

Animals↗
PubMed1996

Respiratory infections of sheep.

Sheep respiratory infections appear as differing clinical syndromes. Mild, acute infections are usually due to parainfluenza 3 (PI3) virus. A mild but chronic respiratory problem in lambs under 1 year old is thought to be caused by Mycoplasma ovipneumoniae probably in association with Pasteurella and PI3. Acute bacterial pneumonia usually results from infection with Pasteurella of biotype A. Infection with PI3 can initiate invasion by Pasteurella. Bordetella parapertussis infection has also been implicated. Serotypes of biotype T P. haemolytica cause an acute septicaemia. Stressful management practices may be a predisposing factor. Chronic proliferative pneumonia results from infection by retroviruses of pulmonary adenomatosis or maedi-visna. Both infections have incubation periods extending into years. The former produces fatal tumorous masses in the lungs. Diagnostic tests are being actively sought. Maedi-visna can present as several clinical problems, frequently as an insidious but fatal proliferative pneumonia.

Adenomatosis, Pulmonary↗
PubMed1988

Lesions and retroviruses associated with naturally occurring ovine pulmonary carcinoma (sheep pulmonary adenomatosis).

Five sheep with ovine pulmonary carcinoma were markedly dyspneic and had sporadic coughing; two had copious watery nasal exudate. In four, lesions consisted of multifocal nodules of neoplastic cuboidal epithelial cells in acinar or papillary patterns. Electron microscopically, cells had microvilli, tight junctions, and cytoplasmic lamellar bodies typical of alveolar type II cells. One sheep had a single lung tumor of nonciliated bronchiolar epithelial cells. Vacuolated alveolar macrophages surrounded adenomatous foci. One sheep had a metastatic lesion in the caudal mediastinal lymph node. All sheep had histologic lesions of lymphoid interstitial pneumonia (LIP, ovine progressive pneumonia) consisting of peribronchiolar and interstitial lymphoid hyperplasia, and fibromuscular proliferation; all had serum precipitating antibodies to ovine lentivirus. Lung fluids or tumor homogenates contained a 26-kd peptide that crossreacted with a primate-derived type D retrovirus as detected by immunoblotting or interspecies competition radioimmunoassay. Ovine lentivirus was isolated from concentrated lung fluids or tumor tissues of four sheep tested and from tumor cell DNA of one animal transfected into ovine muscle cells. These studies document the presence of type D-related retrovirus antigen in ovine pulmonary carcinoma (OPC) in the United States and indicate that lentivirus-induced LIP is a lesion frequently associated with this disease.

Animals↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMedDate not supplied

Maedi-visna virus and its relationship to human immunodeficiency virus.

Maedi-visna is a slow virus infection of sheep leading to a progressing lymphoproliferative disease which is invariably fatal. It affects multiple organs, but primarily the lungs where it causes interstitial pneumonia (maedi). Infection of the central nervous system was commonly observed in Icelandic sheep (visna), infection of mammary glands (hard udder) in sheep in Europe and the USA, and infection of the joints in sheep in the USA. The name ovine progressive pneumonia (OPP) is commonly used in the USA and ovine lentivirus (OvLV) infection is also a name used for maedi-visna. A related infection of goats, caprine arthritis-encephalitis (CAE), is common in Europe and the USA. The natural transmission of maedi-visna is mostly by the respiratory route, but also to newborn lambs by colostrum and milk. Intrauterine transmission seems to be rare and venereal transmission is not well documented. Macrophages are the major target cells of maedi-visna virus (MVV), but viral replication is greatly restricted in the animal host, apparently due to a posttranscriptional block. The low-grade viral production in infected tissues can explain the slow course of the disease in sheep. The lesions in maedi-visna consist of infiltrates of lymphocytes, plasma cells, and macrophages, and are detectable shortly after experimental transmission. Several studies indicate that the lesions are immune mediated and that cytotoxic T-lymphocytes may be important effector cells. The persistence of the MVV infection is explained by a reservoir of latently infected blood and bone marrow monocytes, which migrate into the target organs and mature into macrophages with proviral DNA transcription, but limited replication of virus. The MVV particles are morphologically similar to those of other retroviruses and the mode of replication follows the same general pattern. The genome organization and gene regulation resembles that of other lentiviruses. In addition to gag, pol and env, MVV has three auxiliary genes (tat, rev and vif), which seem to have similar functions as in other lentiviruses, with a possible exception of the tat gene. A determination of the 9200 nucleotide sequence of the MVV genome shows a close relationship to CAE virus, but limited sequence homology with other lentiviruses, and only in certain conserved domains of the reverse transcriptase and possibly in the surface protein. MVV infection in sheep and HIV-1 infection in humans have a number of features in common such as a long preclinical period following transmission, and a slow development of multiorgan disease with fatal outcome. A brief early acute phase, which is terminated by the immune response, is also an interesting common feature. Like HIV-1, MVV is macrophage tropic and the early stages of the HIV-1 infection which affect the central nervous system and the lungs are in many ways comparable to maedi-visna. In contrast to HIV-1, MVV does not infect T-lymphocytes and does not cause T-cell depletion and immunodeficiency. This is responsible for the difference in the late stages of the HIV-1 and MVV infections and the final clinical outcome. Despite limited sequence homology, certain proteins of MVV and HIV-1 show structural and functional similarities. Studies of MVV may therefore help in the search for new drugs against lentiviruses, including HIV-1.

Animals↗
PubMed1993

Pathogenesis of lymphoid interstitial pneumonia in natural and experimental ovine lentivirus infection.

Ovine lentivirus (OvLV), as a member of the lentivirinae subfamily of Retroviridae, shares morphological, genomic, and cytopathic features with human immunodeficiency virus (HIV). Although OvLV infection does not induce profound immune deficiency in sheep, it has many similarities with HIV infection, such as the capacity to infect macrophages, undergo antigenic variation in vivo, and induce slow progressive diseases involving the pulmonary, lymphoid, and central nervous systems. Studies of the pathogenesis of disease in sheep naturally or experimentally infected by OvLV are providing clues to the pathogenesis of HIV infection, including the significance of viral load, the emergence of cytopathic variants, the mechanisms and significance of viral antigenic variation, and viral neutralization, and mechanisms of lymphoproliferation and tissue destruction induced by the virus. Preliminary evidence suggests that infection by other microbial agents, including Mycoplasma species, may play a cofactor role in the pathogenesis of lentivirus-associated lymphoid interstitial pneumonia in sheep, but further studies are required to address this issue.

Animals↗