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At least 73 records · Page 4Linked to original sources
PubMed1979

Immune response of various animals to Akabane disease live virus vaccine.

When various animals and routes of inoculation were examined for antibody response to Akabane disease live virus vaccine, the intracerebral (ic) inoculation of mice induced a better antibody response than the subcutaneous (sc) inoculation of calves, guinea pigs, hamsters, mice, or rats. Immunogenicity was compared among lots of this vaccine by performing ic inoculation of mice and sc inoculation of calves and guinea pigs. As a result, there was no distinct significant difference between any two lots of the vaccine, regardless of the animal species used. There was a tendency that the larger the dose of inoculation of the virus, the earlier the production of neutralizing (NT) antibody took place in calves inoculated with the vaccine, and the higher the antibody titer and the rate of taking a turn for positivity for antibody became in these calves. When calves immunized with the vaccine and cows in the field possessing NT antibody were given booster inoculation with the vaccine, the antibody titer showed a significant increase in almost all the calves and cows that exhibited an NT antibody titer of 4 or less at the time of booster inoculation. There were, however, no changes in antibody titer in such calves and cows as presenting an NT antibody titer of 8 or more. Calves and pregnant cows immunized with the vaccine were prevented from viremia and fetal infection when challenged by inoculation with virulent virus.

Animals↗
PubMed1981

Experimental infection of bulls with Akabane virus.

Eight bulls were inoculated with Akabane virus and the clinical effects, development of viraemia and serological response to infection were followed. In addition semen was collected regularly from each bull both before and after inoculation. The bulls had a viraemia which occurred between days 2 and 9 after inoculation and which lasted for three to five days. Virus neutralising antibodies were detected in the serum of all bulls by days 7 to 10. Semen samples were tested for virus by inoculation of tissue cultures and by subcutaneous injection of susceptible cattle. Akabane virus was not detected in the semen using either method. The semen was usually of a standard acceptable for artificial breeding. The results of this study suggest that Akabane virus infection of the bull would not affect reproduction.

Animals↗
PubMed1994

Akabane virus.

Akabane virus, an arthropod-borne Bunyavirus, is the major cause of epizootics of congenital malformations in ruminants in Australia, Japan, Korea, and Israel, and is suspected to be a cause of sporadic outbreaks elsewhere. Blood-sucking insects, such as biting midges, transmit the virus horizontally to vertebrates. Climatic factors influence the seasonal activity and geographic range of the vector population and, therefore, occurrence of related disease. Inoculated ruminants seroconvert rapidly after a short subclinical viremia. Infection is of consequence only if ruminants are pregnant and not protected by adequate specific neutralizing antibodies. In naive pregnant animals, virus may spread hematogenously to replicate and persist in trophoblastic cells of placental cotyledons and subsequently invade the fetus. A distinct tropism for immature rapidly dividing cells of the fetal central nervous system and skeletal muscle results in direct virus-induced necrotizing encephalomyelitis and polymyositis. If fetuses survive, such injury may manifest as arthrogryposis, hydranencephaly, porencephaly, microencephaly, hydrocephalus, or encephalomyelitis at term. The earlier in gestation that fetal infection occurs, the more severe the lesions, reflecting the large population of vulnerable cells and lack of fetal immunocompetency at earlier stages of pregnancy. Injury during the period of critical cell migration and differentiation in organogenesis may substantially disrupt structural development in target organs. Late gestational infections cause nonsuppurative inflammation in the brain and spinal cord, premature birth, or fetal death with stillbirth or abortion. Affected neonates are nonviable. Control is by vaccination but is not always justified economically. Akabane viral infections must be differentiated from infections with other teratogenic viruses (including related Bunyaviruses), inherited conditions, and maternal intoxications. Diagnosis is made by serology and viral isolation.

Animals↗
PubMed1994

The distribution of Akabane virus in the Middle East.

Serological evidence was used to confirm an outbreak of Akabane disease in cattle in the Turkish Province of Aydin in 1980. Thereafter, serum collections from the Middle East were screened for the presence of neutralizing antibodies to Akabane virus. The results indicate that the virus was present in a number of provinces on the south Turkish coast in 1979 and 1980 but that it probably did not persist into 1981; the virus had also been present on Cyprus in 1980 and on at least one previous occasion. There was also evidence of limited virus transmission in the Orontes river valley in Syria in 1979 and less precise evidence to show that occasional infection occurred in the lower Jordan river valley. The failure of Akabane virus to persist in southern Turkey for more than two years indicates that this area is open to epidemic rather than endemic infection. The presence of neutralizing antibodies in the eastern Turkish Provinces of Gaziantep and Diyarbakir suggests that this might be the route whereby Akabane virus occasionally invades the Middle East region.

Animals↗
PubMed1981

Distribution and prevalence of Mermet virus infections in the central United States.

Tests were run on 3,198 bird sera for neutralizing antibody of Mermet virus. The birds were mostly House Sparrows (Passer domesticus) captured in the central U.S. Antibody was detected in birds from Texas, Mississippi, Tennessee, Ohio, Indiana, Illinois, and Wisconsin, but not Kentucky or Missouri. Antibody prevalence differed by location and between years in similar locations. These results confirmed the widespread activity of Mermet virus in the central U.S., suggested irregular activity of the virus, and provided the first evidence that Mermet virus activity occurs in Mississippi, Indiana, and Wisconsin. No antibody to Mermet virus was found in paired sera from 966 humans with suspected arboviral infection.

Animals↗
PubMed1979

An attenuated strain of Akabane virus: a candidate for live virus vaccine.

An attempt was made to attenuate the high virulent OBE-1 strain of Akabane virus by adaptation to low temperature. In it the virus was subjected to passage through HmLu-1 cell cultures at 30 degrees C. Cloning was carried out on the virus which had undergone 20 passages through these cultures to select a strain adapted to low temperature. Finally, ten clones were obtained. As a result, nine strains of clone in which virus replication was poor in HmLu-1 cell cultures at 40 degrees C were obtained. Of them, five strains of clone produced uniform plaques. Of these strains, one, or the TS-C2 strain, was selected. It was considerably lower both in peripheral infectivity to suckling mice and in intracerebral infectivity to 3-week-old mice than the OBE-1 strain. Calves and pregnant cows inoculated with the TS-C2 strain by the intracerebral, intravenous, or subcutaneous route were free from pyrexia, leukopenia, and viremia. Virus recovery was negative from various organs and fetuses. All the animals inoculated, however, were found to have neutralizing antibody produced. The results mentioned above suggested that the TS-C2 strain might have been so attenuated as to be available as a candidate strain for a live virus vaccine.

Animals↗
PubMed1979

Encephalomyelitis in mice experimentally infected with Akabane virus.

Lesions in the central nervous system of mice, induced by intracerebral injection of Akabane virus, were observed by the fluorescent antibody technique and histological method. Fluorescent antigens were recognized in the cytoplasm of nerve cells, but were not detected exactly in any other part. Fluoresced nerve cells were distributed almost all over the central nervous system, especially in medulla oblongata and spinal cord. The appearance of fluorescent antigens was followed by histological changes. So-called Nissl's acute severe degeneration was observed in nerve cells in the area where the fluorescent antigens were distributed. Spongy foci were seen in medulla oblongata and spinal cord. Virus was recovered from brain and spinal cord, but not from any other visceral organ or blood. Akabane virus showed an affinity to nerve cells and caused primary nonpurulent encephalomyelitis when inoculated intracerebrally to mice.

Animals↗
PubMed1997

Restriction fragment length polymorphism analysis of Akabane virus nucleoprotein gene.

The nucleoprotein genes of Akabane virus S RNA segment from 21 Japanese and two Australian isolates were amplified by the reverse transcriptase-polymerase chain reaction (RT-PCR) using a primer set containing the initiation and termination codon of the gene. The RT-PCR products were sufficiently produced from the purified virion RNAs of all the isolates, and then analyzed by enzymatic digestion with 11 restriction endonucleases. Digestion with the eight restriction enzymes revealed sequence variation of the isolates. Restriction fragment length polymorphism (RFLP) profiles obtained by digestion revealed the existence of four major groups (genogroups) among the isolates. The two Australian isolates had extremely different RFLP profiles than the Japanese isolates. The data demonstrate the usefulness of analyzing the RFLP patterns to understand the genetic variability of AKA virus isolated in Japan and Australia.

Animals↗
PubMed1998

Aino virus antigen in brain lesions of a naturally aborted bovine fetus.

A bovine fetus aborted at 187 days of gestation was serologically and immunohistopathologically examined. Serum and cerebrospinal fluid samples had high titers of virus-neutralizing antibody for Aino virus. A severe necrotizing encephalopathy was noted. Aino virus antigen was demonstrated in neuroglial cells within the brain lesion. The destruction of developing neuronal cells appeared to be a significant feature of the pathogenesis of lesions due to Aino virus infection in the central nervous system.

Abortion, Veterinary↗
PubMed2000

Preferential infection of neuronal and astroglia cells by Akabane virus in primary cultures of fetal bovine brain.

Akabane virus is a member of the genus Bunyavirus; it is pathogenic for ruminants and transmitted by arthropod vectors. Infection of adult cattle and sheep causes a transient viremia without obvious clinical signs, while infection of pregnant animals often causes fetal abnormalities including hydranencephaly, poliomyelitis and arthrogryposis. Infectious virus or viral antigens is present in the brain, spinal cord and skeletal muscle of infected fetuses. To understand the interaction between Akabane virus and bovine brain cells, we investigated the viral tropism using primary cultures of fetal bovine brain. The cultured neuronal cells, astroglia cells and microglia cells were distinguished by cell type specific antisera. Akabane virus was found to infect neuronal cells and astroglia cells, which led to degenerative death. No microglia cells were found infected. In some brain cultures, we observed different sensitivities of the cells to two Akabane virus strains: an attenuated strain infected and spread more readily than wild type virus. This difference was not observed in a hamster fibroblast cell line. Both viral and host determinants might be involved in the different susceptibility of brain cells to Akabane virus infection.

Animals↗
PubMed2004

Akabane virus in Israel: a new virus lineage.

This report describes the first molecular characterization of Akabane virus (AKAV) in Israel. The virus was recognized by real-time RT-PCR in extracts from Culicoides imicola insects trapped at the Volcani Center located in the center of Israel. This is also the first report on the use of real-time RT-PCR to identify the virus. The quantitative capability of this technique was applied, and it was calculated that the insect extract contains 1.5 x 10(5) copies of the genome segment S. Following amplification of the small (S) genome segment, its nucleotide sequence was determined to have 93.4% identity or greater with the S segment of other AKAV isolates. The deduced amino acid (aa) sequence of the combined nucleocapsid and the non-structural protein showed more than 96.6% identity. Phylogentic trees constructed using the combined deduced nucleocapsid and the non-structural protein aa sequences showed that the Israeli isolate forms a fourth cluster of AKAV, indicating a separate virus lineage. Attempts to isolate the virus by inoculation to Vero cells and by intracerebral inoculation to mice were unsuccessful.

Animals↗
PubMed1979

Congenital abnormalities in newborn lambs following Akabane virus infection in pregnant ewes.

To clarify the pathogenicity of Akabane virus for ovine embryos, pregnant ewes were inoculated intravenously with the virus. As a result, all of them were affected with viremia and showed an increase in neutralizing antibody 2 weeks after inoculation. The virus was recovered from many organs of embryos which were inoculated with it at 29--45 days of pregnancy and sacrificed 9--30 days later. In particular, some of these embryos which were sacrificed 15 days after inoculation were found suffering from systemic infection. A large quantity of virus was recovered from the organs all over the body of them. No virus, however was recovered from any organ of embryos which were inoculated with the virus at 81 days of pregnancy and sacrificed 30 days later. Abnormal changes were observed in neonatal lambs born from ewes inoculated with the virus at 30--50 days of pregnancy. They were especially severe when the virus was inoculated at 30 days of pregnancy. They consisted of ankylosis of the limbs, scoliosis, hydranencephaly, porencephaly, stillbirth with dwarfism, and death after birth with dwarfism and weakness. Nothing abnormal was found in any neonatal lambs born from ewes inoculated with the virus at 91--101 days of pregnancy. When embryos exceeded 64 days of intra-uterine life more than 29 days after virus inoculation, it was possible to detect immunoglobulin, IgM or IgG or both, and antibody from the serum. Attempts failed to detect either immunoglobulin from embryos less than 59 days of intrauterine life. No IgA was detected from the serum of any embryo. In almost all the neonatal lambs born from ewes inoculated with the virus at 28--101 days of pregnancy, neutralizing antibody was detected from the serum at the time of birth.

Animals↗
PubMed1981

Developmental disorders of the fetus in some arthropod-borne virus infections.

A number of arboviruses have been associated with congenital defects in domestic aminals and man. In this review comparison is made of the temporal association between epidemics of arboviruses affecting man and animals in which there is an obvious relationship between the infection and the fetal defects, and arboviruses which cause no overt clinical symptoms in the vertebrate host but result in deformities of the fetus. The danger to the fetus following the use of live attenuated virus vaccines against several important arbovirus diseases is also examined. It is concluded that arboviruses which are capable of infecting humans or animals without producing overt clinical signs, and attenuated vaccine viruses pose the greatest threat to the fetus.

Animals↗
PubMed1978

A survey of antibody to Aino virus in cattle and other species in Australia.

A serological survey of healthy cattle in Australia showed that antibodies to Aino virus were present in serums from cattle in northern Australia and down the east coast as far as central New South Wales in 1975, 1976 and 1977, but occurred with a lower frequency than antibodies to Akabane virus. In contrast to the findings with Akabane virus, no neutralising antibodies to Aino virus were detected in serums from camels, dogs or horses. Antibodies to both viruses were detected in buffaloes and sheep, but not in humans or any of the Australian indigenous species so far tested. All positive serums originated from within the known range of Culicoides brevitarsis.

Animals↗
PubMed2001

Diagnosis of Oropouche virus infection using a recombinant nucleocapsid protein-based enzyme immunoassay.

Oropouche (ORO) virus is an emerging infectious agent that has caused numerous outbreaks of an acute febrile (dengue-like) illness among humans in Brazil, Peru, and Panama. Diagnosis of ORO virus infection is based mainly on serology. Two different antigens, hamster serum antigen (HSA) and Vero cell lysate antigen (VCLA), are currently used in enzyme immunoassays (EIAs) in Brazil and Peru, respectively, to investigate the epidemiology of ORO virus infection. Both antigens involve use of infectious virus, and for this reason their use is restricted. Consequently, the frequency and distribution of ORO virus infection are largely unexplored in other countries of South America. This report describes the use of a bacterially expressed recombinant nucleocapsid (rN) protein of ORO virus in EIAs for the diagnosis of ORO virus infection. The data revealed that the purified rN protein is comparable to the authentic viral N protein in its antigenic characteristics and is highly sensitive and specific in EIAs. Among 183 serum samples tested, a high degree of concordance was found between rN protein-based EIA and HSA- and VCLA-based EIAs for the detection of both ORO virus-specific immunoglobulin M (IgM) and IgG antibodies. The high sensitivity, specificity, and safety of the rN protein-based EIA make it a useful diagnostic technique that can be widely used to detect ORO virus infection in South America.

Animals↗
PubMed2002

Encephalomyelitis associated with akabane virus infection in adult cows.

Between August and September 2000, five 2-7-year-old cows in Korea exhibited neurologic signs and were diagnosed as infected with Akabane virus based on the results of histopathology, immunohistochemistry, serology, and reverse transcription polymerase chain reaction (RT-PCR) analysis. Immunohistochemistry and RT-PCR were equally effective and sensitive for diagnosing Akabane virus infection during the early stage of infection. Typical lymphohistiocytic inflammation characterized by perivascular mononuclear cell infiltration, gliosis, neuronophagia, and neuronal loss was noted in the brain and the ventral horn gray matter of the spinal cord. The lesions in the brain were most prominent in the pons and medulla oblongata. Akabane virus antigen was detected in the brain and spinal cord, mainly in degenerating neurons and glial cells. RT-PCR analysis revealed a target band of expected size in four cows. This is the first report on an outbreak of natural Akabane virus infection in adult cattle.

Animals↗
PubMed2006

Highly effective inhibition of Akabane virus replication by siRNA genes.

Since 2002 there has been a rise in arthrogryposis/hydranencephaly (AGH) incidence in Israel, caused by Akabane (AKA) and, possibly, Aino viruses. To test the ability to control the disease, three siRNA genes targeted to the S genome segment were designed and prepared in the form of siRNA cassettes. For the design all published S segment were aligned and two conserved target sequences with 100% homology were chosen. A third conserved target that was found exhibited only one base change found in the two Australian isolates and was also designed and tested. It was demonstrated that cells transfected with single siRNA genes showed 99% inhibition, as measured by real-time RT-PCR, virus titration and immunofluorescence. When cells were transfected with all three genes together the inhibition levels were increased and reached almost 100%.

Animals↗