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At least 19 recordsLinked to original sources
PubMed1994

Identification of naturally occurring monoclonal antibody escape variants of louping ill virus.

Louping ill virus isolates from Great Britain, Ireland and Norway were compared antigenically by indirect immunofluorescence, haemagglutination-inhibition and neutralization tests using a panel of five envelope-specific and five non-structural protein NS1-specific monoclonal antibodies raised against louping ill virus. The viruses were grouped according to their reactivities with the antibodies. Group 1, members of which were isolated between 1931 and 1987, consisted of 13 viruses that reacted with all antibodies, whereas group 2, members of which were isolated after 1980, consisted of five viruses that were positive with only eight of the 10 monoclonal antibodies. The two monoclonal antibodies that did not react with the group 2 viruses are known to be neutralizing antibodies and the amino acids that they recognize in the viral envelope protein have been identified. We therefore refer to the group 2 viruses as naturally occurring monoclonal antibody escape variants. When compared with group 1 viruses, the escape variants showed reduced virulence for mice in terms of the time taken to kill and/or the proportion that died, following intraperitoneal inoculation. The nucleotide and deduced amino acid sequences of the envelope gene of one escape variant were compared with those of several group 1 viruses. A single amino acid substitution at residue 308 was detected in the envelope protein of the escape variant which corresponds precisely to the position in experimentally selected attenuated monoclonal antibody escape mutants. The importance and potential implications of these naturally occurring variants in louping ill epizootiology and vaccine-based control are discussed.

Animals↗
PubMed1991

Louping ill in man: a forgotten disease.

Louping ill disease of sheep has been recognised in Scotland for centuries. It causes encephalitis and is transmitted by the sheep tick, Ixodes ricinus. Human infection was first reported in 1934. Thirty-one cases of human infection have now been described. Four clinical syndromes are seen, an influenza-like illness, a bi-phase encephalitis, a poliomyelitis-like illness and a hemorrhagic fever. Certain occupational groups, e.g. laboratory personnel working with the virus and those who kill injected sheep, are at increased risk of acquiring louping ill infection. In many instances, infection is subclinical. Eight new human cases are described. Six were in crofters or shepherds in the north and west of Scotland, one was in a general practitioner in the Western Isles and the eighth was in a butcher in Edinburgh. Louping ill disease should not be forgotten in cases of unexplained encephalitis in those whose lifestyle exposes them to the virus.

Animals↗
PubMed1986

Response of sheep to experimental concurrent infection with tick-borne fever (Cytoecetes phagocytophila) and louping-ill virus.

The pathogenesis of concurrent Cytoecetes phagocytophila and louping-ill virus infection was studied in two experiments. In the first experiment 18 four- to seven-year-old rams were used. Ten were infected with C phagocytophila and five days later eight of these animals and the remaining eight sheep were infected with louping-ill virus. The two rams infected with C phagocytophila alone developed no clinical signs apart from a transient pyrexia, while only three of the eight rams infected with louping-ill virus alone showed mild clinical signs. In marked contrast, all eight dually infected sheep developed severe clinical signs with pronounced depression and dysentery and three died and five were killed in extremis. They developed higher titres of viraemia and the antibody response was depressed while necrotising lesions affecting a variety of organs were detected at post mortem examination. Rhizomucor pucillus was recovered from these lesions in seven of the eight sheep. A second experiment using 10 sheep, five aged seven months and five aged two to three years, confirmed the findings of the first experiment indicating that the age of the animal had not significantly influenced the initial result. It was concluded that C phagocytophila infection could enhance the pathogenicity of louping-ill virus and that, operating together, the two pathogens facilitated fungal invasion. It is postulated that sudden deaths in sheep recently transferred to tick-infested pastures may be due to this newly described syndrome.

Animals↗
PubMed1991

Genomic sequence of the structural proteins of louping ill virus: comparative analysis with tick-borne encephalitis virus.

The genomic RNA of louping ill virus coding for capsid, premembrane, membrane, and envelope proteins was cloned and sequenced. Hydrophilicity profiles of the deduced amino acid sequence shared homologous functional domains with other flaviviruses. The premembrane and envelope proteins contain N-glycosylation sites and conserved cysteine residues which are important for maintaining the secondary structures of the proteins. Sequence comparisons of louping ill envelope protein showed greater homology with tick-borne than mosquito-borne flaviviruses and greater homology with the western than the far eastern subtype of tick-borne encephalitis virus. With the capsid and membrane proteins, the degree of homology between louping ill and the western subtype was greater than that between the two subtypes, indicating very close evolutionary relationships between louping ill and the western subtype of tick-borne encephalitis. Thus, louping ill and tick-borne encephalitis may be varieties of a common tick-borne ancestral virus. The average amino acid sequence diversity between members of the tick-borne serogroup was significantly lower than that of mosquito-borne serogroups, suggesting that tick-borne flaviviruses have been subjected to different evolutionary immune selection pressure from the mosquito-borne viruses. Using the published model of tick-borne encephalitis envelope protein and our sequence data on louping ill virus, we have identified three discontinuous peptides (amino acids 81-88, 207-212, and 230-234) which may represent critical molecular determinants within the receptor binding site of tick-borne flaviviruses and may provide a specific genetic marker for these viruses.

Amino Acid Sequence↗
PubMed1993

Sequencing and antigenic studies of a Norwegian virus isolated from encephalomyelitic sheep confirm the existence of louping ill virus outside Great Britain and Ireland.

We have carried out an antigenic analysis and nucleotide sequence comparison of the envelope glycoprotein of recognized louping ill virus strains isolated from Scotland with that of a Norwegian virus known to cause encephalomyelitis in sheep. Monoclonal antibodies with defined specificity for the louping ill virus envelope glycoprotein failed to distinguish between the Norwegian virus and prototype louping ill virus in indirect immunofluorescence, haemagglutination inhibition and neutralization tests. Nucleotide sequencing of the envelope glycoprotein and alignment of the deduced amino acid sequence with other known sequences revealed that the Norwegian virus closely resembles (> 95% identity for nucleotide and > 98% identity for amino acid sequences) louping ill virus. Maximum variation in identities among four strains of louping ill virus were 4.4% and 1.8% respectively for nucleotide and amino acid alignments. We conclude that sheep encephalomyelitis in Norway is caused by louping ill virus. These results imply that other viruses present in Europe and known to cause encephalitis/encephalomyelitis of sheep could be caused by louping ill virus.

Animals↗
PubMed1983

Experimental louping-ill virus infection of black grouse (Tetrao tetrix).

Louping-ill virus was injected into the tarsal pads of four black grouse and the course of infection monitored. All developed viraemia of low intensity that lasted for four days and thereafter produced high titres of haemagglutination inhibiting antibody. No clinical signs were detected and mild neuropathological changes were present in only 1/4 brains collected on day 17 after inoculation. The mild response of black grouse to infection with louping-ill virus is thus similar to that found in other woodland and forest birds and contrasts with the generally fatal response of moorland and tundra grouse species. These findings give further support to the concept that louping-ill has been introduced to the moorland habitat only in the relatively recent past.

Animals↗
PubMed1980

Evaluation of the double immunodiffusion test for the diagnosis of louping ill infection.

The usefulness of the double immunodiffusion test for the diagnosis of louping ill infection was investigated. Whereas louping ill viral antigen was not detected in brain material from field cases of the infection, its presence was readily confirmed in suckling mouse brain isolates of the virus. The double immunodiffusion test was found to be unreliable as a serological test for the retrospective diagnosis of louping ill infection in the horse.

Animals↗
PubMed1987

A disease resembling louping-ill in sheep in the Basque region of Spain.

A clinical syndrome resembling louping-ill which primarily affects lambs and yearlings in the Basque region of Spain is described. The disease has been observed for several years during May and June after the sheep flocks have been taken to the mountain grazings where the sheep tick (Ixodes ricinus) is known to occur. Examination of the brain from one of the affected animals revealed histological changes indistinguishable from those caused by louping-ill virus. In addition antibody that reacted with louping-ill virus antigen was detected in the serum of 57 per cent of the sheep tested from the affected flocks but in only 0.8 per cent of sera from flocks free of the disease. These preliminary results suggest that louping-ill or a related tick-borne virus is responsible for ovine encephalomyelitis in Spain.

Animals↗
PubMed1971

Field trials of an inactivated oil-adjuvant vaccine against louping-ill (Arbovirus group B).

A single dose of inactivated louping-ill oil-adjuvant vaccine elicited a sero-logically detectable immune response in sheep lasting for at least 1 year. These sheep when exposed to a natural focus of louping-ill virus were completely protected from clinical disease and 1 year after vaccination were able to pass on a substantial maternal immunity to their lambs.Twenty-nine per cent of unvaccinated sheep, exposed at the same time, died from clinical louping-ill; half of the survivors showed positive sero-conversion and became immune, while the other half remained susceptible. The incidence of fatal encephalomyelitis in sheep which were known to have circulated virus exceeded 50% in 2 out of 3 trials conducted simultaneously in different locations in Scotland in 1969.

Adjuvants, Immunologic↗
PubMed2000

The role of lambs in louping-ill virus amplification.

In some areas of Scotland, the prevalence of louping-ill virus has not decreased despite the vaccination of replacement ewes for over 30 years. The role of unvaccinated lambs in viral persistence was examined through a combination of an empirical study of infection rates of lambs and mathematical modelling. Serological sampling revealed that most lambs were protected by colostral immunity at turnout in May/June but were fully susceptible by the end of September. Between 8 and 83% of lambs were infected over the first season, with seroconversion rates greater in late rather than early summer. The proportion of lambs that could have amplified the louping-ill virus was low, however, because high initial titres of colostral antibody on farms with a high force of infection gave protection for several months. A simple mathematical model suggested that the relationship between the force of infection and the percentage of lambs that became viraemic was not linear and that the maximum percentage of viraemic lambs occurred at moderately high infection rates. Examination of the conditions required for louping-ill persistence suggested that the virus could theoretically persist in a sheep flock with over 370 lambs, if the grazing season was longer than 130 days. In practice, however, lamb viraemia is not a general explanation for louping-ill virus persistence as these conditions are not met in most management systems and because the widespread use of acaracides in most tick-affected hill farming systems reduces the number of ticks feeding successfully.

Animals↗
PubMed1992

Nucleotide sequence of the envelope glycoprotein of Negishi virus shows very close homology to louping ill virus.

Negishi virus, a member of the family Flaviviridae, was originally isolated in Japan, during an outbreak of Japanese encephalitis. Antigenically, however, Negishi virus resembles the tick-borne rather than the mosquito-borne flaviviruses. Monoclonal antibodies that bind louping ill virus showed a close antigenic relationship between louping ill and Negishi virus. The genes encoding the envelope glycoprotein of Negishi virus (strain 3248/49/P10) and louping ill virus (strain SB526) were cloned and sequenced. They showed a very close homology at both the nucleotide and deduced amino acid levels. Comparison with the known sequence of another strain of louping ill virus (strain 369/T2) and with other tick-borne flaviviruses showed that Negishi virus was more closely related to louping ill virus than to the other tick-borne viruses. The significance of this observation for virus evolution, virus distribution in the environment, and the potential use of nucleotide sequencing for rapid and precise identification of flaviviruses are discussed.

Amino Acid Sequence↗
PubMed1984

Transmission of louping-ill virus in goat milk.

The course of louping-ill virus infection was examined in lactating goats. Seven goats were inoculated subcutaneously and titres of virus in blood and milk were monitored. All goats became viraemic with maximum titres of between 10(1.6) and 10(4.0) plaque forming units (pfu)/0.2 ml. Virus was also detected in the milk of all goats at maximum titres of between 10(0.6) and 10(5.7) pfu/0.2 ml. Only one of these goats exhibited clinical signs which were transient. In contrast, five of the 13 kids sucking these goats became infected and all showed marked clinical signs and one died and two were killed in extremis. It is considered that goats do not represent an efficient maintenance host for louping-ill virus but the excretion of virus in milk could represent a public health hazard.

Animals↗
PubMed1997

The epidemiology of louping-ill, a tick borne infection of red grouse (Lagopus lagopus scoticus).

The epidemiology of louping-ill in red grouse was studied in northern Britain concentrating on the possible role of other species and mechanisms of disease persistence. This tick borne viral disease caused heavy mortality in red grouse, particularly chicks. Louping-ill induced mortality reduced the strength of the density dependence that generates the tendency of grouse populations to cycle and in some populations may cause population sinks. Four routes of transmission were examined and non-viraemic transmission of virus between ticks cofeeding on hares was considered significant. Field data supported the hypothesis that disease dynamics is influenced greatly by mountain hares, both as passive amplifiers and as hosts for the tick vector. Genetic variation in louping-ill within Britain was small.

Animals↗
PubMed1980

Immunosuppression in toxoplasmosis: further studies on mice infected with louping-ill virus.

Mice were infected with an avirulent cyst-producing strain of Toxoplasma gondii and given injections of louping-ill virus 7 days later; control mice were given virus but not Toxoplasma. Test and control mice were then killed, in groups, 2, 4, 6, 8 and 10 days later. In the dually infected mice viraemia was later, greater and more prolonged; titres of virus recovered from brain and spleen were greater; production and haemagglutinating antibody to louping-ill virus was later and less, and inflammation in the brain was more severe, than in mice given virus alone. We suggest that T. gondii suppressed the immunity of mice, making them more susceptible to the virus, and that a significant proportion of the increased number of inflammatory cells observed in the brain could have been toxoplasma specific and not virus-specific and hence contributed to the increased susceptibility of the dually infected mice to louping-ill virus.

Animals↗
PubMed1977

The occurrence of antibody to Babesia and to the virus of louping-ill in deer in Scotland.

Sera of wild red deer from 16 localities in Scotland were tested by the indirect fluorescent antibody technique for antibody to Babesia and by the haemagglutination inhibition test for antibody to the virus of louping-ill. Babesial antibody was detected in sera from all localities in proportions ranging from 22 to 100 per cent. Antibody to louping-ill virus could not be demonstrated in sera from five of the localities and in the other 11 was found less frequently than was antibody to Babesia. Sera from male and female deer were positive for louping-ill in almost equal proportions whereas the incidence of babesial antibody was significantly lower in females than in mature males. This difference could be explained by the habits of the deer. The variable occurrence of louping-ill antibody suggested that red deer are tangential hosts for the virus.

Animals↗
PubMed1976

The effect of colostrum-derived antibody on louping-ill virus infection in lambs.

The influence of colostrum-derived antibody to louping-ill virus on the course of experimental infection was investigated in lambs. Lambs that had high titres of antibody were refractory to infection. Lambs that had low titres of antibody did not develop a viraemia but either showed an antibody reaction or were sensitized as judged by the immune response, which was typical of an anamnestic response, after rechallenge. Animals that had no antibody 34-20 days before challenge had either no or very slight viraemia, but did develop an antibody response with titres as high as those of control lambs by day 21. Lambs that had been negative for longer periods responded in a similar fashion to controls. These findings are discussed in relation to the occurrence of disease in lambs kept in louping-ill endemic areas. It is concluded that in such areas infections of lambs are likely to be of minor importance as a cause of mortality and of little epidemiological significance.

Animals↗
PubMed1981

Experimental louping-ill virus infection of cattle.

The response of six calves to subcutaneous inoculation with louping-ill virus was studied. All developed viraemia of low intensity which lasted two to four days followed by the appearance of haemagglutination inhibiting serum antibody. IgM was the predominant class of antibody until day 14. Only one calf developed clinical signs; following a brief period of incoordination on day 7 it became recumbent and was killed on day 12. Severe meningoencephalitis was detected in this calf and mild changes were observed in one of the five survivors which were killed on day 14 or 20. These findings are discussed in relation to the epidemiology of louping-ill and the diagnosis of the disease in cattle.

Animals↗