Encephalitis Viruses, Tick-Borne
Encephalitis, Tick-Borne
Viral Envelope Proteins
Recombinant Semliki Forest virus particles encoding the prME or NS1 proteins of louping ill virus protect mice from lethal challenge. (1/9)
Recombinant Semliki Forest virus (rSFV) vaccines encoding louping ill virus (LIV) genes prME and NS1 were examined. Cells transfected with rSFV-prME RNA showed correct processing of the precursor prME and the release into the medium of M and E proteins in particulate form, whilst rSFV-NS1-transfected cells secreted glycosylated, heat-labile NS1 dimers. Mice immunized with rSFV particles produced antibodies against prME and NS1 that were mainly of the IgG2a subtype, indicating that a T-helper 1 immune response was induced. Immunization with prME- or NS1-encoding particles induced T-cell proliferation. Mice vaccinated intraperitoneally (i.p.) with rSFV-prME and/or rSFV-NS1 were significantly protected from lethal i.p. challenge by two strains of LIV, the virulent LI/31 strain, from which the commercial LIV vaccine is derived, and the less-virulent LI/I antibody-escape variant. Intranasal (i.n.) vaccination was protective for rSFV-prME only against LI/31 challenge and not against challenge with LI/I. Immunization with rSFV-NS1 was protective against i.p. and i.n. challenge with both virus strains when given i.p., but was not protective when given i.n. For unvaccinated mice infected with LIV, all animals showing clinical signs had severe degenerative and inflammatory lesions in the central nervous system. None of the rSFV-vaccinated mice that survived challenge showed central nervous system pathology, with the exception of mild leptomeningitis in a minority of LI/31-infected mice. This suggests that protection following immunization with rSFV must occur at early stages of LIV infection. (+info)Experimental infection of monkeys with viruses of the tick-borne encephalitis complex: degenerative cerebellar lesions following inapparent forms of the disease or recovery from clinical encephalitis. (2/9)
Rhesus, patas and vervet monkeys were infected i.c. or i.n. with three viruses of the tick-borne encephalitis complex (TBE) as follows: Turkish tick-borne encephalitis virus (TTE), Louping-ill virus and Central European tick-borne encephalitis virus (CETE). The incidence of overt clinical signs of disease varied according to the virus that was used for the inoculations. TTE proved to be more pathogenic for monkeys than the other two members of the complex, whilst CETE was the least pathogenic. Injections of specific antiserum soon after infection tended to increase both the incidence of clinical signs and the moratlity. A proportion of animals with inapparent infections and a number of monkeys that recovered from the acute phase of the disease developed degenerative lesions in the cerebellum, often superimposed on the involuting inflammatory changes. The changes affected either a few only or many folia of the cerebellum and consisted of neuronal and spongy degeneration of the Purkinje and granular layers, usually accompanied by marked astrocytic proliferation and hypertrophy in the granular and molecular layers. (+info)The effect of colostrum-derived antibody on louping-ill virus infection in lambs. (3/9)
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. (+info)Studies of louping-ill virus (Flavivirus group) in wild red grouse (Lagopus lagopus scoticus). (4/9)
Studies were made to find evidence of louping-ill virus infection in free-living red grouse and relate this to their breeding success. In areas where ticks were abundant 61 (84%) adult grouse had antibody to the virus compared with 1 (10%) in areas where ticks were relatively scarce. Of 162 chicks tested 25 were shown to be viraemic. Infected chicks were of significantly less weight than comparably aged uninfected birds and the probability that they died was much greater than that of uninfected birds. It is concluded that the relatively poor breeding success in areas of high tick numbers was principally due to infection with louping-ill virus. The susceptibility of the red grouse to infection is discussed. (+info)Effect of chronic Trypanosoma brucei infection on the course of louping ill virus infection in mice. (5/9)
The course of louping-ill virus infection in mice chronically infected with Trypanosoma brucei was investigated. The mean survival time of mice infected with virus alone was 10.2 days, compared to 12.8 days in mice infected with T. brucei 14 days before virus challenge, and the cumulative mortality in the two groups was 62.5 and 90%, respectively. Virus was only inconsistently detected in the blood of mice given virus alone but was regularly present at high titers for up to 12 days in the blood of mice previously infected with T. brucei. Titers of virus in brains were also higher in dually infected mice, and encephalitis was of greater severity. These results indicate that the immunosuppressive effect of chronic trypanosomiasis may markedly increase susceptibility to acute virus infection. In addition, it is concluded that vector-vertebrate relationships of arthropod-transmitted viruses may be altered by concurrent trypanosome infection. (+info)Louping ill in goats, Spain, 2011. (6/9)
(+info)Field trials of an inactivated oil-adjuvant vaccine against louping-ill (Arbovirus group B). (7/9)
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. (+info)Immunosuppression in toxoplasmosis: further studies on mice infected with louping-ill virus. (8/9)
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. (+info)Louping Ill is a viral disease that primarily affects sheep and cattle, but can also infect humans. It is caused by the Louping Ill virus, which belongs to the family of viruses known as Bunyaviridae. The name "Louping Ill" comes from the characteristic leaping or hopping gait that infected animals may display due to damage to their central nervous system.
In humans, Louping Ill is typically transmitted through the bite of an infected tick, although it can also be spread through contact with infected animal blood or tissue. The virus attacks the nervous system and can cause symptoms such as fever, headache, muscle pain, and stiffness. In severe cases, it can lead to encephalitis (inflammation of the brain), meningitis (inflammation of the membranes surrounding the brain and spinal cord), or paralysis.
Louping Ill is primarily found in the United Kingdom, particularly in Scotland and Northern Ireland, as well as parts of Europe and Africa. It is preventable through vaccination of at-risk animals and the use of tick control measures. There is no specific treatment for Louping Ill in humans, but supportive care can help manage symptoms and promote recovery.
Tick-borne encephalitis (TBE) viruses are a group of related viruses that are primarily transmitted to humans through the bite of infected ticks. The main strains of TBE viruses include:
1. European tick-borne encephalitis virus (TBEV-Eu): This strain is found mainly in Europe and causes the majority of human cases of TBE. It is transmitted by the tick species Ixodes ricinus.
2. Siberian tick-borne encephalitis virus (TBEV-Sib): This strain is prevalent in Russia, Mongolia, and China, and is transmitted by the tick species Ixodes persulcatus.
3. Far Eastern tick-borne encephalitis virus (TBEV-FE): Also known as Russian spring-summer encephalitis (RSSE) virus, this strain is found in Russia, China, and Japan, and is transmitted by the tick species Ixodes persulcatus.
4. Louping ill virus (LIV): This strain is primarily found in the United Kingdom, Ireland, Portugal, and Spain, and is transmitted by the tick species Ixodes ricinus. It mainly affects sheep but can also infect humans.
5. Turkish sheep encephalitis virus (TSEV): This strain is found in Turkey and Greece and is primarily associated with ovine encephalitis, although it can occasionally cause human disease.
6. Negishi virus (NGS): This strain has been identified in Japan and Russia, but its role in human disease remains unclear.
TBE viruses are members of the Flaviviridae family and are closely related to other mosquito-borne flaviviruses such as West Nile virus, dengue virus, and Zika virus. The incubation period for TBE is usually 7-14 days after a tick bite, but it can range from 2 to 28 days. Symptoms of TBE include fever, headache, muscle pain, fatigue, and vomiting, followed by neurological symptoms such as meningitis (inflammation of the membranes surrounding the brain and spinal cord) or encephalitis (inflammation of the brain). Severe cases can lead to long-term complications or even death. No specific antiviral treatment is available for TBE, and management typically involves supportive care. Prevention measures include avoiding tick-infested areas, using insect repellents, wearing protective clothing, and promptly removing attached ticks. Vaccination is also recommended for individuals at high risk of exposure to TBE viruses.
Tick-borne encephalitis (TBE) is a viral infectious disease that causes inflammation of the brain (encephalitis). It is transmitted to humans through the bite of infected ticks, primarily of the Ixodes species. The TBE virus belongs to the family Flaviviridae and has several subtypes, with different geographical distributions.
The illness typically progresses in two stages:
1. An initial viremic phase, characterized by fever, headache, fatigue, muscle pain, and sometimes rash, which lasts about a week.
2. A second neurological phase, which occurs in approximately 20-30% of infected individuals, can manifest as meningitis (inflammation of the membranes surrounding the brain and spinal cord), encephalitis (inflammation of the brain), or meningoencephalitis (inflammation of both the brain and its membranes). Symptoms may include neck stiffness, severe headache, confusion, disorientation, seizures, and in severe cases, coma and long-term neurological complications.
Preventive measures include avoiding tick-infested areas, using insect repellents, wearing protective clothing, and promptly removing attached ticks. Vaccination is available and recommended for individuals living or traveling to TBE endemic regions. Treatment is primarily supportive, focusing on managing symptoms and addressing complications as they arise. There is no specific antiviral treatment for TBE.
Viral envelope proteins are structural proteins found in the envelope that surrounds many types of viruses. These proteins play a crucial role in the virus's life cycle, including attachment to host cells, fusion with the cell membrane, and entry into the host cell. They are typically made up of glycoproteins and are often responsible for eliciting an immune response in the host organism. The exact structure and function of viral envelope proteins vary between different types of viruses.