Aride virus, a new ungrouped arbovirus infecting Amblyomma loculosum ticks from roseate terns in the Seychelles.
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In Africa, many Aedes mosquitos are involved in yellow fever and dengue transmission. Their control can be carried out either in a "prophylactic" way, when no disease occurs, or in a "curative" one, when virus is detected in the human community. In the first event, control is confounded with sanitation measures; in the second event, insecticidal control is needed against both larvae and adults. Larvae populations are destroyed by means of insecticidal deposits in the breeding-sites. Control of adults is achieved by thermal fogs or U.L.V. applications of organophosphorous compounds dispensed from ground or aerial generators. The insecticide susceptibility level of every Aedes populations involved in arbovirus transmission must be periodically determined with all the insecticides available.
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Normal and undernourished mice inoculated orally and intraperitoneally with cocal virus show panencephalitis and acute poliomyelitis, which is more accentuated in cases of malnutrition. Speculations are made regarding viral penetration and progression in the nervous system.
Two Australian members of the Simbu group, Douglas and Tinaroo viruses, were found to be distinct, by virus-neutralization tests, from three previously known Simbu group viruses isolated in Australia, namely Akabane, Aino and Peaton viruses. A low-titre, two-way, cross-reaction was noted between Akabane and Tinaroo viruses. Antibody to Tinaroo and Douglas viruses was detected in serum from cattle, buffalo, sheep, goats and deer but not in humans, pigs, kangaroos and wallabies. The results for horses were inconclusive. The distribution of antibodies to each virus falls mainly within the geographical distribution of the biting midge Culicoides brevitarsis, an insect from which each virus has been isolated.
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Aedes aegypti (L.) mosquitoes showed a significant reduction in susceptibility to infection with Ross River virus and Murray Valley encephalitis virus when they were fed on a blood-virus mixture containing rabbit antibodies to mosquito midgut components. Presence of the antibodies did not demonstrably affect virus titres in infected mosquitoes, nor the transmission of virus from infected mosquitoes to vertebrates.
Ross River virus has been incriminated in the etiology of many sporadic and epidemic cases of polyarthritis in Australia and the Pacific. Both synovium and synovial exudate fluid recovered from the knee of an epidemic polyarthritis patient showed a predominantly mononuclear leucocyte infiltrate. Infectious virus could not be recovered from the synovial exudate. Functional natural killer cells were detected in the synovial fluid. Their level of cytotoxic activity was similar to that detected in the peripheral circulation.
Serum antibodies to Ross River virus and Murray Valley encephalitis virus were measured during 1974-1975 in residents of Echuca, an urban Murray Valley community. A representative group of volunteers was obtained by random selection of households. The prevalence of antibodies to both viruses increased progressively with age. Prevalence was equal in both sexes for both viruses in all age groups, indicating that the risk of infection was mainly determined by geography rather than by personal activities. Antibody levels remained unchanged in the following year when there was no disease activity in the area. The stability of antibody levels permitted retrospective estimates of mean rates of infection. These were approximately 0.4% per annum for both viruses when age was used as the index for years of exposure. With allowance for other factors, the best estimate for both virus infections is probably closer to 1%. The morbidity rate for Ross River virus infection appeared to be low. It is concluded that infection with Ross River virus and with Murray Valley encephalitis-related viruses is endemic in the Murray Valley.
A sero epidemiological study was carried out on human sera from all regions of New South Wales for the presence of antibodies to nine bunyaviruses viz Aino, Akabane, Belmont, Gan Gan, Kowanyama, mapputta, Peaton, Tinaroo, Trubanaman and the orbivirus Corriparta. Neutralising antibodies were found in titres up to 1280 to Gan Gan and to 640 to Trubanaman viruses, prevalences 4.7% and 1.4% respectively. Neutralisation titres up to 40 were found to Belmont, Aino, Peaton and Corriparta viruses but the significance of these is uncertain since they may represent either non-specific inhibitors or cross reacting antibodies to related but currently unknown viruses. No antibodies were found to Akabane, Kowanyama, Mapputta or Tinaroo viruses in New South Wales sera. Gan Gan virus appeared to be pathogenic for man being associated with an acute epidemic polyarthritic like illness. Trubanaman virus is suspected of being pathogenic. This is the first report of the pathogenicity of these Australian bunyaviruses.
Although there is no recognized transmission of human arboviral infections in the UK, concerns about the possible spread of West Nile virus (WNV) have precipitated coordinated activities around both surveillance and response. The Department of Health has chaired a UK WNV task force since the end of 2000. This is a multidisciplinary group of senior representatives from Agencies and Government Departments involved in human and animal health, entomology and academic departments. Activities include surveillance for WNV infections in humans, and in dead birds, mosquitoes and horses. All have been negative for WNV. A WNV contingency plan was produced in 2004, and this could be used as a generic plan for an effective and coordinated response in the event of the emergence of a new vector-borne zoonotic infection.
Cytoplasmic extracts of chicken embryo fibroblast cells infected with Semliki Forest virus were subjected to isopycnic centrifugation in discontinuous sucrose gradients. Seven distinct bands were usually formed. The four upper bands contained predominantly smooth membranes and the lowest band was enriched in rough endoplasmic reticulum. One fraction (fraction 5), banding at a density of 1.16 g/cm(3), was found to be heavily enriched in pulse-labeled ribonucleic acid (RNA), viral RNA polymerase, and viral RNA forms associated with RNA replication. Thus, fraction 5 evidently contained a membrane-associated viral replication complex of a type previously defined in picornavirus infections. Fraction 5 was also consistently enriched with unique membranous structures previously observed in intact cells as type 1 cytopathic vacuoles (CPV-1). When the CPV-1 in fraction 5 were isolated from cells briefly incubated with (3)H-uridine and (3)H-adenosine prior to cell disruption, a large proportion was found to be labeled by high-resolution autoradiography. Thus, ultrastructural, biochemical, and biological evidence were all consistent with the interpretation that the CPV-1 membranes represent a significant element of the viral replication complex.
Unique cytoplasmic structures, herein designated as type I cytopathic vacuoles (CPV-I), are found in chick embryo cells early in the logarithmic phase of Semliki Forest virus replication. High resolution autoradiography demonstrated that the CPV-I are loci of (3)H-uridine incorporation. This evidence correlates well with previous biochemical data and electron microscopy of the subcellular fractions active in Semliki Forest virus ribonucleic acid synthesis. Origin of the CPV-I within host cell cytoplasm is confirmed by the distribution of electron-dense tracer particles and sequential ultrastructural observations.
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