Methods for Recovering African Horsesickness Virus from Horse Blood1

Ozawa, Y.; Salama, S. A.; Dardiri, A. H.

doi:10.1159/000393518

Cited by 11 publications

(8 citation statements)

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“…However, in 1953, McIntosh [10] suggested that, in the circulatory system, AHSV is present in or on RBC membranes and such cell-associated virus may exist concurrently with serum antibodies. To prevent neutralization of AHSV after lysis of RBC by ultrasonication [11,12], the practice at this Institute has been to collect blood in heparin and to thoroughly wash the RBC before lysis and assay. The results recorded here show that antibodies and detectable amounts of antigen were not concurrently present in serum and heparinized blood collected from the three ponies which died.…”

Section: Discussionmentioning

confidence: 99%

The detection of African horse sickness virus antigens and antibodies in young equidae

et al. 1992

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SUMMARYFour ponies were each inoculated with a different serotype of African horse sickness virus (AHSV) which had been passaged through cell culture in order to achieve attenuation. Three of the ponies died suddenly after showing mild clinical signs, the fourth pony remained clinically normal and was killed at day 38. Infectious AHSV was isolated from blood samples collected at intervals from all four ponies. Positive antigen ELISA reactions were only observed with blood samples from two of the ponies on the two days preceding death. Specific AHSV antibodies were detected by ELISA in serum samples from the other two ponies although one eventually died. African horse sickness viral antigens were detected by ELISA in post-mortem tissue samples collected from all four ponies. No infectious virus could be detected in tissue samples taken post-mortem from the pony which survived African horse sickness (AHS) infection. In the event of a suspected outbreak of AHS it is recommended that sera and heparinized blood should be tested for specific antibodies and AHSV antigen respectively. When available, post-mortem tissues, including spleen, heart, lung and liver, should also be tested for AHSV antigen. Although the ELISA used for the detection of AHSV antigen is highly sensitive and specific, negative ELISA results should be confirmed by virus isolation attempts.

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Section: Discussionmentioning

confidence: 99%

The detection of African horse sickness virus antigens and antibodies in young equidae

et al. 1992

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“…Titers of BTV in the erythrocyte fraction were very similar to those in unseparated blood cells. We previously have established that virus is not associated with either neutrophils or platelets late in the course of infection.32 Prolonged erythrocyte-associated viremia that persists despite the presence of specific neutralizing antibody would, therefore, appear to be a characteristic of several different orbiviral infections of animals, including those of African horse sickness virus, Colorado tick fever virus, and Palyam subgroup viruses such as Chuzan virus infection of cattle.4s6J8, 24 Although we confirmed that viremia is highly cell associated in BTV-infected cattle, the pathogenesis of BTV infection of blood cells was not definitively established. The data suggest that infection of blood cells is not a consequence of infection of hematopoietic precursors in bone marrow as virus was present in blood and a variety of tissues before it was isolated from bone marrow; furthermore, BTV was inconsistently isolated in relatively low titers from bone marrow, and infected cells were not demonstrated in bone marrow by immunohistochemical staining.…”

Section: Imentioning

confidence: 99%

The Pathogenesis of Experimental Bluetongue Virus Infection of Calves

et al. 1990

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Abstract. Eleven seronegative calves were intravenously inoculated with bluetongue virus (BTV) serotype 10, and two calves were inoculated with a placebo. Cellular association of BTV during viremia was investigated in three of the calves by titrating virus present in plasma and different blood cell fractions at weekly intervals after infection. Viremia persisted 35 to 49 days in individual calves. Virus was transiently isolated from blood mononuclear cells and plasma collected from two of the calves but was consistently isolated from erythrocytes throughout infection of all three animals. Titers of BTV present in the erythrocyte fraction were comparable to those of the unseparated blood cell fraction. Tissue tropism of BTV was determined by viral isolation from tissues collected from calves euthanatized at 1, 2, 3, 4, 5, 7, 14, 28, 42, and 56 (2 calves) days after inoculation with BTV. Tropism was also determined by immunohistochemical staining of selected tissues with an avidinbiotin complex immunoperoxidase staining procedure using three BTV-specific monoclonal antibodies. The BTV infected calves remained healthy throughout the study. Virus was isolated from at least one tissue collected from calves euthanatized at 1 through 28 days after inoculation, but not thereafter. High titers of BTV were present in the lungs, prescapular and mesenteric lymph nodes, thymus, and spleen of calves euthanatized at 1 to 4 days after inoculation, whereas BTV was either not isolated or isolated in low titer from bone marrow collected from these animals. Very low numbers of infected cells were detected by immunohistochemical staining of sections of spleen (days 1 and 2 after inoculation), prescapular lymph nodes (days 1, 2, 3, and 4), lung (day 3), thymus (day 4), lip (day 5), and trapezius muscle (day 7). The morphology and anatomic location of at least some of the infected cells in sections of lymph node, spleen, and thymus were most consistent with their being mononuclear phagocytes, whereas the infected cells in the sections of lip and trapezius muscle were located within or immediately adjacent to arterioles and probably were endothelial cells. It is proposed that after intravenous inoculation of calves with BTV, viral replication initially occurs in mononuclear phagocytic cells and subsequently in vascular endothelium. The intimate association of BTV with circulating blood cells, especially erythrocytes, apparently impedes prompt clearance resulting in prolonged viremia. The data suggest that although BTV infection of cattle is characterized by prolonged viremia, viral replication in tissues is transient, and a truly persistent infection does not occur in BTV infected calves. Bluetongue virus; cattle; viremia. Bluetongue is an insect-transmitted, non-contagious viral disease of domestic and wild r u m i n a n t~.~~~J 1,20, 30 The causative agent is bluetongue virus (BTV), a member of the Reoviridae and prototype virus of the genus orbivirus. The consequences of BTV infection of cattle and sheep frequently are different;...

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“…Virus is present in the blood 4 days before the signs of the disease and 2 days after (Goldsmit, 1968) and may reach a titre of 1068 LD50 per ml (Ozawa, Salama & Dardiri, 1972). Virus persists at low titre in the blood in the presence of antibody for long periods after recovery from the disease.…”

Section: And Vector Hostmentioning

confidence: 99%

Possible spread of African horse sickness on the wind

Sellers

Pedgley

Tucker

1977

J. Hyg.

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SUMMARYAnalyses of outbreaks of African horse sickness showed that movement of infected Culicoides midges on the wind was most likely responsible for the spread of the disease over the sea from Morocco to Spain in 1966, from Turkey to Cyprus in 1960, and from Senegal to the Cape Verde Islands in 1943. The pattern of spread of the epidemic in the Middle East in 1960 could have been laid down by the infected midges carried on spells of south-east winds, and analyses of outbreaks in Algeria in 1965 and India in 1960 also suggested windborne spread of the disease. Each spread occurred when the presence of virus, host and vector coincided either with a spell of winds unusual for a particular time of year (Spain, Cyprus, Cape Verde Islands and Algeria) or with a series of disturbances usual at that time of the year (Middle East and India). Inferred flight endurance of the midge varied up to at least 20 h and flight range from 40 to 700 km. Flight occurred when temperatures were likely to have been in the range of 15–25 °C if it was at night or 20 to about 40 °C if it was by day.It is suggested that likely movements of midges on the wind can be estimated from synoptic weather charts, and should be taken into account when planning control of the disease in the face of an outbreak. Such control includes a ban on movement of horses, vaccination and spraying of insecticide.The risk of spread to countries outside the endemic areas should be assessed by reference to possible wind dispersal of infected midges.

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Methods for Recovering African Horsesickness Virus from Horse Blood1

Cited by 11 publications

References 0 publications

The detection of African horse sickness virus antigens and antibodies in young equidae

The detection of African horse sickness virus antigens and antibodies in young equidae

The Pathogenesis of Experimental Bluetongue Virus Infection of Calves

Possible spread of African horse sickness on the wind

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