Seroprevalence of Visna-Maedi Virus (VMV) and Border Disease Virus (BDV) in Van province and around / Seroprevalência de Visna-Maedi Virus (VMV) e Border Disease Virus (BDV) na Província de Van e Proximidades

The present study investigated the seroprevalance of Visna Maedi Virus (VMV) and Border Disease Virus (BDV) infections in sheeps in regions in and around Van province, Turkey. Sample materials were taken from 360 sheep sent to slaughterhouses around Van. All serum samples were examined using ELISA for antibodies for Visna Maedi (VMV) and Border Disease (BDV) viruses. Of these, 38 (10.5%) tested positive for Visna Maedi virus antibodies and 163 (45.2%) for Border Disease virus antibodies. Varying numbers of samples were positive for both virus antibodies across the towns of Ercis, Çaldiran, Erçek and Baskale in Van, Agri and Hakkari provinces. Both infections should be eliminated by informing veterinarians and animal owners, identifying and eliminating persistently infected animals from flocks, and conducting appropriate eradication measures. Economic support should be provided for this.(AU)

O presente estudo investigou a seroprevalência de infecções por Visna Maedi Virus (VMV) e Border Disease Virus (BDV) em ovelhas nas redondezas da província de Van, na Turquia. Amostras foram retiradas de 360 ovelhas enviadas a um matadouro próximo de Van. Todas as amostras foram examinadas usando ELISA para anticorpos de visna Maedi (VMW) e Border Disease (BDV). Destes, 38 (10.5%) foram positivos para anticorpos virais de Visna Maedi e 163 (45.2%) para anticorpos virais de Border Disease. Números variados de amostras foram positivos para ambos os anticorpos nos municípios de Ercis, Çaldiran, Erçek e Baskale, nas províncias Van, Agri e Hakkari. Ambas as infecções devem ser eliminadas informando veterinários e proprietários, identificando e eliminando animais persistentemente infectados de rebanhos, e conduzindo medidas apropriadas de erradicação. Suporte financeiro deve ser providenciado para tal.(AU)

Experimental infection with chamois border disease virus causes long-lasting viraemia and disease in Pyrenean chamois (Rupicapra pyrenaica).

Since 2001, severe outbreaks of disease associated with border disease virus (BDV) infection have been reported in Pyrenean chamois. The disease is characterized by variable degrees of cachexia, alopecia and neurological manifestations prior to death. The aim of this study was to investigate this disease under experimental conditions. To assess viral virulence, humoral immune response, dissemination and probable routes of transmission, seven chamois (five seronegative and two seropositive for BDV) were inoculated with a BDV isolated from a naturally infected chamois. A group of three chamois were maintained as uninfected controls. The five seronegative chamois became viraemic from day 2 post-inoculation (p.i.) until their death (three animals) or the end of the experiment (on day 34 p.i.) and developed neutralizing antibodies from day 18 p.i. until the end of the study. Continuous shedding of the virus was detected by RT-PCR in oral, nasal and rectal swabs in viraemic chamois from day 5 p.i. Despite none of the viraemic chamois showing obvious neurological signs, all of them had a non-suppurative meningoencephalitis as seen in naturally infected chamois. The two inoculated BDV-seropositive chamois did not become viraemic. This study confirms that BDV is the primary agent of the disease that has been affecting chamois populations in recent years in the Pyrenees and that previously acquired humoral immunity is protective.

The envelope glycoprotein E2 is a determinant of cell culture tropism in ruminant pestiviruses.

Bovine viral diarrhoea virus (BVDV) isolates infect cultured Madin-Darby bovine kidney (MDBK) cells as efficiently as sheep kidney cells. In contrast, border disease virus (BDV) propagates poorly in MDBK cells but infects sheep cells very efficiently. The envelope glycoprotein E2 has been shown to be essential for virus infectivity. To explore the potential role of E2 in pestivirus host range in cell cultures, we engineered a chimeric BVDV with the E2 coding region from BDV. As expected, the BVDV-E2(bdv) chimera retained the ability of BDV to multiply in sheep cells but experienced a remarkable reduction in its ability to propagate and form plaques in MDBK, a phenotype that is characteristic of the E2 donor, BDV31 virus. Control chimeric BVDV bearing a type II E2 demonstrated that the heterologous E2 does not impair replication in MDBK or lamb cells. These results establish a role for E2 in determining the tropism of a pestivirus in cell culture.