Avian Orthoavulavirus 1 Vaccination Failure in Minnesota Turkeys.

Minnesota is the leading state in number of turkeys produced in the United States. Turkey flocks in the field are usually vaccinated several times with live avian orthoavulavirus 1 (AOAV-1) vaccines starting as early as 2 wk of age (WOA). During the years 2018-2019, many turkey flocks were diagnosed with low-virulence AOAV-1 infection around 9 WOA that led to respiratory disease, although they were previously vaccinated. This study was designed to investigate the immunity against AOAV-1 in Minnesota turkey flocks in the field and experimentally after vaccination. We reviewed antibody titers against AOAV-1 from turkey flocks tested by ELISA at Minnesota Poultry Testing Laboratory (n = 1292). Up to 9 WOA, more than 85% of the field flocks tested had unprotective antibody titers against AOAV-1. However, commercial poults at 3 WOA experimentally vaccinated by eye-drop method had an ELISA geometric mean titer of 6011 at 7 WOA. Oropharyngeal virus shedding after vaccination was 10%, 70%, 80%, and 40% at 1, 3, 5, and 7 days postvaccination, respectively. This study demonstrates that experimentally vaccinated turkeys respond very well to AOAV-1 vaccine when properly administered. However, there is clear vaccination failure in the field, where vaccine is commonly administered in drinking water, a method that is more susceptible to failure because of many variables in this procedure. We recommend choosing the most effective method of vaccine administration. Given the high incidence of inadequate immunity induced in commercial turkeys on mass application of live AOAV-1 vaccines in water, alternative application methods and subsequent monitoring of the serologic antibody response must be undertaken to ensure a proper immune response.

Artículo regular­Fracaso de la vacunación contra el Orthoavulavirus aviar 1 en pavos de Minnesota. Minnesota es el estado líder en número de pavos producidos en los Estados Unidos. Las parvadas de pavos en el campo generalmente se vacunan varias veces con vacunas vivas con Orthoavulavirus Aviar 1 (AOAV-1) comenzando desde las 2 semanas de edad (WOA). Durante los años 2018­2019, muchas parvadas de pavos fueron diagnosticadas con infección por Orthoavulavirus Aviar 1 de baja virulencia alrededor de las nueve semanas de edad que condujeron a una enfermedad respiratoria, aunque las aves fueron vacunadas previamente. Este estudio fue diseñado para investigar la inmunidad contra Orthoavulavirus Aviar 1 en parvadas de pavos de Minnesota en el campo y experimentalmente después de la vacunación. Se revisaron los títulos de anticuerpos contra Orthoavulavirus Aviar 1 de parvadas de pavos analizados por ELISA en el Laboratorio de Diagnóstico Avícola de Minnesota (n = 1292). Hasta las nueve semanas de edad, más del 85% de las parvadas de campo analizadas tenían títulos de anticuerpos no protectores contra Orthoavulavirus Aviar 1. Sin embargo, los pavipollos comerciales a las tres semanas de edad vacunados experimentalmente por el método de gota ocular tenían un título medio geométrico de ELISA de 6011 a las siete semanas de edad. La diseminación del virus orofaríngeo después de la vacunación fue del 10%, 70%, 80% y 40% a los 1, 3, 5 y 7 días después de la vacunación, respectivamente. Este estudio demuestra que los pavos vacunados experimentalmente respondieron muy bien a la vacuna con Orthoavulavirus Aviar 1 cuando se administra correctamente. Sin embargo, existe un claro fracaso de la vacunación en el campo, donde la vacuna se administra comúnmente en el agua potable, un método que es más susceptible al fracaso debido a muchas variables en este procedimiento. Se recomienda elegir el método de administración de vacunas más eficaz. Considerando la alta incidencia de inmunidad inadecuada inducida en pavos comerciales con la aplicación masiva de vacunas vivas con Orthoavulavirus Aviar 1 en agua, se deben llevar a cabo métodos de aplicación alternativos y monitoreo posterior de la respuesta de anticuerpos serológicos para asegurar una respuesta inmune adecuada.

Antiviral activity and RNA polymerase degradation following Hsp90 inhibition in a range of negative strand viruses.

We have analyzed the effectiveness of Hsp90 inhibitors in blocking the replication of negative-strand RNA viruses. In cells infected with the prototype negative strand virus vesicular stomatitis virus (VSV), inhibiting Hsp90 activity reduced viral replication in cells infected at both high and low multiplicities of infection. This inhibition was observed using two Hsp90 inhibitors geldanamycin and radicicol. Silencing of Hsp90 expression using siRNA also reduced viral replication. Hsp90 inhibition changed the half-life of newly synthesized L protein (the large subunit of the VSV polymerase) from >1 h to less than 20 min without affecting the stability of other VSV proteins. Both the inhibition of viral replication and the destabilization of the viral L protein were seen when either geldanamycin or radicicol was added to cells infected with paramyxoviruses SV5, HPIV-2, HPIV-3, or SV41, or to cells infected with the La Crosse bunyavirus. Based on these results, we propose that Hsp90 is a host factor that is important for the replication of many negative strand viruses.

Characterization of Bangor virus proteins by using monoclonal antibodies.

A new virus was isolated from a finch in quarantine in Northern Ireland in 1973. The virus had the morphological characteristics of a paramyxovirus, and was named Bangor virus (BaV). In order to identify the structural proteins of BaV and to investigate the biological characterization of the virus, 28 monoclonal antibodies (mAbs) directed against BaV were prepared. Eight of these mAbs reacted with the nucleocapsid protein (NP), 10 with hemagglutinin-neuraminidase (HN) protein, and 10 with fusion (F) protein. With the aid of these mAbs, the structural proteins of BaV were determined, namely, p52, gp74, gp63, and gp51 were identified as the NP, HN, F0, and F1 proteins, respectively. The biological activities of the mAbs directed against the envelope glycoproteins of BaV were examined. Intriguingly, it was found in the neutralization assay that four mAbs directed against the HN protein of BaV can enhance the fusion of HeLa cells infected with BaV, showing the presence of a potential third function of the HN protein that affects the fusion activity of the F protein. Furthermore, all of the anti-F protein mAbs showed neutralizing activity.