Infección por el virus de la Lengua azul: activación de señales celulares que inducen apoptosis / Bluetongue virus infection: signaling pathway activated during apoptosis

El virus de la Lengua azul (VLA) es un ARN virus de doble cadena que induce apoptosis tanto en cultivos celulares como en tejidos blanco. Con el fin de dilucidar el mecanismo de apoptosis en la infección por el VLA, en el presente trabajo examinamos en detalle, por la técnica de Western blot, las señales celulares de caspasas, Bax, citocromo c, Smac/DIABLO y factor nuclear kappa B (NF-kB) que se activan en la infección viral. Hemos comprobado que luego de la infección in vitro con el VLA, se detectó la activación de la caspasa 8 y con ello el mecanismo extrínseco de la apoptosis. También detectamos por primera vez no sólo la activación de miembros de la familia Bcl-2 (Bax), sino también la liberación del citocromo c y la proteína Smac/DIABLO, confirmando que en la infección por el VLA está involucrado el mecanismo secuencial intrínseco de la apoptosis. Asimismo, demostramos que la infección por el VLA activa el NF-kB y que la apoptosis es sustancialmente reducida mediante la inhibición del mismo. La activación de las señales celulares tales como Bax, citocromo c, Smac/DIABLO y NF-kB presentados en este trabajo, esclarecen los mecanismos apoptóticos durante la infección por el VLA para una mayor comprensión del papel primario que juega la apoptosis en la patogénesis del virus.

Bluetongue (BTV) is a double-stranded RNA virus that induces apoptosis both in mammalian cell cultures and in target tissues. To elucidate the apoptosis pathways in BTV infection, we have examined in detail the apoptosis mechanism by examination of caspases, Bax, cytochrome c, Smac/DIABLO and NF-kB signalling pathways. In this report, after cell infection with BTV, the activation of caspase 8 was detected, proving the extrinsic receptor binding apoptotic pathway. Apoptosis followed a sequential pathway involving the detection of activated Bcl-2 family members. Furthermore, its translocation to the mitochondria, as well as the release of cytochrome c and Smac/Diablo confirmed that BTV apoptosis involves the sequential intrinsic pathway. In addition, we demonstrated that NF-kB was activated following BTV infection and cell treatment with an inhibitor peptide before BTV infection, prevented NF-kB activation and substantially reduced cellular apoptosis. Our accumulating data concerning the activation of Bax, cytochrome c, Smac/DIABLO and NF-kB clarify the mechanism of apoptosis during BTV infection, and confer a better understanding of the primary role of apoptosis in BTV pathogenesis.

Feline immunodeficiency virus infection: a comparative study of different diagnostic techniques

Avaliou-se a técnica de imunofluorescência indireta (IFA) na detecção de anticorpos contra o vírus da imunodeficiência felina (FIV) numa pesquisa epidemiológica do FIV na Argentina. A IFA foi modificada e comparada com duas outras técnicas imunológicas: western blot (WB) e imunocromatografia em camadas (SI) com kit comercial e também com reação em cadeia de polimerase (PCR) para detecção do DNA proviral. A IFA mostrou ser um teste com alta sensibilidade e especificidade e poderá ser empregada como ferramenta útil em estudos epidemiológicos. A baixa porcentagem de reatividade não específica pode ser esclarecida com testes mais avançados ou usando métodos alternativos.

Virus de la inmunodeficiencia felina: producción de interferón gamma en cultivos de linfocitos T infectados / Feline immunodeficiency virus infection: interferon gamma secretion in a T-lymphoblastoid infected cell line

Feline immunodeficiency virus (FIV) was first isolated in 1987 from a cat with an acquired immunodeficiency syndrome (AIDS)-like disease. Since then, FIV has been subject of intensive research. Perturbation in cytokine production observed in human immunodeficiency virus infection (HIV) is paralleled in the FIV-infected cat. Interferon gamma (IFN-gamma) is a type 1 lymphokine that exert protective effects during infection through upregulation of cellular immunity and phagocytic functions. The present study was carried out to examine the expression of IFN-gamma in a feline T-lymphoid cell line (Fel-039) infected with FIV as well as the viral replication in these cells after addition of recombinant-type feline IFN (rIFn). We found a marked inhibition of IFN-gamma release in Fel-039 cells infected with FIV which might be pivotal for high viral replication. Infection of Fel-039 cells with FIV resulted in an increase of the reverse transcriptase (RT) activity in the culture supernatant. When the cells were cultured in the presence of rIFN a significant dose-dependent inhibition of RT activity of FIV was detected without cytotoxicity. On the basis of these in vitro results, we suggest that IFN therapies aimed at restoring depleted level of this important cytokine in FIV infected T-cells make this compound a promising candidate for development of suitable drugs for AIDS treatment.