The focus of this review is to summarize the biology of BHV-1 and how this relates to BRDC. The ability of BHV-1 to enter permissive cells, infect sensory neurons and promote virus spread from sensory neurons to mucosal surfaces following reactivation from latency is also regulated by several viral glycoproteins. Two viral genes, the latency related gene and ORF-E are abundantly expressed during latency, suggesting that they regulate the latency-reactivation cycle. Periodically BHV-1 reactivates from latency, virus is shed, and consequently virus transmission occurs. Agradeceria cualquier ayuda en este sentido porque ya lo he probado y buscado todo y no hay manera, y estas imagenes me hacen falta urgentemente.
Following acute infection, BHV-1 establishes latency in sensory neurons of trigeminal ganglia (TG) and germinal centers of pharyngeal tonsil. Bhv 1 Codec He probado a descargar el citado codec pero no hay manera de dar con el en internet. Consequently, the ability of BHV-1 to impair the immune response can lead to BRDC.
Following acute infection of calves, BHV-1 can also infect and induce high levels of apoptosis of CD4+ T-cells. BHV-1 encodes at least three proteins that can inhibit specific arms of the immune system: (i) bICP0 inhibits interferon-dependent transcription, (ii) the UL41.5 protein inhibits CD8+ T-cell recognition of infected cells by preventing trafficking of viral peptides to the surface of the cells and (iii) glycoprotein G is a chemokine-binding protein that prevents homing of lymphocytes to sights of infection. BHV-1-induced immune suppression initiates bovine respiratory disease complex (BRDC), which costs the US cattle industry approximately 3 billion dollars annually. Infection of cattle by bovine herpesvirus type 1 (BHV-1) can lead to upper respiratory tract disorders, conjunctivitis, genital disorders and immune suppression.
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