Microbiol. Veterinary Microbiology 88: 315–334. Cells were infected with VSVΔM51, KM100 and BHV-1gfp at MOIs of 0.5 and 5. A 336-bp intergenic region between the gB and UL 26/UL26.5/UL24 genes (indicated hereafter as UL26) (GenBank accession number AJ004801) was found to be suitable for the insertion of the 8.8-kb spanning BAC mini-F plasmid sequence. The LAT locus encodes additional transcripts (). In addition, Ras is able to mediate cellular responses to virus infection by mediating the activity of antiviral pathways (28–32).
pastoris was mixed with 5 μl SacI-linearized recombinant plasmid (∼1 μg/μl) and incubated for 5 min at 0°C in a cuvette (0.2-cm gap; Bio-Rad). When nuclear extracts were IP with the anti-Flag antibody to IP bICP0, several diffuse bands, in addition to the immunoglobulin G heavy chain, were detected when the Western blot was probed with the anti-IRF7 antibody (Fig. The PCR product was inserted as a KpnI/SalI fragment into pEYFP-N1 (Clontech, Mountain View, CA), creating pUL48-YFP. Although TG is the major site for α-herpesvirus latency following infection, several studies demonstrate that persistence or latency can occur in nonneural sites. Nonadherent cells contained mainly DC and were further enriched by centrifugation in Nycodenz gradients (d = 1.068; Nycomed Pharma, Oslo, Norway). HSV-1 establishes latency in ganglionic sensory neurons (33, 61) and the latency-associated transcript (LAT) is abundantly transcribed in latently infected neurons (52, 58).
Shortly after exposure of cells to UV-irradiated virus, which was capable of receptor binding and endocytosis, the early PI3K/Akt and MAPK/Erk1/2 pathways activation was induced, but it was insufficient to induce the late stage phosphorylation (Figure 3). gE is a type I transmembrane protein, whereas Us9 is a type II tail-anchored membrane protein. Importantly, the rates of expression of UL47 in the two viruses were similar, as were the expression kinetics of the bTIF protein encoded by UL48 (Fig. The ability of bICP0 to associate with chromatin remodeling enzymes, histone deacetylase 1 (HDAC1) and p300, stimulates viral gene expression and productive infection (Zhang and Jones, 2001; Zhang et al., 2006). To date, bICP0 is the only BHV-1 gene that has been demonstrated to inhibit the activity of human (Henderson et al., 2005; Saira et al., 2007, 2009) and bovine (da Silva et al., 2011) IFN-β promoters. Nous avons conclu que l’exposition préalable au BHV-1 mais non au BVDV de type 2 était une cause nécessaire des maladies respiratoires associées à M.
In herpes simplex virus type 1 (HSV-1), VP22 interacts with another tegument protein, VP16, and its gene is classified as essential (8). 71:6786–6795, 1997), suggesting that certain aspects of a lytic infection occur in neurons and that these factors influence LRT splicing. The economic losses due to BRDC alone cost the U.S. The affection of these three organ systems determines the clinical signs observed after EHV-1 infection, which are respiratory distress including nasal discharge, dyspnoea, and coughing, late-time abortions in pregnant mares, and neurological disease. F., Amin, A.S. Growth arrested MDBK cells were mock infected or infected with BHV-1 at an MOI of 10.
The MDBK cell line at second passage level showed characteristic cytopathic effect viz. Extracellular virions of the UL47 deletion mutant contained reduced amounts of gD, gB, gC, and VP22 but similar amounts of VP16 compared to those of wild-type or revertant virus particles. We detected a high concentration of HSV-1-reactive IgG in immune milk. The genomes of large DNA viruses have generally evolved by three mechanisms: mutation during viral DNA replication, acquisition of cellular genes, and recombination between strains of the same viral species. In addition, we found that a gD-null virus (a virus containing no gD on its virion) could infect gD-expressing cells, but not normal MDBK cells. Kurokawa and H.
Necropsy findings in 10 of 22 cattle included hyperemia and softening of the rostral portions of the telencephalic cortex, with flattening of gyri, and malacia. The aim of the present study was to address the effects of BHV-1 on iron metabolism in Madin-Darby bovine kidney (MDBK) cells at different times of post-infection. The natural port of entry is the mucous membrane of upper respiratory and genital tracts and the disease is characterised by (muco) purulent nasal discharge, and by conjunctivitis. BHV-1 is also a contributing factor in Bovine Respiratory Disease Complex (BRDC), otherwise known as shipping fever.