Specific Detection and Identification of Herpes B Virus by a PCR-Microplate Hybridization Assay

Amplification of the A, C, and E regions successfully generated products from SMHV/pBV-DNA but not from HSV-1, HSV-2, HCMV, and SCMV isolates (Fig. The relative positions of all fragments used for B virus genome sequencing are shown in Fig. The insertion of the stop codon linker into the BglII site results in a 1,157-bp amplimer (lane 4) that, when cut with SpeI, yields 856-bp and 301-bp fragments (lane 3). The products (10 μL) were then analyzed by electrophoresis on 1% agarose gels. ELISA antigens from four BV isolates, one from each macaque species, were prepared. At 72 h postinfection, virus-containing medium from the transfected cells was harvested and titrated by a plaque assay on Sf-9 cell monolayers.

HSV-1 strain KOS (ATCC VR-1493) was grown and titrated on Vero cells maintained in minimum essential medium (MEM) supplemented with 2% FBS. The amplified cDNA libraries were resolved using a 6% polyacrylamide Tris-borate-EDTA (TBE) gel. Microplate hybridization was performed as previously described (12, 15) with some modifications. L-cells and Gro2C and Sog9 cells were a generous gift from F. HSV-1 (KOS/tk12) and vesicular stomatitis virus were kindly provided by P. After 3 days of culture of the remaining cells, the nonadherent (granulocyte-rich) cells were removed by washing and the adherent cells were supplemented with fresh medium.

In our work from MD lymphocytes in vivo, BCL2 protein was unchanged suggesting that any BCL2 functional-deregulation may occur prior to the CD30lo to CD30hi transition in the lymphoma environment. At Sangeh, three troops of macaques, a total of >200 monkeys, range throughout the monkey forest, along a road lined with merchants’ shops, and into the adjacent town. We reasoned that transcriptional retargeting of γ34.5 might provide a means to achieve selective virulence for tumors while retaining attenuated virulence for normal tissues. The ligation mixtures were transformed into E. Therefore myeloid infection seems more likely to be important for establishing MuHV-4 host colonization than for maintaining it. I.

Electroporated cells were then returned to the flask, fed the next day, and split 1:2 when they reached confluence at 2 days post electroporation. During latency, only a few regions are transcriptionally active. The repression of viral protein synthesis during latency has led to the prevalent view of latency as being a quiescent and antigenically silent infection that is ignored by host immunity. NKT cells influence diverse immune responses, including immunity to tumors and infectious diseases, as well as autoimmune diseases and allergies (5). Several mechanisms have been identified by which HSV-1 inhibits recognition by CD8+ T cells. Conversely, Myb34.5’s oncolytic efficacy against a variety of human glioma cells in culture and in vivo was enhanced compared to that of HSVs with γ34.5 mutations, and in fact, it was comparable to that of the wild-type F strain and of viral mutants that possess a wild-type γ34.5 gene.

In captivity, as well as in the wild, mature macaques are more likely than immature animals to have been infected with, and shed, the virus. These results were further confirmed by BV infection. Owing to the biosafety concerns, little research has been conducted directly using BV; most of the knowledge on this virus is extrapolated from study of its closely related viral species of the subfamily Alphaherpesvirinae, herpes simplex virus (HSV) type 1 (HSV-1) and HSV-2 [6]. After 1 yr, local evolution required surgery followed by irradiation. Airborne transmission is postulated to have occurred as a result of clinical circumstances in two reported cases, but there is no strong evidence to support the hypothesis of aerosol infection. In addition, binding of the gB-Fc fusion protein to CHO cells was severely impaired in the presence of soluble heparin, as well as when heparan sulfate-deficient mutant CHO cells were used.

It contains the expected signal and transmembrane sequence motifs as well as a putative site of protease cleavage. HHV-6 isolates can be differentiated into two groups, variants A and B (HHV-6A and HHV-6B). Description: Clinical Infectious Diseases publishes clinically relevant articles on the pathogenesis, clinical investigation, medical microbiology, diagnosis, immune mechanisms, and treatment of diseases caused by infectious agents. Human herpesvirus-6A (HHV-6A) and HHV-6B integrate their genomes into the telomeres of human chromosomes, however, the mechanisms leading to integration remain unknown. Kaposi’s sarcoma-associated herpesvirus (KSHV) is the etiologic agent of primary effusion lymphoma (PEL), multicentric Castleman’s disease (MCD), and the inflammation-driven neoplasm Kaposi’s sarcoma (KS).