Epidemiology of cercopithecine herpesvirus 1 (B virus) infection and shedding in a large breeding cohort

Our aim was to examine the risk of exposure to CeHV-1 from Sangeh’s macaques. PROPHYLAXIS: Yes, individuals thought to be at high risk for infection following a bite, laceration, or puncture wound when working with infected neural tissue are administered antivirals (4, 6). Viral DNA from the E2490 strain was extracted and purified as previously described (11). fusata, M. ). Unfortunately, FMAU has been reported to be toxic to humans at elevated doses used for cancer chemotherapy (1, 13); FMAU can be incorporated into uninfected cell DNA by host DNA polymerase, suggesting the basis of its toxicity in vivo (11).

Little is known about the shedding rate of MaHV1 in macaques outside the laboratory setting, the frequency of transmission to humans, or the incidence of MaHV1 encephalitis among humans (particularly those with frequent contact with macaques). (25) observed that a PCR test developed by using primers based on the DNA sequence from a cynomolgus monkey BV isolate failed to detect BV isolates from rhesus monkeys. Antigens may also suffer from lot-to-lot variation, compromising outcome measures based on assays using these antigens. Imperfect complementarity to a sequence in the 3′ untranslated region (3′ UTR) usually results in the inhibition of translation of the target mRNA, while perfect complementarity to a region in the coding sequence usually results in the cleavage of the target mRNA. Alphaherpesviruses share a strategy to enter host cells (1–3). Currently, most reports of virus-encoded miRNAs are associated with herpesviruses.


Both of the neurotropic viruses establish latency in the sensory nerve ganglia of their natural hosts (2, 34). To identify particular gB epitopes responsible for HSPG-independent binding, we used a panel of monoclonal antibodies (MAbs) to gB to block gB binding. On direct intracerebral inoculation in BALB/c mice, the 50% lethal dose (LD(50)) for Myb34.5 was 2.7 x 10(7) PFU while that for HSVs with mutations in the gamma34.5 gene could not be technically achieved with available viral stocks and it was estimated as >1 x 10(7) PFU. LANA2 is a potent inhibitor of p53-induced transcription in reporter assays. Neutralizing antibodies could only partially inhibit the switch. The Nov.

66:2754-2762, 1992). These results clarify some of the initial events in HHV-8 entry and can be used for the design of targeted preventive therapies. gB targets DR molecules on their biosynthetic route, after the MHC class II invariant chain is released from the DR heterodimer. The lower pathogenicity of KOS as related to gBKOS, is furthermore associated with the change of Ser to Thr at aa 313 (locus III/D2). In addition, entry may involve plasma membrane rearrangement, signaling events, and/or recruitment of additional cellular molecules. We cloned gB from HSV-1 strain 17 and demonstrate association of the virus envelope protein to three HLA-DR allotypes.

Whereas the immunophenotype of KSHV-infected cells in MCD and malignant KSHV+ PEL cells was similar (PAX5, Bcl-6-; PRDM1/BLIMP1, IRF4/MUM1+; Ki67+), the MCD KSHV-infected cells differed, as they expressed OCT2, cytoplasmic lambda immunoglobulin; variably expressed CD27; lacked CD138; and were Epstein-Barr virus negative. In contrast to B cells of normal donors, CLL B cells were resistant to the cytopathic effects of infection by rdHSV-1 and maintained high-level expression of the transgene for several days in vitro. To examine the association of HVEM and nectin-1 with lipid rafts, we analyzed whether they partitioned into nonionic detergent-insoluble glycolipid-enriched membranes (DIG). To address this, we mutated the furin cleavage site (R-R-K-R) of the MuHV-4 gB. Figure 1 Proteomics based network model showing differential expression of proteins in canonical cancer pathways and the intricate involvement of Meq, via hypothesized CD30-NF-κB-Meq pathway. While macaques infected with this virus are usually asymptomatic, zoonosis caused by the virus in human is one of the most deadly acquired infections.

The Diagnostic Laboratories are adjacent to the B Virus Research Laboratories, facilitating exchange of the most up-to-date strategies for identification of B virus infections whether in the natural host or in zoonotically infected humans. It has always been associated with human herpesvirus type 8 (HHV-8) and in 80% of cases has also been associated with Epstein-Barr virus (EBV). Herpesvirus B (Cercopithecine herpesvirus 1) has been implicated as the cause of approximately 40 cases of meningoencephalitis affecting persons in direct or indirect contact with laboratory macaques.