Sequence and Genetic Arrangement of the U(S) Region of the Monkey B Virus (Cercopithecine Herpesvirus 1) Genome and Comparison with the U(S) Regions of Other Primate Herpesviruses

The sequence of the unique short (U(S)) region of monkey B virus (BV) was determined. The 13 genes identified are arranged in the same order and orientation as in herpes simplex virus (HSV). These results demonstrate that the BV U(S) region is entirely colinear with that of HSV type 1 (HSV-1), HSV-2, and simian agent 8 virus

Simian Foamy Virus Infections in a Baboon Breeding Colony

AbstractThe prevalence, transmission, and variation of simian foamy viruses (SFVs) in baboons was investigated. Over 95% of adult baboons in the breeding colony as well as recently imported adult animals had high titers of anti-SFV serum IgG. Maternal antibody was detectable in infants' serum up to 6 months of age. Approximately 30% of infants in breeding harems experienced SFV infections by 1 year of age. Shedding of SFV in oral secretions was common, with 13% of samples from normal adult animals and 35% from immunosuppressed animals containing infectious SFV. SFV was isolated from three baboon subspecies (olive, yellow, and chacma baboons) and sequences from both the pol and the LTR regions of the provirus were amplified by PCR and sequenced. Phylogenetic analysis indicated that all baboon isolates formed a single lineage distinct from SFVs of other African monkey species. Within the baboon SFV lineage, two distinct clades were apparent, which consisted of isolates from yellow and olive baboons and isolates from chacma baboons. Competition ELISAs indicated that, while SFV isolates of these two groups were very closely related, antigenic differences do exist between them. SFV isolates from a drill and a mandrill were distinct from baboon SFV isolates, both genetically and antigenically

Sensitivity of Monkey B Virus (Cercopithecine herpesvirus 1) to Antiviral Drugs: Role of Thymidine Kinase in Antiviral Activities of Substrate Analogs and Acyclonucleosides▿

Herpes B virus (B virus [BV]) is a macaque herpesvirus that is occasionally transmitted to humans where it can cause rapidly ascending encephalitis that is often fatal. To understand the low susceptibility of BV to the acyclonucleosides, we have cloned, expressed, and characterized the BV thymidine kinase (TK), an enzyme that is expected to “activate” nucleoside analogs. This enzyme is similar in sequence and properties to the TK of herpes simplex virus (HSV), i.e., it has a broad substrate range and low enantioselectivity and is sensitive to inhibitors of HSV TKs. The BV enzyme phosphorylates some modified nucleosides and acyclonucleosides and l enantiomers of thymidine and related antiherpetic analogs. However, the potent anti-HSV drugs acyclovir (ACV), ganciclovir (GCV), and 5-bromovinyldeoxyuridine were poorly or not phosphorylated by the BV enzyme under the experimental conditions. The antiviral activities of a number of marketed antiherpes drugs and experimental compounds were compared against BV strains and, for comparison, HSV type 1 (HSV-1) in Vero cell cultures. For most compounds tested, BV was found to be about as sensitive as HSV-1 was. However, BV was less sensitive to ACV and GCV than HSV-1 was. The abilities of thymidine analogs and acyclonucleosides to inhibit replication of BV in Vero cell culture were not always proportional to their substrate properties for BV TK. Our studies characterize BV TK for the first time and suggest new lead compounds, e.g., 5-ethyldeoxyuridine and pencyclovir, which may be superior to ACV or GCV as treatment for this emerging infectious disease