California herpes dating
2011]) in which viral descendants follow the phylogenetic history of their host species. These viruses have been characterized in monkeys, where each host species is infected with a single, species-specific virus.Herpes simplex viruses in primates exemplify this phenomenon and evidence of codivergence dates back at least to the ancestor of New World and Old World primates (Simiiformes) 44.2 Ma (Eberle and Black 1993; Luebcke et al. Humans are the only primate species in which more than one herpes simplex virus has been characterized: HSV-1 and HSV-2 (table 1).
Under the BSREL model, one set of origin scenarios is clearly favored (table 2).All scenarios imply a 6 Ma t MRCA for HSV-2/Ch HV and a t MRCA Evolutionary scenarios that could produce the human and chimpanzee herpes simplex virus phylogeny via viral cross-species transmission. Nodes representing the common ancestor of humans and chimpanzees, around 6 Ma, are indicated with asterisks. The herpes simplex virus substitution rate is estimated to be around 10 substitutions/site/year (Sakaoka et al. 2011), which suggests that t MRCAs on the order of tens of millions of years could be reliably inferred.Scenarios Evolutionary scenarios that could produce the human and chimpanzee herpes simplex virus phylogeny via viral cross-species transmission. Nodes representing the common ancestor of humans and chimpanzees, around 6 Ma, are indicated with asterisks. However, such analyses may be misleading because, unlike phylogeny-based molecular clocks, they do not account for shared evolutionary history (Drummond et al. Recent methodological developments in the dating of RNA viruses have suggested that standard evolutionary models used in molecular dating can underestimate the time to most recent common ancestor (t MRCA) (e.g., in measles virus, Ebola virus, avian influenza virus, and coronaviruses) (Wertheim and Kosakovsky Pond 2011; Wertheim et al. This bias has been attributed to the action of strong purifying selection over long evolutionary time scales, and selection-informed models have been shown to improve branch length estimation (Wertheim and Kosakovsky Pond 2011); even under these models, however, many viruses are likely too old to produce reliable t MRCA estimates. To resolve the origin of HSV-1 and HSV-2, we propose a novel computational hypothesis testing approach that combines realistic codon-substitution evolutionary models that allow for selection strength heterogeneity with a penalized likelihood molecular clock estimation procedure.Under both general sets of hypotheses (viral lineage duplication [fig. 3]), the t MRCA of either HSV-1/Ch HV or HSV-2/Ch HV should correspond to the divergence between their human and chimpanzee hosts around 6 Ma (fig. We also performed dating analysis using only glycoprotein B (g B) sequences, which have been sampled in a greater number of taxa, permitting the inclusion of an additional calibration point in New World monkeys (see Materials and Methods). 2012), BMCMC dating results support neither the lineage duplication nor the cross-species transmission hypotheses for the origin of HSV-1 and HSV-2.
The phylogenetic relationships among the primate simplex viruses were all well supported in the BMCMC analyses in both data sets (posterior probability = 1.0; online); the topologies are in agreement with previous viral analyses (Luebcke et al. 2013) and generally congruent with the host phylogeny (fig. Surprisingly, in the concatenated glycoprotein analysis, neither the HSV-1/Ch HV t MRCA (mean = 10.2 Ma, 95% highest posterior density [HPD] = 6.2–14.5 Ma) nor the HSV-2/Ch HV t MRCA (mean = 3.2 Ma, 95% HPD = 1.5–5.4) corresponded to the speciation between their human and chimpanzee hosts around 6 Ma (fig. Although the split between humans and chimpanzees is likely better reflected by a continuous process whereby alleles segregate over a period of time between 5 and 7 Ma (Kumar et al. We continued with an in-depth analysis of the g B data set, because it contains three additional host species for molecular clock calibration and validation.A t MRCA for HSV-2 and Ch HV at 6 Ma is rejected in favor of an unconstrained model ( substitution model, a 6 Ma t MRCA for HSV-1/Ch HV also provided a better fit than a 6 Ma t MRCA for HSV-2/Ch HV (table 2).