Aim Successful colonization after long‐distance dispersal (LDD) depends on the availability of suitable habitats and competitive ability. In this study, we address the hypothesis that two widely distributed sister grass lineages (broad‐ and fine‐leaved Loliinae; hereafter BL and FL) that differ in their habitat requirements and competitive ability also differ in their biogeographic history, with particular reference to LDD. Location Global. Methods We reconstructed a comprehensive phylogeny of Loliinae, based on nuclear and plastid markers and estimated divergence times using fossil calibrations. Biogeographical events were estimated using analysis of range evolution, comparing different models. Numbers and rates of dispersals were estimated for BL and FL using stochastic mapping with best‐performing and baseline biogeographical models, and examined for correlation with distance, disjunction type, and phenotypic syndrome. Results The most recent common ancestor of Loliinae likely split at the Oligocene‐Miocene transition (22.50 ± 3.95 Ma), pre‐dating previous estimates, whereas the ancestors of the BL and FL Loliinae likely began to diversify in the Early Miocene (18.91 ± 4.15 and 17.50 ± 3.50 Ma, respectively). A model of range evolution integrating founder events and scaling of dispersal by shortest distance between areas performed best amongst a set of alternative models and recovered a mean of 83 dispersal events in Loliinae. Overall dispersal rates were significantly higher in BL than in FL. Per‐route dispersal rates showed a significant negative exponential relationship to shortest distance but were not affected by phenotypic syndrome or disjunction type. Main conclusions Loliinae originated in the Northern Hemisphere and evolved through recurrent LDDs. Higher competitive ability, potentially related to the broad‐leaved syndrome (i.e. tall strong‐rhizomatous plants, long‐living individuals, occupancy of more stable habitats), may explain higher observed dispersal rates in BL compared with FL Loliinae. However, the dominant factor impacting dispersal in both BL and FL Loliinae is the distance between suitable areas.

The Pooideae are a highly diverse C3 grass subfamily that includes some of the most economically important crops, nested within the highly speciose core-pooid clade. Here, we build and explore the phylogeny of the Pooideae within a temporal framework, assessing its patterns of diversification and its chromosomal evolutionary changes in the light of past environmental transformations. We sequenced five plastid DNA loci, two coding (ndhF, matk) and three non-coding (trnH-psbA, trnT-L and trnL-F), in 163 Poaceae taxa, including representatives for all subfamilies of the grasses and all but four ingroup Pooideae tribes. Parsimony and Bayesian phylogenetic analyses were conducted and divergence times were inferred in BEAST using a relaxed molecular clock. Diversification rates were assessed using the MEDUSA approach, and chromosome evolution was analyzed using the chromEvol software. Diversification of the Pooideae started in the Late-Eocene and was especially intense during the Oligocene-Miocene. The background diversification rate increased significantly at the time of the origin of the Poodae + Triticodae clade. This shift in diversification occurred in a context of falling temperatures that potentially increased ecological opportunities for grasses adapted to open areas around the world. The base haploid chromosome number n = 7 has remained stable throughout the phylogenetic history of the core pooids and we found no link between chromosome transitions and major diversification events in the Pooideae.

Herpes simplex virus 1 (HSV-1) and HSV-2 are large, double-stranded DNA viruses that cause lifelong persistent infections characterized by periods of quiescence and recurrent disease. How HSV evolves within an infected individual experiencing multiple episodes of recurrent disease over time is not known. We determined the genome sequences of viruses isolated from two subjects in the Herpevac Trial for Women who experienced primary HSV-2 genital disease and compared them with sequences of viruses isolated from the subsequent fifth or sixth episode of recurrent disease in the same individuals. Each of the HSV-2 genome sequences was initially obtained using next-generation sequencing and completed with Sanger sequencing. Polymorphisms over the entire genomes were mapped, and amino acid variants resulting from nonsynonymous changes were analyzed based on the secondary and tertiary structures of a previously crystallized protein. A phylogenetic reconstruction was used to assess relationships among the four HSV-2 samples, other North American sequences, and reference sequences. Little genetic drift was detected in viruses shed by the same subjects following repeated reactivation events, suggesting strong selective pressure on the viral genome to maintain sequence fidelity during reactivations from its latent state within an individual host. Our results also demonstrate that some primary HSV-2 isolates from North America more closely resemble the HG52 laboratory strain from Scotland than the low-passage-number clinical isolate SD90e from South Africa or laboratory strain 333. Thus, one of the sequences reported here would be a logical choice as a reference strain for inclusion in future studies of North American HSV-2 isolates. The extent to which the HSV-2 genome evolves during multiple episodes of reactivation from its latent state within an infected individual is not known. We used next-generation sequencing techniques to determine whole-genome sequences of four viral samples from two subjects in the Herpevac Trial. The sequence of each subject's well-documented primary isolate was compared with the sequence of the isolate from their fifth or sixth episode of recurrent disease. Only 19 genetic polymorphisms unique to the primary or recurrent isolate were identified, 10 in subject A and 9 in subject B. These observations indicate remarkable genetic conservation between primary and recurrent episodes of HSV-2 infection and imply that strong selection pressures exist to maintain the fidelity of the viral genome during repeated reactivations from its latent state. The genome conservation observed also has implications for the potential success of a therapeutic vaccine.

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