One sentence summary:Sustained SARS-CoV-2 transmission networks became established in Europe and the US several weeks later than previously estimated. Abstract:Accurate understanding of the global spread of emerging viruses is critically important for public health response and for anticipating and preventing future outbreaks. Here, we elucidate when, where and how the earliest sustained SARS-CoV-2 transmission networks became established in Europe and the United States (US). Our results refute prior findings erroneously linking cases in January 2020 with outbreaks that occurred weeks later. Instead, rapid interventions successfully prevented onward transmission of those early cases in Germany and Washington State. Other, later introductions of the virus from China to both Italy and Washington State founded the earliest sustained European and US transmission networks. Our analyses reveal an extended period of missed opportunity when intensive testing and contact tracing could have prevented SARS-CoV-2 from becoming established in the US and Europe.

We determined the complete mitochondrial genome sequences of two species of gall midges (Diptera: Cecidomyiidae), as well as partial sequence from a third cecidomyiid and a species from a related family, the Sciaridae. The sciarid sequence has a number of rearrangements of tRNA genes, relative to other dipterans, but is otherwise unremarkable. In contrast, the cecidomyiid genomes possess a number of very unusual features. First, the two complete sequences are very small compared with other dipteran mitochondrial genomes. The genome of Mayetiola destructor is only 14,759 bp while that of Rhopalomyia pomum is only 14,503 bp, comparable with genome sizes observed in some arachnids. Second, all three cecidomyiid species have very high A + T content—more than 83% for the coding region. Third, all three cecidomyiid species possess a number of rearrangements of tRNA genes, including variations within the family. Fourth, the most extraordinary feature of cecidomyiids examined in this study is an extreme truncation of all tRNA genes, including the loss of TΨC arms and apparent absence of the 3′ part of the aminoacyl stems.The truncated tRNA genes of cecidomyiids are very similar to those previously reported for spiders and appear to represent a second, independent origin of these structural features. It is likely that they are made functional through RNA editing, perhaps using the 5′ end of the aminoacyl stem as a template for the construction of the required 3′ end.

Viral phylogenies provide crucial information on the spread of infectious diseases, and many studies fit mathematical models to phylogenetic data to estimate epidemiological parameters such as the effective reproduction ratio (Re) over time. Such phylodynamic inferences often complement or even substitute for conventional surveillance data, particularly when sampling is poor or delayed. It remains generally unknown, however, how robust phylodynamic epidemiological inferences are, especially when there is uncertainty regarding pathogen prevalence and sampling intensity. Here we use recently developed mathematical techniques to fully characterize the information that can possibly be extracted from serially collected viral phylogenetic data, in the context of the commonly used birth-death-sampling model. We show that for any candidate epidemiological scenario, there exists a myriad of alternative, markedly different and yet plausible “congruent” scenarios that cannot be distinguished using phylogenetic data alone, no matter how large the dataset. In the absence of strong constraints or rate priors across the entire study period, neither maximum-likelihood fitting nor Bayesian inference can reliably reconstruct the true epidemiological dynamics from phylogenetic data alone; rather, estimators can only converge to the “congruence class” of the true dynamics. We propose concrete and feasible strategies for making more robust epidemiological inferences from viral phylogenetic data.