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Biology subjects

Wilms, H. T.

Publications and source records attributed to Wilms, H. T..

2 recordsLinked to original sources

Robust Inference of Phage Host Infection Dynamics from Sparse Single-Cell Transcriptomic Profiles in Pseudomonas aeruginosa

Phage therapy is providing a benefit to a limited number of people. To date those who have received phage therapy typically have done so via an IND expanded access mechanism, colloquially referred to as compassionate release, new clinical trials are underway, and the advent of phage therapy seems to be at hand. However, a recurring question remains, which phages to use for which bacteria. By understanding how a phage interacts with its bacterial host we will move closer to being able to provide an answer to this pressing question. By using bacterial single cell RNA sequencing (scRNAseq) during phage infection we can look at the most fundamental interaction between the phage and its host. We have observed phage gene expression consistent with well described expression profiles seen in bulk expression data. Phage genes in our scRNAseq data followed the early, mid, and late gene expression profile. Using a machine learning algorithm (Support Vector Machine) we were able to distinguish time of infection from phage genes. We also observed that phage infection is likely not random. When infected with two genetically distinct phages the likelihood of finding both inside a single cell was not consistent with Poisson distribution.

microbiology↗

Leukemic fusion genes repress viral gene expression and expel adenovirus from persistently infected human B lymphocytes but evidence of the virus lingers behind

Species C adenoviruses infect virtually all children in the first few years of life. These viruses can establish asymptomatic persistent infections in mucosal-associated lymphocytes and can infect lymphocytes in utero. Although adenovirus is a DNA tumor virus, it has not yet been shown to initiate cancer in humans. Epidemiological studies of B cell precursor acute lymphoblastic leukemia (ALL), point towards an infectious etiology. The ETV6/RUNX1 fusion protein results from a chromosomal translocation t(12; 21) believed to initiate ALL. This translocation can be detected in utero and has been identified in as much as 40% of clustered cases of leukemia, which are those most likely to have been initiated by an infectious agent. Infectious agents have not yet been detected in leukemic cells, causing speculation that the oncogenic agent has been lost in the transformed progeny through a "hit and run" mechanism. In the current study, we attempt to model the "run" of adenovirus in B-lymphocytes by forcing expression of leukemic fusion genes to determine if they create an environment that is refractory to adenovirus persistence. Here we show that the common leukemic fusion proteins, ETV6/RUNX1 or RUNX1/MTG8, reduce adenovirus persistence in a B-lymphocyte line but do not dampen the initial acute infection phase. Further, we show that ETV6/RUNX1 can bind to the viral genome and that some viral gene expression appears to be suppressed through the activities of HDACs in ETV6/RUNX1-expressing cells. Finally, we show that the expression of virally silenced cellular genes remains repressed even after the loss of the virus from infected cells. The results of the current study provide support for how adenovirus could be lost from translocation containing lymphocytes and provide evidence that adenovirus can leave a lasting imprint on cells previously infected in the form of an epigenetic echo.

cancer biology↗