MicroRNA-145 regulates oncolytic herpes simplex virus-1 for selective killing of human non-small cell lung cancer

Additionally, subcutaneous models of HCC were established to evaluate the in vivo anti-tumor efficacy of G47Δ. Oncolytic herpes simplex virus (oHSV) may represent a promising therapy for cancer. Viruses are obligate, intracellular parasites. The purpose of this study was to investigate whether miRNA-145 regulated oncolytic herpes simplex virus-1 (HSV-1) can selectively kill NSCLC cells with reduced collateral damage to normal cells. Glioblastoma multiforme (GBM) brain tumors are extremely resistant to all currently approved therapies, including surgical resection, radiotherapy, and chemotherapy. That’s a big risk, but, it is being attempted, so we can treat HIV. In this weeklong Special Report, BU Today talks to Boston University researchers in several fields about why medical personnel confront the risks; the ethical and political dilemmas presented by the outbreak; how the virus kills; efforts to design effective therapies; and other aspects of this unprecedented outbreak of Ebola.

Electron microscopy was used to determine whether human breast cancer and bone marrow cells are permissive for JS1/34.5-/47- infection. Genital herpes simplex infections are generally limited to epithelia and neurons. We investigated the role of human interleukin-15 (IL-15) in this phenomenon and report here that HSV-1-mediated enhanced NK activity was abrogated by neutralizing antibodies for IL-15 but not for other cytokines (i.e., IL-2, IL-12, gamma interferon [IFN-γ], tumor necrosis factor alpha, or IFN-α). oerstedii, S. Cold sores are one example of a herpes virus. Back then, we had the Aeromonas and Pseudomonas infections to watch out for! This phenomenon has been shown in test tube laboratory experiments, but now researchers at the University of North Carolina School of Medicine have demonstrated that the same phenomenon occurs in a humanized mouse model, suggesting a promising new target for tackling the virus, which has killed nearly 30 million people worldwide since it first appeared three decades ago.

As expected, the expression of miRNA-145 in NSCLC cells was much lower than that in normal cells (see Figure 1). NV1066 is an oncolytic HSV-1 mutant that contains the marker gene for enhanced green fluorescent protein. New genomic analysis has found that oral herpes may have been around since before our split with chimpanzees happened about 6 million years ago. Terrifying. The polymer has a triple-action process that inhibits and kills the viral molecules. In fact, people have more bacteria cells in their bodies than human cells. In the present study, HEK-293 cells that stably and inducibly produce NGF were further stably transfected with herpes simplex virus-thymidine kinase gene as a suicide gene (hNGF-EcR-293-TK) in order to shut off the NGF secretion and kill the cells upon treatment with ganciclovir (GCV).

Viruses are responsible for many other serious, often deadly, diseases including acquired immunodeficiency syndrome (AIDS), Ebola hemorrhagic fever, infectious hepatitis and herpes. eGFP-positive or negative status was recorded for each specimen and compared to results obtained by conventional cytologic evaluation. The ribonucleotide reductase has cellular homologues that could provide the missing function in trans. Oncolytic replication-competent herpes simplex virus type-1 (HSV) mutants have the ability to replicate in and kill malignant cells. Effectively using one disease to fight another, the team created the T-VEC drug by modifying the original herpes virus to become a cancer-killing machine. Primary EOC cultures obtained from patients who varied in their responses to platinum/paclitaxel induction chemotherapy displayed similar sensitivity to HSV-R3616. Vaccines and antibiotics had apparently tamed the microbial world; indeed, molecular biologist were domesticating viruses and bacteria in the laboratory, using them as tools to study human genes.

That’s when a new, invasive species turned up on the scene, homo sapiens—our direct ancestors. We studied the kinetics of production of two monocyte-derived cytokines, interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF alpha), induced by Epstein-Barr virus (EBV) and herpes simplex virus type 1 (HSV-1) in peripheral blood mononuclear cell cultures and in fractionated cell populations. The chimeric virus infected a significantly greater number of cells than the γ134.5-deleted virus in both hypoxia and normoxia in all three xenolines at 10 MOI (). Peritoneal exudate and alveolar macrophages were found to be the most active effector cells, followed by blood neutrophils and monocytes. Life is often defined as a comparison between animate and inanimate objects. Cytotoxic colonies were derived from HSV-induced cell lines of three donors who, in previous experiments, had shown a prevalence of gamma delta+ or alpha beta+ effector cells. Moreover, this product is a new drug, as defined by section 201(p) of the Act, 21 U.S.C.

But the prospect of commercializing the technology has created huge financial incentives for biotechnology and pharmaceutical companies who have invested hundreds of millions of dollars in xenotransplantation. We developed a model using human dorsal root ganglion (DRG) xenografts in severe combined immunodeficient (SCID) mice to investigate VZV infection of differentiated neurons and satellite cells in vivo. During the past two years a little-publicized health battle has been waged out of the glare of the media.