Many mammalian viruses have properties that can be commandeered for the treatment of cancer. These characteristics include preferential infection and replication in tumor cells, the initiation of tumor cell lysis, and the induction of innate and adaptive anti-tumor immunity. Furthermore, viruses can be genetically engineered to reduce pathogenicity and increase immunogenicity resulting in minimally toxic therapeutic agents. Talimogene laherparepvec (T-VEC; Imlygic™), is a genetically modified herpes simplex virus, type 1, and is the first oncolytic virus therapy to be approved for the treatment of advanced melanoma by the US FDA. T-VEC is attenuated by the deletion of the herpes neurovirulence viral genes and enhanced for immunogenicity by the deletion of the viral ICP47 gene. Immunogenicity is further supported by expression of the human granulocyte-macrophage colony-stimulating factor (GM-CSF) gene, which helps promote the priming of T cell responses. T-VEC demonstrated significant improvement in durable response rate, objective response rate, and progression-free survival in a randomized phase III clinical trial for patients with advanced melanoma. This review will discuss the optimal selection of patients for such treatment and describe how therapy is optimally delivered. We will also discuss future directions for oncolytic virus immunotherapy, which will likely include combination T-VEC clinical trials, expansion of T-VEC to other types of non-melanoma skin cancers, and renewed efforts at oncolytic virus drug development with other viruses.

A commonly seen phenomenon in the hospital and critical care setting is anaphylaxis. This acute systemic inflammatory reaction can lead to anaphylactic shock in severe cases and potentially be fatal. The role of platelets in anaphylactic reactions is not well established; however, platelets, among other mediators such as platelet-activating factor, have been shown to promote a prothrombotic state shortly after an acute hypersensitivity reaction. In addition, the aggregation of platelets promoted by platelet-activating factor and other mediators can also lead to thrombocytopenia. We present a case of a 57-year-old woman who developed severe anaphylaxis while receiving chemotherapy with paclitaxel suspended in Cremophor, a well-known allergen. She was profoundly thrombocytopenic following the reaction and was treated with therapeutic anticoagulation, with no thrombus formation.

Hyper-eosinophilic syndrome (HES) can be fatal if left untreated; and it is difficult to make a diagnosis early on due to the symptoms overlapping with many other conditions. For patients presenting with eosinophilia and end-organ damage, clinicians should have a high degree of suspicion for HES. Treatment with steroids can prevent further progression or can lead to complete resolution of the symptoms.