Bridging the health security divide: department of defense support for the global health security agenda.

In 2011, President Obama addressed the United Nations General Assembly and urged the global community to come together to prevent, detect, and fight every kind of biological danger, whether a pandemic, terrorist threat, or treatable disease. Over the past decade, the United States and key international partners have addressed these dangers through a variety of programs and strategies aimed at developing and enhancing countries' capacity to rapidly detect, assess, report, and respond to acute biological threats. Despite our collective efforts, however, an increasingly interconnected world presents heightened opportunities for human, animal, and zoonotic diseases to emerge and spread globally.

RIG-I enhanced interferon independent apoptosis upon Junin virus infection.

Junin virus (JUNV) is the etiological agent of Argentine hemorrhagic fever (AHF), a human disease with a high case-fatality rate. It is widely accepted that arenaviral infections, including JUNV infections, are generally non-cytopathic. In contrast, here we demonstrated apoptosis induction in human lung epithelial carcinoma (A549), human hepatocarcinoma and Vero cells upon infection with the attenuated Candid#1 strain of, JUNV as determined by phosphatidylserine (PS) translocation, Caspase 3 (CASP3) activation, Poly (ADP-ribose) polymerase (PARP) cleavage and/or chromosomal DNA fragmentation.

Potent inhibition of Junín virus infection by interferon in murine cells.

The new world arenavirus Junín virus (JUNV) is the causative agent of Argentine hemorrhagic fever, a lethal human infectious disease. Adult laboratory mice are generally resistant to peripheral infection by JUNV. The mechanism underlying the mouse resistance to JUNV infection is largely unknown.

Endothelial cell permeability and adherens junction disruption induced by junín virus infection.

Junín virus (JUNV) is endemic to the fertile Pampas of Argentina, maintained in nature by the rodent host Calomys musculinus, and the causative agent of Argentine hemorrhagic fever (AHF), which is characterized by vascular dysfunction and fluid distribution abnormalities. Clinical as well as experimental studies implicate involvement of the endothelium in the pathogenesis of AHF, although little is known of its role. JUNV has been shown to result in productive infection of endothelial cells (ECs) in vitro with no visible cytopathic effects.