In conclusion, Q7R is an extremely potent anti-PEDV substance which reduces PEDV growth, inhibits Inhibition of PEDV replication by Q7R is independent of its antioxidant activity. Vero cells were infected with PEDV (MOI = 10) in the presence of Q7R. Relative ROS generation in Vero cells exposed to Q7R of 1, 10, 100 and 500 μg/ml for the indicated times. NAC exposed to 10 μg/ml for the indicated times. Redox-sensitive fluorescence probe DCFH-DA (20 μM) was added to the phosphate buffered-saline (pH 7.2) after harvest of Vero cells infected with PEDV at 6 h. Representative images of ROS-induced DCF fluorescence of infected cell at 6 h post-infection are shown at a flow cytometry histogram. All data represent mean values of six independent measurements ± S.D. Ctr2, control treated with DCFH-DA; NAC 10, treated with N-acetyl L-cysteine of 10 μg/ml; PEDV, infected with PEDV for 6 h; Q7R 500, treated with Q7R of 500 μg/ml. the CPE and DNA fragment of infected cells regardless of its antioxidant activity and then didn't directly interact with PEDV particles and affect the initial stage of PEDV infection by obstructing with its viral mRNA production. It will be interesting to further investigate the antiviral activity of the Q7R in preventing various PEDV-mediated injuries in in vivo pathological situations.  Use of Recombinant Adenovirus Vectored Consensus IFN-α to Avert Severe Arenavirus Infection Several arenaviruses can cause viral hemorrhagic fever, a severe disease with case-fatality rates in hospitalized individuals ranging from 15-30%. Because of limited prophylaxis and treatment options, new medical countermeasures are needed for these viruses classified by the National Institutes of Allergy and Infectious Diseases (NIAID) as top priority biodefense Category A pathogens. Recombinant consensus interferon alpha (cIFN-α) is a licensed protein with broad clinical appeal. However, while cIFN-α has great therapeutic value, its utility for biodefense applications is hindered by its short in vivo half-life, mode and frequency of administration, and costly production. To address these limitations, we describe the use of DEF201, a replication-deficient adenovirus vector that drives the expression of cIFN-α, for pre- and post-exposure prophylaxis of acute arenaviral infection modeled in hamsters. Intranasal administration of DEF201 24 h prior to challenge with Pichindé virus (PICV) was highly effective at protecting animals from mortality and preventing viral replication and liver-associated disease. A significant protective effect was still observed with a single dosing of DEF201 given two weeks prior to PICV challenge. DEF201 was also efficacious when administered as a treatment 24 to 48 h post-virus exposure. The protective effect of DEF201 was largely attributed to the expression of cIFN-α, as dosing with a control empty vector adenovirus did not protect hamsters from lethal PICV challenge. Effective countermeasures that are highly stable, easily administered, and elicit long lasting protective immunity are much needed for arena and other viral infections. The DEF201 technology has the potential to address all of these issues and may serve as a broad-spectrum antiviral to enhance host defense against a number of viral pathogens. The Arenaviridae family of viruses has several members that can cause viral hemorrhagic fever, an acute, often-fatal, viral syndrome characterized by intense fever, malaise, and less frequently, bleeding and neurologic manifestations. Case fatality rates of hospitalized patients suffering from arenaviral hemorrhagic fever (AHF) range from 15-30% [1, 2, 3, 4] . Arenaviruses known to cause AHF include Junín, Machupo, Guanarito, Sabiá, and Chapare in the South American continent, and Lassa and Lujo in west and southern Africa, respectively. Primary transmission of the arenaviruses from respective rodent reservoir hosts to humans occurs via exposure to contaminated excreta [5] . Person-to-person transmission can occur through contact with blood or other body fluids during the care and management of infected individuals [1, 6] . Notably, these viruses are considered a threat to national security and are classified as highest priority pathogens by the NIAID [7] .