Severe acute respiratory syndrome coronavirus infection in vaccinated ferrets.

Background: Development of vaccines to prevent severe acute respiratory syndrome (SARS) is limited by the lack of well-characterized animal models. Previous vaccine reports have noted robust neutralizing antibody and inflammatory responses in ferrets, resulting in enhanced hepatitis.

Methods: We evaluated the humoral immune response and pathological end points in ferrets challenged with the Urbani strain of SARS-associated coronavirus (SARS-CoV) after having received formalin-inactivated whole-virus vaccine or mock vaccine.

Evaluation of inactivation methods for severe acute respiratory syndrome coronavirus in noncellular blood products.

Background: Severe acute respiratory syndrome coronavirus (SARS-CoV) has been detected in the blood of infected individuals, which may have the potential to contaminate donated blood and plasma-derived products in the event of a future outbreak. Effective methods for inactivating the SARS-CoV in protein solutions are described in this report.

Study Design And Methods: Heat, ultraviolet (UV) irradiation, octanoic acid, and solvent/detergent (S/D) methods were tested individually for their ability to inactivate SARS-CoV in protein solutions appropriately mimicking blood-derived products.

New antiviral pathway that mediates hepatitis C virus replicon interferon sensitivity through ADAR1.

While many clinical hepatitis C virus (HCV) infections are resistant to alpha interferon (IFN-alpha) therapy, subgenomic in vitro self-replicating HCV RNAs (HCV replicons) are characterized by marked IFN-alpha sensitivity. IFN-alpha treatment of replicon-containing cells results in a rapid loss of viral RNA via translation inhibition through double-stranded RNA-activated protein kinase (PKR) and also through a new pathway involving RNA editing by an adenosine deaminase that acts on double-stranded RNA (ADAR1). More than 200 genes are induced by IFN-alpha, and yet only a few are attributed with an antiviral role.

Inactivation of the coronavirus that induces severe acute respiratory syndrome, SARS-CoV.

Severe acute respiratory syndrome (SARS) is a life-threatening disease caused by a novel coronavirus termed SARS-CoV. Due to the severity of this disease, the World Health Organization (WHO) recommends that manipulation of active viral cultures of SARS-CoV be performed in containment laboratories at biosafety level 3 (BSL3). The virus was inactivated by ultraviolet light (UV) at 254 nm, heat treatment of 65 degrees C or greater, alkaline (pH > 12) or acidic (pH < 3) conditions, formalin and glutaraldehyde treatments.

Cytokine and chemokine gene expression after primary and secondary respiratory syncytial virus infection in cotton rats.

The induction of pro- and anti-inflammatory cytokines and chemokines was studied in the lungs of cotton rats after primary or secondary infection with respiratory syncytial virus (RSV). Increases in messenger RNA (mRNA) levels of all genes analyzed were observed during the course of primary infection. In general, mRNA expression peaked between postinfection days 1 and 4 and returned to near-normal levels by day 10.