Evaluating a surveillance system: live-bird market surveillance for highly pathogenic avian influenza, a case study.

Introduction: Highly pathogenic avian influenza H5N1 was first reported in poultry in Nigeria in February 2006. The only human case that occurred was linked to contact with poultry in a live bird market (LBM). LBM surveillance was instituted to assess the degree of threat of human exposure to H5N1.

Wild-type rabies virus phosphoprotein is associated with viral sensitivity to type I interferon treatment.

Rabies virus (RABV) is a single-stranded, negative-sense RNA virus that causes a fatal neurological disease in humans and animals. Our previous studies have shown that lab-adapted, but not wild-type (wt), RABV enhances innate immune responses including type I interferon (IFN) and chemokines. To determine if treatment with type I IFN can inhibit RABV infection, mouse neuroblastoma and baby hamster kidney cells were treated with IFN-α before being infected with lab-adapted or wt RABV.

Rabies virus-induced apoptosis involves caspase-dependent and caspase-independent pathways.

Previously, it has been shown that the laboratory attenuated rabies virus CVS-B2C, but not the wild-type virus SHBRV, induces apoptosis in mice and the induction of apoptosis is mediated by viral glycoprotein. Induction of apoptosis by CVS-B2C limits the spread of the virus in the CNS. In the present study, we characterized the pathways by which CVS-B2C induces apoptosis.

Attenuated rabies virus activates, while pathogenic rabies virus evades, the host innate immune responses in the central nervous system.

Rabies virus (RV) induces encephalomyelitis in humans and animals. However, the pathogenic mechanism of rabies is not fully understood. To investigate the host responses to RV infection, we examined and compared the pathology, particularly the inflammatory responses, and the gene expression profiles in the brains of mice infected with wild-type (wt) virus silver-haired bat RV (SHBRV) or laboratory-adapted virus B2C, using a mouse genomic array (Affymetrix).

Homologous protection but lack of heterologous-protection by various species and types of Bartonella in specific pathogen-free cats.

Cat-scratch disease (CSD) is caused by Bartonella henselae, and possibly by B. clarridgeiae. In immuno-compromised persons, B.