It's not a mouse, it's a hamster!

Abstract

A new hamster model for visceral leishmaniasis has been developed that might provide vital insight into the mechanisms of the disease in humans (P.C. Melby et al. J. Immunol. 166, 1912–1920, 2001). The clinical features of Leishmania donovani infection of Syrian hamsters closely resemble human infection; both species experience progressive increases in visceral parasite burden, cachexia, splenomegaly and hypergammaglobulinaemia. The study found that, although a strong Th1-like immune response is initiated in Leishmania-infected hamsters, macrophages in this species fail to produce the effector molecule nitric oxide. The failure of humans to control visceral leishmaniasis is also thought to be because of defective nitric oxide production. In mice, the most commonly used rodent model for leishmaniasis, infection is controlled by macrophage nitric oxide production. SHK