HIV infection in humans is characterized not only by the loss of antigen-specific CD4+ T helper cells, but by an additional wide range of immune dysfunctions that include the innate immune response. This dysfunction likely contributes to the susceptibility of AIDS patients to opportunistic infections. The group around Gregg Dean used the feline equivalent of HIV, infection with feline immunodeficiency virus (FIV) to study suppression of the innate immune response in an elegant model by infection such FIV-infected and SPG cats with Listeria monocytogenes, an opportunistic bacterial pathogen in cats and many other mammals including humans. The importance of their study lies first in the fact that they clearly demonstrate suppression of natural killer (NK) cell responses in FIV-infected cats. This suppression of an antigen-independent arm of the lymphocytic response makes these cats more susceptible to Listeria monocytogenes, resulting in delayed clearance only by antigen-specific T cells. In addition, they have established a mammalian model of HIV infection that will allow detailed model study of the impairment of the innate immune response in immunodeficiency retroviral infections. In previous work they have established that exogenous IL-15 rescues the NK cell responses and resistance to Listeria monocytogenes in FIV-infected cats, suggesting the IL-15 deficiency may underlie the impaired NK response. These result may be help to further dissect molecular mechanisms of the innate immune impairment in HIV patients and guide studies to correct them.