Asset Liability Management How Matched is this Company?

S u m m a r y Insurance companies are coming under increasing attack: by voters for premium levels, by Congress for the tax burden and by citizens action groups for solvency. We must continue to broaden our methods of evaluating and managing insurance companies. Asset/Liability Management is emerging as a useful tool. This paper begins by reviewing Asset/Liability Management basics. The discussion is pragmatic rather than theoretical, presenting techniques in use. A new method for evaluating the duration of inflation sensitive assets is presented. Then, by examining the inflation adjusted duration, the increased risk to surplus in an inflationary environment is shown. Several sensitivity analyses are presented. Each changes the duration of a single variable and looks at the effect on surplus risk exposure. These variables are bond duration, real estate duration, and liability duration. The results are then combined into a two-way sensitivity matrix. Last, cash flow immunization is analyzed for mismatches. This paper shows liability duration is sensitive to rising inflation. Surplus is hit twice, once by dropping asset values and again by increasing liabilities. Real estate and inflation sensitive special investments can ameliorate the impact. However, real estate behaves more like a medium term bond than an inflation hedge. Reducing the duration mismatch and adding inflation hedging instruments is prudent when inflation is expected to rise. Cet article commence par réviser les bases de la gestion des actifs et des engagements. La discussion est pragmatique plutôt que théorique et présente des techniques utilisées

Inflammatory monocytes require type I interferon receptor signaling to activate NK cells via IL-18 during a mucosal viral infection

The requirement of type I interferon (IFN) for natural killer (NK) cell activation in response to viral infection is known, but the underlying mechanism remains unclear. Here, we demonstrate that type I IFN signaling in inflammatory monocytes, but not in dendritic cells (DCs) or NK cells, is essential for NK cell function in response to a mucosal herpes simplex virus type 2 (HSV-2) infection. Mice deficient in type I IFN signaling, Ifnar(-/-) and Irf9(-/-) mice, had significantly lower levels of inflammatory monocytes, were deficient in IL-18 production, and lacked NK cell-derived IFN-gamma. Depletion of inflammatory monocytes, but not DCs or other myeloid cells, resulted in lower levels of IL-18 and a complete abrogation of NK cell function in HSV-2 infection. Moreover, this resulted in higher susceptibility to HSV-2 infection. Although Il18(-/-) mice had normal levels of inflammatory monocytes, their NK cells were unresponsive to HSV-2 challenge. This study highlights the importance of type I IFN signaling in inflammatory monocytes and the induction of the early innate antiviral response