Compared to other poxviruses, such as vaccinia virus, mechanisms that account for APV pathogenesis is poorly understood. APVs have evolved a variety of elegant mechanisms to deliver their genes and accessory proteins into host cells. Like many other DNA viruses, APV probably devotes much of its genes to allow it to evade host immune responses. Such viral genes commonly encode proteins that are critical for the virus to undergo molecular transformation that leads to successful membrane fusion, penetration and intracellular transport. These includes genes that encodes proteins which act on early innate pathways such as pathways involving interferon [40] , pattern recognition receptors as Toll-like receptor (TLR) [41] , chemokines [42] and cytokines [43] , as well as pathways that act on subsequent adaptive responses [44, 45] . The infection of a cell by a virus is a complex process, during which the virus must overcome several host factors restriction points and the host immune response. Host protein interaction networks and biochemical pathways are in most cases altered by the viral proteins that free the virus from normal cellular controls and allow nucleotide metabolism in cells that have shut down DNA synthesis [46] . Hence, understanding viral protein functions and their interactions with host proteins is a prerequisite, not only to understand the infection biology of the virus-host system in question, but also for the rational development of target vaccines, based on specific antigens and possibly immunomodulatory factors, as well as antiviral compounds.