Phylogenetic Dependency Networks

Since its identification as the pathogenic cause of Acquired Immunodeficiency Syndrome (AIDS) in the early 1980s, Human Immunodeficiency Virus Type 1 (HIV) has emerged as a major global pandemic with an estimated 33 million infected individuals worldwide at the end of 2007 [1]. Specifically targeting the so-called “helper T cells” that help coordinate the adaptive immune response, HIV causes a progressive deterioration of immune function, leaving the infected individual susceptible to a range of opportunistic infections that eventually lead to AIDS and death. Although improvements in antiretroviral therapy have dramatically reduced HIV-related morbidity and mortality among those with access to treatment [2], the search for an effective HIV vaccine continues. One of the enduring challenges facing HIV vaccine design is the remarkable rate of viral mutation and adaptation that allows the virus to evade the adaptive immune response of the host. As the immune system learns to target the virus, novel viral mutations that allow the virus to escape the attack provide an advantage over virus particles (virions) lacking the mutations. These escape mutations thus come to dominate the viral population in the host via natural selection and the immune system is left learning to target what must appear to be a novel pathogen, causing the process to repeat. The result has been devastating to HIV vaccine design. The goal of a vaccine is to train the host immune system to recognize the virus before exposure, but when the virus is constantly changing, it is extremely difficult to predict what the attacking virus will look like or how