peritoneal macrophages in the mouse are activated after latent infection of the herpesvirus, and since macrophages play an important role in immunity, this provides the mouse with a stronger, active immune system at the time of bacterial exposure. It was found that the latent herpesvirus caused an increase in interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α), cytokines which both lead to activation of macrophages and resistance to bacterial infection. Influenza and Mycobacterium tuberculosis Variations within the human genome can be studied to determine susceptibility to infectious diseases. The study of variations within microbial genomes will also need to be evaluated to use genomics of infectious disease within public health. The ability to determine if a person has greater susceptibility to an infectious disease will be valuable to determine how to treat the disease if it is present or prevent the person from getting the disease. Several infectious diseases have shown a link between genetics and susceptibility in that families tend to have heritability traits of a disease. During the course of the past influenza pandemics and the current influenza epizootic there has been evidence of family clusters of disease. Kandun, et al. found that family clusters in Indonesia in 2005 resulted in mild, severe and fatal cases among family members. The findings from this study raise questions about genetic or other predispositions and how they affect a persons susceptibility to and severity of disease. Continued research will be needed to determine the epidemiology of H5N1 infection and whether genetic, behavioral, immunologic, and environmental factors contribute to case clustering. Host genetic factors play a major role in determining differential susceptibility to major infectious diseases of humans. Infectious diseases in humans appear highly polygenic with many loci implicated but only a minority of these convincingly replicated. Over the course of time, humans have been exposed to organisms like Mycobacterium tuberculosis. It is possible that the human genome has evolved in part from our exposure to M. tuberculosis. Animal model studies and whole genome screens can be used to identify potential regions on a gene that suggest evidence of tuberculosis susceptibility. In the case of M. tuberculosis, animal model studies were used to suggest evidence of a locus which was correlated with susceptibility, further studies were done to prove the link between the suggested locus and susceptibility. The genetic loci that have been identified as associated with susceptibility to tuberculosis are HLA-DR, INF-γ,