Lalor et al. showed NP+M2 to be protective in mice, but only when formulated with Vaxfectin and in a vaccine dose 6.6 times greater than that used in this study. However, in ferrets, in the absence of HA, this combination only resulted in delayed illness and death [20] . Price et al. showed that NP+M2 protects ferrets against H5N1 in a triple-prime rAd boost regimen similar to the one used here, but this difference in results may be due to the higher dose of DNA in the primary immunization (ten-fold greater than the present study) as well as a much lower viral challenge dose (56LD 50 [21] compared to 3610 5 6LD 50 in this study). However, due to differences in experimental parameters such as the immunization regimen and assay standardization, direct comparisons of NP and M2 immune responses between studies are difficult. In addition, different vaccinations may alter various antibody and cellular immune responses which may affect the protective immunity in various animal models. Nonetheless, the evidence suggests while NP or NP+M2 may provide moderate levels of protection against low dose viral challenges in ferrets, they are insufficient against high challenge doses of HPAI. On the other hand, HA elicits effective immune protection even against very high HPAI viral challenge doses. Although vaccines encoding NP or M2 alone are not required for protection against H5N1, they could potentially augment HA-encoded vaccines, particularly when there is a mismatch between the vaccine and viral HA proteins. Studies in mice have shown that M2 antibodies may help to reduce viral replication [8, 9, 52, 53] , while studies in ferrets have shown M2 to be associated with reductions in viral recovery [20, 54] . However, based on our H5N1 challenge results in ferrets, HA DNA immunization is superior to NP and M2 DNA immunization in terms of protection. These highly conserved viral genes may require combinatorial vaccination with HA to be suitable candidates for universal influenza vaccines. The Impact of Contact Tracing in Clustered Populations The tracing of potentially infectious contacts has become an important part of the control strategy for many infectious diseases, from early cases of novel infections to endemic sexually transmitted infections. Here, we make use of mathematical models to consider the case of partner notification for sexually transmitted infection, however these models are sufficiently simple to allow more general conclusions to be drawn. We show that, when contact network structure is considered in addition to contact tracing, standard “mass action” models are generally inadequate. To consider the impact of mutual contacts (specifically clustering) we develop an improvement to existing pairwise network models, which we use to demonstrate that ceteris paribus, clustering improves the efficacy of contact tracing for a large region of parameter space. This result is sometimes reversed, however, for the case of highly effective contact tracing. We also develop stochastic simulations for comparison, using simple re-wiring methods that allow the generation of appropriate comparator networks. In this way we contribute to the general theory of network-based interventions against infectious disease. Modelling has become a central tool in understanding the epidemiology of infectious disease, and designing control strategies. One control method, contact tracing, has been considered in a large number of disease contexts. These include the 2003 SARS pandemic [1, 2] , the 2001 UK FMD epidemic [3] [4] [5] [6] , contingency planning for deliberate release of smallpox [7, 8] , and control of sexually transmitted infections [9] [10] [11] . A particular benefit of tracing is that it allows targeting of control, at the cost of effort spent on finding the individuals at risk.