In the future, we plan to add an epidemiology-based ontology and develop a separate query tool. This is in part a substitute for a markup language. This tool will identify all models within the MREP (using the ontology information) that reference specific model parameters and connect those parameters to the values assigned by the study developers. This will provide a convenient mechanism for identifying and comparing assumptions across models within the MREP. Escape from Autologous Neutralizing Antibodies in Acute/Early Subtype C HIV-1 Infection Requires Multiple Pathways One aim for an HIV vaccine is to elicit neutralizing antibodies (Nab) that can limit replication of genetically diverse viruses and prevent establishment of a new infection. Thus, identifying the strengths and weaknesses of Nab during the early stages of natural infection could prove useful in achieving this goal. Here we demonstrate that viral escape readily occurred despite the development of high titer autologous Nab in two subjects with acute/early subtype C infection. To provide a detailed portrayal of the escape pathways, Nab resistant variants identified at multiple time points were used to create a series of envelope (Env) glycoprotein chimeras and mutants within the background of a corresponding newly transmitted Env. In one subject, Nab escape was driven predominantly by changes in the region of gp120 that extends from the beginning of the V3 domain to the end of the V5 domain (V3V5). However, Nab escape pathways in this subject oscillated and at times required cooperation between V1V2 and the gp41 ectodomain. In the second subject, escape was driven by changes in V1V2. This V1V2-dependent escape pathway was retained over time, and its utility was reflected in the virus's ability to escape from two distinct monoclonal antibodies (Mabs) derived from this same patient via introduction of a single potential N-linked glycosylation site in V2. Spatial representation of the sequence changes in gp120 suggested that selective pressure acted upon the same regions of Env in these two subjects, even though the Env domains that drove escape were different. Together the findings argue that a single mutational pathway is not sufficient to confer escape in early subtype C HIV-1 infection, and support a model in which multiple strategies, including potential glycan shifts, direct alteration of an epitope sequence, and cooperative Env domain conformational masking, are used to evade neutralization. The current AIDS pandemic is the result of genetically diverse viral subtypes and circulating recombinant forms (CRFs) of HIV-1 group M, of which subtypes A, C, and D account for a majority of infections worldwide [1, 2] . A key source of this genetic diversity is the viral env gene, which encodes the envelope (Env) glycoproteins, gp120 and gp41 (reviewed in [3] ). On the virion, monomers of non-covalently associated gp120 and gp41 subunits trimerize to form 'spikes', and together these facilitate entry into a target cell. Env has a complex conformation and undergoes substantial rearrangements in both subunits upon gp120 binding to CD4 and coreceptor [4, 5, 6] . Env also contains the principal targets for neutralizing antibodies (Nab) [7, 8] , and epitopes are targeted in both Env subunits [9] . However, many potential neutralization targets are transiently or not exposed on the trimeric form of virion-associated Env, including the V3 domain, CD4-induced epitopes, and the CD4 binding site [10, 11, 12] . Despite these limitations, most HIV-1 infected patients develop robust Nab responses against their autologous virus, particularly those infected with subtype C [13, 14, 15, 16, 17, 18, 19] .