Research interests of the Hu lab include pathogenic mechanisms of HIV-1 infection and approaches to prevent or control such infections. A host factor, TRIM5α, restricts HIV-1 replication in many Old World primates. New World primates, on the other hand, utilize TRIMCyp, which is a TRIM5-cyclophilin A fusion protein resulting from retrotransposition of CypA gene into intron 7 of TRIM5. Recently, this laboratory discovered that Old World monkeys, like their New World counterparts, also express TRIMCyp, but do so through a different retrotransposition event than New World monkeys. Such an example of convergent evolution suggests that selection by retroviruses may have played an important role in the genesis of diverse primate species. Better understanding of the mechanisms by which primates control retroviruses may yield insights for novel targets for antiviral therapy and help the development of appropriate animal models for HIV pathogenesis. This lab also studies approaches for the prevention and treatment of AIDS. One of the key targets for the development of AIDS vaccines is the highly glycosylated surface antigen of HIV. These glycans contribute to viral escape of host immune responses. We are interested in how changes in specific glycan moieties affect the function and antigenicity of HIV-1 envelope proteins and how such information may be used for the design of safe and effective HIV vaccines.