Please activate JavaScript!
Please install Adobe Flash Player, click here for download


titative traits. These cells also allow the re-assessment of haplotypes that are possibly associated with differences in gene expression, by the mea- surement of allele differential expression (Yan, 2002, Pastinen, 2004). Innate cellular defense. While certain host proteins are necessary for infection and for sustaining viral replication, others represent antiviral factors (Figure 1). Some cellular antiviral factors can be selectively suppressed by viral proteins, as shown by the interaction between human APOBEC3G, a cytidine deaminase, and the HIV-1 Vif protein (Sheehy, 2002, Mariani, 2003, Harris, 2003, Mangeat, 2003, Lecossier, 2003). An early interplay between incoming retroviral preintegration complexes and the nuclear proteins INI1 (integrase interactor 1) and PML (promyelocytic leukemia protein) creates an antiviral state that interferes with the immediate-early steps of HIV-1 infection (Turelli, 2001). ZAP, a zinc finger protein, inhibits production of retroviral RNA (Gao, 2002). Other antiretroviral factors target the capsid protein, imposing a post-entry block (Hatziioannou, 2003, Stremlau, 2004). Murr1, a gene product known previously for its involvement in copper regulation, acts as a genetic restriction factor that inhibits HIV-1 growth in unstimulated CD4+ T cells through its effects on the proteasome (Ganesh, 2003).This growing list of specific antiretroviral factors adds to the current knowledge on antiviral innate defense mechanisms that implicate interferon responses mediated by double stranded RNA- dependent protein kinase, the MX proteins, and RNase L-mediated degradation of viral RNAs (Goff, 2003). Two antiviral proteins, APOBEC3G and TRIM5␣, underscore the con- cept that the biological barrier preventing the entry of simian immuno- deficiency viruses into the human population as zoonotic infections is potentially quite fragile. A single APOBEC3G residue, aspartic 128 in human, lysine in African green monkeys controls the ability of the HIV-1 Vif protein to bind and inactivate this host defense factor (Schrofelbauer, 2004, Mangeat, 2004). HIV-1 efficiently enters the cells of Old World monkeys but encounters a block before reverse transcription by modulating the uncoating of a retroviral capsid (Stremlau, 2004). The cytoplasmic body component TRIM5␣ restricts HIV-1 infection in Old World monkeys while the simian immuno- 22