Master of Science
Microbiology and Immunology
Dr. Stephen Barr
Understanding how the immune system reacts to HIV infection and why normal antiviral defenses are insufficient to fight infection is a key step towards creating better therapies. Several interferon-induced proteins, such as the tripartite motif protein TRIM22, are capable of restricting HIV-1 replication; however single nucleotide polymorphisms (SNPs) can dramatically impact the actions of these proteins. While the trim22 gene contains numerous SNPs, no study has addressed how these may affect TRIM22 functions. Here we provide the first direct comparison of two TRIM22 unique isoforms. Through confocal microscopy we observed these isoforms exhibit different patterns of localization. In vitro studies revealed these isoforms exhibit different capacities in their ability to restrict release of infectious HIV-1 particles. Both isoforms also restricted transcription from the HIV-1 and cytomegalovirus promoters to varying degrees. Collectively, these data suggest that TRIM22 antiviral activity is variable between isoforms, and that SNPs may alter its biological characteristics.
Hattlmann, Clayton, "Restriction of HIV-1 replication by unique TRIM22 isoforms." (2012). Electronic Thesis and Dissertation Repository. Paper 392.