HIV Molecular Virology The principal focus in this laboratory is detailed analysis of a step in HIV replication called reverse transcription, during which process, HIV is able to convert its genetic material composed of RNA into a form compatible with human DNA
Laboratory Head: Dr David Harrich
Research Highlights Revealed that an HIV protein called Tat directly stimulates reverse transcriptase activity. Experiments suggested TAR forms a unique ribonucleoprotein complex, and additional critical RNA elements regulating reverse transcription have been identified. Showed, for the first time, that protein kinase C regulated an early event during HIV-1 but not through cellular receptors. Demonstrated that protein methylation is critical for HIV-1 infectivity. Cellular factors that are important for reverse transcription are being characterised.
HIV Virology researchers from left – Ann Apolloni and Haran Sivakumaran
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Over the last several years, research in this laboratory, and that of others world wide, has revealed complex interactions between viral proteins, unexpected roles for virus RNA, and requirements for cell factors to support virus growth. HIV is, in most respects, a typical retrovirus. The virus particle is 100 nm in diameter and surrounded by a cell-derived lipid membrane. Within the virus are the structural proteins including reverse transcriptase, and the genomic RNA. Reverse transcriptase is a viral enzyme and its role is to convert the viral
genomic RNA into DNA so that the genomic material is compatible with the cell. Studies by other laboratories, and confirmed by this one, have shown that virions contain very little if any DNA. Given that the virus machinery is designed to convert RNA to DNA using reverse transcriptase, it has been puzzling why reverse transcription is repressed in virions. A clear understanding of how HIV regulates reverse transcription, and how cellular factors impact this process have potential to identify novel antiviral strategies.