The Hajduk laboratory is mainly interested in the molecular and biochemical basis of parasitic and viral diseases. Several basic molecular pathways in African trypanosomes, the cause of human sleeping sickness, are under investigation. These include:

- RNA processing and trafficking

- Antigenic variation

- Mitochondrial biogenesis and developmental control of gene expression

A unique aspect of the biology of trypanosomes is RNA editing. RNA editing results in the post-transcriptional insertion or deletion of nucleotides into mRNA, at specific sites, creating functional open reading frames. The lab is investigating the mechanism of RNA editing and the assembly of proteins and RNAs required for editing. Recently, it has been suggested that the enzymes involved in RNA editing might be potential targets for drug development.

Innate immunity can play an important role in preventing or limiting the effects of a parasitic infection. This laboratory is particularly interested in the biochemical and molecular basis for the non-immune killing of African trypanosomes and Plasmodium falciparum malaria.

Trypanosoma brucei brucei is the causative agent of a bovine disease Nagana, and is killed by a toxic subspecies of human serum high density lipoproteins (HDL) while the human sleeping sickness parasites, T. b. gambiense and T.b.rhodesiense are not. In collaboration with Karen Day's group at Oxford University, this laboratory has begun to explore the role of innate factors in modulation of the severity of malaria in humans and the relationship of this phenomenon to innate resistance to trypanosomes. Recent studies have shown that the same subclass of human HDL that kills trypanosomes is also active against P. falciparum and may be important in limiting the severity of malaria in humans.

Finally, this laboratory has initiated collaborative studies to determine the structure of the HIV-1 initiation complex and the potential for targeting this complex for drug development. The life-cycle of HIV-1 requires the synthesis of a double-stranded DNA copy of the viral RNA genome. Replication is facilitated by the enzyme reverse transcriptase and requires the formation of a binary complex between the retroviral RNA genome and a cellular tRNALys3. The lab has begun to examine the assembly and structure of this initiation complex. Based on the structure of the initiation complex, compounds specifically recognizing the structure of the binary RNA structure will be tested for inhibition of reverse transcription.