Audrey O.T. Lau, MPH, PhD
Audrey O.T. Lau, MPH, PhD
My research focus is on host-pathogen interactions and can be divided into
two aspects: (i) the genomic basis of virulence and (ii) chemotherapeutics.
My goal is to create a knowledge database that will help the field to better
understand disease pathogenesis among apicomplexan parasites and,
eventually, to develop novel treatments for combating diseases such as
malaria and babesiosis. The protozoan my laboratory studies is Babesia sp.
which not only offers as a great model system for understanding
apicomplexans in general as all experiments can be performed in the natural
mammalian and tick (Rhipicephalus microplus) hosts, the asexual blood stages
can be routinely propagated in vitro and one species that we work on can be
genetically manipulated by transient and stable transfection, babesiosis is
rapidly emerging as a public health issue in human medicine here in the
United States. My laboratory uses “omic” approaches to answer some
fundamental questions of host cell invasion, egression, immune evasion and
any other phenotypic changes to adapt to the different environmental milieus
for survival. We have sequenced several genomes of virulent and attenuated
Babesia strain and validated novel blood stage microarray. Transcriptomic
analysis through next generation sequencing techonology also provided us a
glimpse into how this pathogen modulates its gene expression pattern as a
result of attenuation. Global genomic and transcriptomic analysis also
reveals targets within this protozoan that may be used as drug candidates.
Overall, the Babesia model system and available molecular tools will
contribute to the better understand this parasite and likely to other
apicomplexans as well.
Cilingir G, Lau AOT and Broschat SL.
ApicoAMP: The first computational model for identifying apicoplast-targeted
transmembrane proteins in apicomplexa. (accepted in Journal of
Pedroni MJ, Sondgeroth KS, Lopez GM, Echaide I and Lau AOT.
Comparative transcriptome analysis of geographical distinct virulent and
attenuated Babesia bovis reveals different attenuation profiles (accepted in
Sondgeroth KS, McElwain TF, Allen AJ, Chen AV and Lau AOT.
Loss of neurovirulence is associated with reduction of cerebral capillary
sequestration during acute Babesia bovis infection. Parasites
and Vectors 6:181 (2013).
Lau AOT, Pedroni MJ and Bhanot P. Target-specific
trisubstituted pyrrole inhibits Babesia erythrocytic growth.
Experimental Parasitology 133: 365-8 (2013).
Pedroni MJ, Luu TNK and Lau AOT. Babesia bovis:
Bipartite signal sequence directs glutamyl tRNA synthetase to the apicoplast.
Experimental Parasitology 131(2): 261-6 (2012).
Cilingir G, Broschat SL and Lau AOT. ApicoAP: Predicting
apicoplast-targeted proteins in multiple Apicomplexans using rule-based
classifiers optimized via a genetic algorithm. PLoS ONE 7(5):
Caballero MC, Pedroni MJ, Palmer GH, Davitt C, Suarez CE and Lau
AOT. Characterization of an acyl carrier protein and LytB within
Babesia bovis apicoplast. Molecular and Biochemical
Parasitology, 181: 125-133 (2012).
Mesplet M, Palmer GH, Pedroni MJ, Florin-Christensen M, Schnittger L and
Lau AOT. Genome-wide analysis of peptidase content and
virulence in a virulent and attenuated Babesia bovis strain pair.
Molecular and Biochemical Parasitology, 179: 111-113 (2011).
Lau AOT, Kalyanaraman A, Echaide I, Palmer GH, Bock R,
Pedroni MJ, Rameshkumar M, Ferreira MB, Fletcher TI and McElwain TF.
Virulence loss in apicomplexans is a reduction of population structure
complexity. BMC Genomics, 12:410 (2011).