||Disease ecology, molecular evolution, microbial ecology/ evolution, host-pathogen interaction
||Microbiology, microbial genomics, virology, bacteriology, deep sequencing, bioinformatics, micro biome
||Systems biology of host-pathogen interactions; high-throughput screening; genomic and genetic analysis
||Bacterial proteomics and evolution of extracytoplasmic proteins with
a focus on the links between cytochromes, disulfide bond formation proteins
and related periplasmic proteases.
||Parasitology; host-pathogen interactions; protease function; drug screening/drug development; chemical-biology
||Origins and evolution of primate lentiviruses and simian Plasmodium parasites
||Influenza, antigenic drift, drug resistance
||Computational biology; evolutionary genomics; neuro-cell biology; yeast functional genomics; phylogenetics; single-cell biology
||Bacterial acquisition of drug resistance; Viral hypermutation; Antibody somatic hypermutation
My group works at the interface of epidemiology, ecology and statistics
to understand and control vector-borne and other infectious diseases.
We have focused our research the past five years on the control of urban
Chagas disease transmission in Peru. Our research team in Peru conducts
epidemiological studies on Chagas disease as well as entomological and
ecological research on disease vectors and reservoirs. In addition the
team uses quantitative and qualitative methods to elucidate the factors
that have led to urbanization of a disease traditionally associated
with rural poverty. My methodological interests include developing new
Bayesian methods to retrace the history of epidemics, and applying techniques
from control theory to optimize interventions against infectious diseases.
||Molecular evolution; population genetics; mathematical biology
||Protein transport, S-layer, cell surface, motility, biofilm, type IV pili, exosortase, evolution, archaea
||Studies in the Roos focus on protozoan parasites in the
phylum Apicomplexa, including Plasmodium (which causes malaria), and Toxoplasma
(a prominent source of congenital neurological birth defects, and an opportunistic
pathogen associated with AIDS and other immunosuppressed conditions).
The large number of parasite genome sequences now available provides one
of the most attractive systems for research in comparative genomics. As
deep-branching eukaryotes that are amenable to experimental manipulation
in the laboratory, these organisms also offer insights into the origins
and evolution of eukaryotic organelles, including novel targets for drug
||My laboratory studies experimental and natural microbial populations
with the general goal of connecting evolutionary and ecological processes
to causes and consequences at the molecular genetic level. Three broad
areas of research are active within my laboratory: 1) the evolution and
evolutionary significance of mutation rates and mutational phenomena;
2) the genetic and ecotypic structure of natural microbial populations;
and 3) evolutionary and ecological genomics. Research in the first area
utilizes experimental populations of Escherichia coli, experimental
and natural populations of Saccharomyces cerevisiae and its sympatric
sister species S. paradoxus, and computer simulation approaches.
Research in the second and third areas focuses on natural populations
of S. cerevisiae and S. paradoxus.
||The Weiser lab examines the pathogenesis of bacterial infection involving
the respiratory tract. Most studies have focused on two pathogens, Streptococcus
pneumoniae (the pneumococcus) and Haemophilus influenzae, which commonly
infect humans and are the major causes of bacterial diseases involving
the airway. A particular interest of the group is in defining the molecular
events involved in colonization of the mucosal surface-the first step
in the pathogenesis of disease. This approach has involved genomic analysis
of both bacterial and host genes whose expression is affected by colonization.
Genomic analysis using microarray technology has been carried out with
in vitro models using respiratory epitheial cells in culture and in vivo
using a mouse model of colonization.
|Jun (Jay) Zhu
||Vibrio cholerae, pathogenesis, epidemic cycles, virulence gene regulation, environmental survival, quorum sensing, biofilm formation