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David R. Allred

photograph of Dr. David Allred

Department of Infectious Diseases and Pathology
PO Box 110880
2015 SW 16th AV
Gainesville, FL  33611-0880
352-294-4126 (office)
352-294-4136 or 294-4132 (labs)
FAX 352-392-9704


  • MS, Biology, Wayne State University, Detroit, 1978
  • PhD, Cell Biology, University of California, Riverside, 1982
  • Postdoctoral, University of Colorado, 1983-1986; University of Florida, 1986-1988

Honors and Awards

  • C.E. Cornelius Young Investigator Faculty Research Award, University of Florida, 1990 
  • Outstanding Faculty Achievement and Performance Award, University of Florida 1995
  • University of Florida Faculty Research Productivity Award, 1999
  • Editorial Board, Molecular and Biochemical Parasitology, 2007
  • Editorial Board, The Open Parasitology Journal, 2007
  • Editorial Board, Eukaryotic Cell, 2008

Research Interests

Mechanisms of persistence in babesial parasites

The focus of the Allred Laboratory is to decipher mechanisms used by various blood-borne parasites to interact with their vertebrate hosts in order to establish and maintain infections. Our current primary focus is on mechanisms used by babesial parasites to survive and establish highly persistent infections in hosts that are immune to disease. We have chosen to focus on Babesia bovis, a bovine parasite that causes a devastating acute disease but which goes on to establish a generally asymptomatic persistent infection lasting many years. Early observations made by others showed that B. bovis-infected red blood cells (IRBCs) carrying mature parasites sequester in the vasculature of the deep organs, and that the surface of IRBCs becomes altered antigenically during parasite development. We have attempted to establish the bases for these behaviors. In the process, we have confirmed the observations of antigenic modification and demonstrated these changes were due, at least in part, to the expression of the parasite-derived protein, VESA1, on the IRBC membrane surface. We have demonstrated VESA1 to undergo rapid antigenic variation during the course of infection in an individual animal. We have subsequently demonstrated a connection between antigenic variation and sequestration, and the sensitivity of cytoadhesion to the presence of antibodies recognizing VESA1. The molecular genetic basis for antigenic variation in B. bovis is currently being pursued. To date, this has resulted in the identification and characterization of the ves multigene family comprised of ves1a and ves1b genes encoding VESA1a and VESA1b, respectively. We have since determined that B. bovis utilizes a mechanism of “segmental gene conversion” to construct mosaic ves genes from bits of many ves genes. The variability in antigenicity and function that can be generated in this way is staggering, and helps to explain how this parasite successfully evades ongoing antibody responses targeting the IRBC. These results explain the logic behind the seemingly incongruous connection of adhesion with a structurally variant protein.

Ongoing projects

We are currently studying the molecular basis for regulation of ves gene expression, including cross-talk among ves loci around the genome. Moreover, we are collaborating on detection of the mechanisms enabling intracellular parasites to export proteins out into the infected host cell, as well as the enzymatic machinery required for gene conversion events in antigenic variation as potential targets for anti-parasite drug development.

Recent Publications

Additional publications here


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