2010 IHII/McLaughlin Colloquium

Abstract Form

Instructions:

  • Each trainee may submit only a single Abstract.
  • Information on position will be used for grouping presentations for judging.
  • Information on Training program will be used to select eligibility to give an oral presentation.
  • Entire abstract should be in one paragraph typed single-spaced not to exceed 300 words, with no tables, figures, or non-keyboard characters.
  • To complete your abstract (see example on next page), please replace all of the text in the example with your abstract using the same format (BOLD and CAPITALIZED title, presenter listed first, Arial 12 font, etc.)
  • After completing the table and inserting your Abstract, save this word file with your last name in the filename and email as an attachment to:
  • Abstracts must be received by 5 PM on March 30, 2010.

Form:

Participant / Last Name: / First Name:
Position / __ Graduate Student
__ Postdoctoral Fellow
__ Clinical Fellow
__ Medical Student
Training program (if applicable)
E-Mail
Mentor

Example Abstract:

EMERGENCE AND PATHOGENESIS OF VENEZUELAN EQUINE ENCEPHALITIS VIRUS SUBTYPE IE

A.P. Adams1, J.D. Pitts2, R.A. Bowen3, J.F. Aronson1, S.C. Weaver1

1Univ. of Texas Medical Branch, Galveston, TX, 2Texas A&M Univ., College Station, TX, 3Colorado State Univ., Fort Collins, CO

The etiologic agents during major Venezuelan equine encephalitis virus (VEEV) outbreaks are subtype IAB or IC, while subtype IE strains are considered enzootic, equine-avirulent, and incapable of exploiting horses as amplification hosts. However, recent Mexican epizootics were shown to originate from an equine-virulent subtype IE VEEV. Equine pathogenesis studies were performed to determine whether the virulence of subtype IE VEEVs correlates with the establishment of infection and/or modulation of the immune response. Groups of horses were inoculated subcutaneously with one of three VEEVs: 1) MX01-32, a virulent subtype IE strain genetically related to the 1996 Mexican epizootic, 2) 68U201, an enzootic subtype IE VEEV, and 3) 3908, a virulent subtype IC VEEV. Horses were monitored for illness and fever and were humanely euthanized at 48 hr or 14 days after infection or when the animals became paralyzed or anorexic. Interferon (IFN) bioassays showed that MX01-32 elicited a diminished and delayed IFN response when compared to 68U201 and 3908. To determine which amino acid residue changes may have facilitated the emergence of virulent subtype IE VEEV, the complete genome of MX01-32 was sequenced and compared to several enzootic and epizootic VEEVs. Virulent (MX01-32) and avirulent (68U201) subtype IE strains differed by 23 deduced amino acid substitutions; 6 of these were found in epizootic VEEVs, suggesting one or more of these substitutions may be responsible for the acquisition of equine virulence. Taken together, these findings suggest that the emergence of an equine-virulent strain of subtype IE VEEV may be related to its ability to interfere with the innate immune response during infection.