POSTDOCTORAL RESEARCH POSITION
NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES

 A postdoctoral position is available immediately for molecular studies on
rotaviruses, agents with segmented double-stranded RNA genomes that are the
primary cause of acute diarrhea in infants and young children. Potential
research areas include describing the mechanism of genome packaging and
replication, identifying determinants affecting viral growth and virulence,
and developing a reverse genetics system. Applicants should have a strong
background in virology, molecular biology, or biochemistry and hold a Ph.D.
or M.D. degree. Salary begins at $31,000 and increases depending on
experience. Please send curriculum vitae and the names of three references
to:

Dr. John T. Patton, Senior Scientist,
Laboratory of Infectious Diseases, NIAID, NIH,
Building 7, Room 117, MSC 0720,
Bethesda, MD 20892.
FAX: (301) 496-8312;
e-mail: jpatton@nih.niaid.gov.
 
NIH is an Equal Opportunity Employer.

 

POSTDOCTORAL  POSITION

HYPOVIRUS  MOLECULAR  BIOLOGY

LABORATORY  OF  DONALD  NUSS

          Position available immediately for a molecular virologist to study  various aspects of hypovirus-mediated attenuation of fungal virulence, described below.  Applicants should send curriculum vitae to Donald Nuss, Director, Center for Agricultural Biotechnology, University of Maryland Biotechnology Institute, Plant Sciences Building, Rm 5115C, College Park, MD  20742-4450.

             Cytoplasmically-transmissible RNA viruses of the genus Hypovirus  cause reduced virulence (hypovirulence) in the chestnut blight fungus Cryphonectria parasitica. The development of a full-length infectious cDNA clone of the prototypic hypovirus CHV1-EP713 (Science 257:800, 1992) has made it possible to engineer hypovirulent C. parasitica  strains with specific phenotypic traits and with improved biological control potential.  The potential for practical and fundamental applications of this group of viruses was further enhanced by the recent construction of an infectious cDNA clone of a second hypovirus, CHV1-Euro7 (J. Virol. 73:985, 1999).  By analogy with plant viruses, CHV1-EP713 and CHV1-Euro7 can be viewed as severe and mild strains, respectively.  By swapping domains of the two viruses, it has been possible to generate chimeric hypovirus-infected fungal isolates that exhibit a spectrum of defined colony and canker morphologies (J. Virol. 74:7562, 2000). These results demonstrated the feasibility of engineering hypoviruses to fine-tune the interaction between a pathogenic fungus and its host.

            Several lines of evidence indicate that hypovirus infection results in alterations of signal transduction pathways involved in normal fungal gene expression (PNAS 92:305, 1995; PNAS 93:7996, 1996; PNAS 93:14127, 1996; MPMI, 10:984, 1997; MPMI, 11:1130, 1998; PNAS 97:412, 2000).  The chimeric hypovirus is also being used to map modifiers of cellular signaling pathways with the aid of fungal strains stably transformed with novel promoter/reporter gene constructs. Correlations established between virus-mediated changes in cellular signaling and virus-mediated alterations in fungus-host pathogenic interactions are expected to provide insights into new strategies for the design of novel antimycotic therapeutic interventions.