Recommended Readings: Michael Strand, Ph.D.

Friday Lecture Series

Polydnaviruses: Viral Mutualists and Nature’s Genetic Engineers

Michael Strand, Ph.D., Regents Professor, department of entomology,

University of Georgia

February 21, 2014

3:45 p.m.-5:00 p.m. (Refreshments, 3:15 p.m., Abby Lounge)

Caspary Auditorium

Recommended Readings

Beck, M. H., & Strand, M. R. (2007). A novel polydnavirus protein inhibits the insect prophenoloxidase activation pathway. Proceedings of the National Academy of Sciences of the United States of America, 104(49), 19267-19272

Burke, G. R., Thomas, S. A., Eum, J. H., & Strand, M. R. (2013). Mutualistic polydnaviruses share essential replication gene functions with pathogenic ancestors. PLoS Pathogens, 9(5)

Strand, M. R., & Burke, G. R. (2012). Polydnaviruses as symbionts and gene delivery systems. PLoS Pathogens, 8(7), 5

Thoetkiattikul, H., Beck, M. H., & Strand, M. R. (2005). Inhibitor κB-like proteins from a polydnavirus inhibit NF-κB activation and suppress the insect immune response. Proceedings of the National Academy of Sciences of the United States of America, 102(32), 11426-11431

Webb, B. A., Strand, M. R., Dickey, S. E., Beck, M. H., Hilgarth, R. S., Barney, W. E., . . . Witherell, R. A. (2006). Polydnavirus genomes reflect their dual roles as mutualists and pathogens. Virology, 347(1), 160-174


Biologists Produce Malaria Vaccine From Algae

Biologists at the University of California, San Diego have succeeded in engineering algae to produce potential candidates for a vaccine that would prevent transmission of the parasite that causes malaria, an achievement that could pave the way for the development of an inexpensive way to protect billions of people from one of the world’s most prevalent and debilitating diseases. Initial proof-of-principle experiments suggest that such a vaccine could prevent malaria transmission.   Read the report of their research in PLoS ONE. 

How The Malaria Parasite “Hides” From the Immune System

A research team at the Walter and Eliza Hall Institute has identified one of the crucial molecules that instructs the parasite how to employ its invisibility cloak to hide from the immune system, and helps its offspring to remember how to ‘make’ the cloak.

Research published in the journal Cell Host & Microbe details the first molecule found to control the genetic expression of PfEMP1 (Plasmodium falciparum erythrocyte membrane protein 1), a protein that is known to be a major cause of disease during malaria infection.

PfEMP1 plays two important roles in malaria infection. It enables the parasite to stick to cells on the internal lining of blood vessels, which prevents the infected cells from being eliminated from the body. It is also responsible for helping the parasite to escape destruction by the immune system, by varying the genetic code of the PfEMP1 protein so that at least some of the parasites will evade detection. This variation lends the parasite the ‘cloak of invisibility’ which makes it difficult for the immune system to detect parasite-infected cells, and is part of the reason a vaccine has remained elusive.