Author
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KREUTZ, LUIZ - IOWA STATE UNIVERSITY |
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Submitted to: Journal of General Virology
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 3/1/1996 Publication Date: N/A Citation: N/A Interpretive Summary: Porcine reproductive and respiratory syndrome virus (PRRSV) is a new virus that recently emerged in the United States. The virus causes reproductive failure in pregnant sows and a flu-like syndrome in animals of all ages. Currently, the disease caused by this virus is a major concern for the pork industry. It has been difficult to isolate and characterize the virus, mainly because it does not replicate in most types of cells grown in laboratories. Our lab has been studying the interaction of this virus with cells in culture and the mechanism that it uses to enter and replicate in these cells. Thus, by recognizing the mechanism of virus infection of cells grown in the laboratory, we hope to improve our understanding of the mechanism by which the virus causes disease in the animal. In this report we identified some requirements of virus infection and means of blocking virus entry into the cells so that it can no longer replicate and destroy the cells. Technical Abstract: The role of the vacuolar type of proton ATPase during the initial stages of porcine reproductive and respiratory syndrome virus (PRRSV) infection was analyzed. Bafilomycin A1 (Baf A1), a macrolide antibiotic which selectively inhibits proton-ATPase, the enzyme responsible for endosome acidification, blocked PRRSV replication, as measured by fluorescent antibody staining and RNA hybridization of infected cells. The target of Baf A1 was during virus entry, and had no effect on virus attachment or after virus uncoating. Thus, the correlation between inhibition of H+-ATPase activity and lack of virus replication indicates the requirement of an acidic pathway during PRRSV entry. |
