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Journal of Virology, May 2002, p. 5156-5166, Vol. 76, No. 10
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.10.5156-5166.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Caveolar Endocytosis of Simian Virus 40 Is Followed by Brefeldin A-Sensitive Transport to the Endoplasmic Reticulum, Where the Virus Disassembles

Leonard C. Norkin,1* Howard A. Anderson,2 Scott A. Wolfrom,1 and Ariella Oppenheim3

Department of Microbiology, University of Massachusetts, Amherst, Massachusetts 01003,1 Laboratory of Immunology, Division of Therapeutic Proteins, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892,2 Department of Hematology, Hebrew University—Hadassah Medical School, Jerusalem, Israel 911203

Received 23 July 2001/ Accepted 4 February 2002

Simian virus 40 (SV40) enters cells by atypical endocytosis mediated by caveolae that transports the virus to the endoplasmic reticulum (ER) instead of to the endosomal-lysosomal compartment, which is the usual destination for viruses and other cargo that enter by endocytosis. We show here that SV4O is transported to the ER via an intermediate compartment that contains ß-COP, which is best known as a component of the COPI coatamer complexes that are required for the retrograde retrieval pathway from the Golgi to the ER. Additionally, transport of SV40 to the ER, as well as infection, is sensitive to brefeldin A. This drug acts by specifically inhibiting the ARF1 GTPase, which is known to regulate assembly of COPI coat complexes on Golgi cisternae. Moreover, some ß-COP colocalizes with intracellular caveolin-1, which was previously shown to be present on a new organelle (termed the caveosome) that is an intermediate in the transport of SV40 to the ER (L. Pelkmans, J. Kartenbeck, and A. Helenius, Nat. Cell Biol. 3:473-483, 2001). We also show that the internal SV40 capsid proteins VP2 and VP3 become accessible to immunostaining starting at about 5 h. Most of that immunostaining overlays the ER, with some appearing outside of the ER. In contrast, immunostaining with anti-SV40 antisera remains confined to the ER.

* Corresponding author. Mailing address: Department of Microbiology, University of Massachusetts, 203 Morrill Science Center IVN, Amherst, MA 01003-5720. Phone: (413) 545-2009. Fax: (413) 545-1578. E-mail: lnorkin{at}microbio.umass.edu.

Journal of Virology, May 2002, p. 5156-5166, Vol. 76, No. 10
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.10.5156-5166.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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