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J. Biol. Chem., Vol. 277, Issue 38, 35019-35024, September 20, 2002

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Stimulation of Enveloped Virus Infection by -Amyloid Fibrils^*

Woj M. Wojtowicz, Michael Farzan^§, John L. Joyal^¶, Kara Carter^¶, Gregory J. Babcock^§, David I. Israel^¶, Joseph Sodroski^§, and Tajib Mirzabekov^¶**

From ^¶ Praecis Pharmaceuticals, Inc., Waltham, Massachusetts 02451-4100 and the  Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, ^§ Department of Pathology, Division of AIDS, Harvard Medical School, and  Department of Immunology and Infectious Disease, Harvard School of Public Health, Boston, Massachusetts 02115

Alzheimer's disease is characterized by deposition of -amyloid peptide (A) into plaques in the brain, leading to neuronal toxicity and dementia. Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system can also cause a dementia, and amyloid deposition in the central nervous system is significantly higher in HIV-1-infected individuals compared with uninfected controls. Here we report that A fibrils stimulated, by 5-20-fold, infection of target cells expressing CD4 and an appropriate coreceptor by multiple HIV-1 isolates but did not permit infection of cells lacking these receptors. A enhanced infection at the stage of virus attachment or entry into the cell. A fibrils also stimulated infection by amphotrophic Moloney leukemia virus, herpes simplex virus, and viruses pseudotyped with the envelope glycoprotein of vesicular stomatitis virus. Other synthetic fibril-forming peptides similarly enhanced viral infection and may be useful in gene delivery applications utilizing retroviral vectors. These data suggest that A deposition may increase the vulnerability of the central nervous system to enveloped viral infection and that amyloidogenic peptides could be useful in enhancing gene transfer by enveloped viral vectors.

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