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Journal of Virology, May 2008, p. 4751-4761, Vol. 82, No. 10
0022-538X/08/$08.00+0 doi:10.1128/JVI.02320-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Annegret Pelchen-Matthews,
Magdalena Deneka, and
Mark Marsh*
Cell Biology Unit, MRC Laboratory for Molecular Cell Biology and Department of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom
Received 26 October 2007/ Accepted 21 February 2008
During the assembly of human immunodeficiency virus type 1 (HIV-1) particles, the tetraspanin CD63 can be incorporated into the viral membrane. Indeed, cell surface tetraspanin microdomains that include CD63 have been proposed as sites for virus release. In addition, antibodies against CD63 can inhibit HIV infection of macrophages. In this cell type, HIV assembles into intracellularly sequestered plasma membrane domains that contain several other tetraspanins, including CD81, CD9, and CD53. CD63 is recruited to this domain following HIV infection. Together, these observations suggest that CD63 may have some function in the assembly of infectious virus particles and/or the infectivity of assembled virions. Here we have used RNA interference to knock down CD63 expression in monocyte-derived primary macrophages. We show that in the absence of CD63, HIV assembly is quantitatively comparable to that seen in CD63-expressing macrophages and that virus assembly occurs on compartments positive for CD81, CD9, and CD53. Moreover, the infectivity of macrophage-derived virus is unaffected by the loss of CD63. Together, our results indicate that at least in tissue culture, CD63 expression is not required for either the production or the infectivity of HIV-1.
Published ahead of print on 5 March 2008.
Present address: Laboratorio de Inmunovirología. Servicio de Enfermedades Infecciosas, Hospitales Universitarios Virgen del Rocio, Avd. Manuel Siurot s/n, 41013 Sevilla, Spain.
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