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Journal of Virology, May 1999, p. 4019-4028, Vol. 73, No. 5
Dermatology Branch,
Received 23 October 1998/Accepted 1 February 1999
Human herpesvirus 6 (HHV-6) has been implicated as a cofactor in
the progressive loss of CD4+ T cells observed in AIDS
patients. Because dendritic cells (DC) play an important role in the
immunopathogenesis of human immunodeficiency virus (HIV) disease, we
studied the infection of DC by HHV-6 and coinfection of DC by HHV-6 and
HIV. Purified immature DC (derived from adherent peripheral blood
mononuclear cells in the presence of granulocyte-macrophage
colony-stimulating factor and interleukin-4) could be infected with
HHV-6, as determined by PCR analyses, intracellular monoclonal
antibody staining, and presence of virus in culture supernatants.
However, HHV-6-infected DC demonstrated neither cytopathic changes nor
functional defects. Interestingly, HHV-6 markedly suppressed HIV
replication and syncytium formation in coinfected DC cultures.
This HHV-6-mediated anti-HIV effect was DC specific, occurred when
HHV-6 was added either before or after HIV, and was not due to
decreased surface expression or function of CD4, CXCR4, or CCR5.
Conversely, HIV had no demonstrable effect on HHV-6 replication. These
findings suggest that HHV-6 may protect DC from HIV-induced
cytopathicity in AIDS patients. We also demonstrate that interactions
between HIV and herpesviruses are complex and that the observable
outcome of dual infection is dependent on the target cell type.
0022-538X/99/$04.00+0
Human Herpesvirus 6 Infects Dendritic Cells and Suppresses Human
Immunodeficiency Virus Type 1 Replication in Coinfected
Cultures
*
Corresponding author. Mailing address: Dermatology
Branch, National Cancer Institute, Building 10/Room 12N238, 10 Center Dr. MSC 1908, Bethesda, MD 20892-1908. Phone: (301) 402-4167. Fax: (301) 402-1439. E-mail:
Andrew_Blauvelt{at}nih.gov.
Journal of Virology, May 1999, p. 4019-4028, Vol. 73, No. 5
0022-538X/99/$04.00+0
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