scholarly journals β‐Herpesvirus (Human Cytomegalovirus and Human Herpesvirus 6) Reactivation in At‐Risk Lung Transplant Recipients and in Human Immunodeficiency Virus–Infected Patients

2002 ◽  
Vol 186 (2) ◽  
pp. 173-180 ◽  
Author(s):  
Alexandra Michaelides ◽  
Eric M. Glare ◽  
Denis W. Spelman ◽  
Steven L. Wesselingh ◽  
Jennifer F. Hoy ◽  
...  
Keyword(s):  
At Risk ◽  
Human Immunodeficiency Virus ◽  
Human Cytomegalovirus ◽  
Lung Transplant ◽  
Human Herpesvirus ◽  
Transplant Recipients ◽  
Human Herpesvirus 6 ◽  
Immunodeficiency Virus ◽  
Herpesvirus 6 ◽  
Lung Transplant Recipients

scholarly journals Human Herpesvirus 6 Infects Dendritic Cells and Suppresses Human Immunodeficiency Virus Type 1 Replication in Coinfected Cultures

1999 ◽  
Vol 73 (5) ◽  
pp. 4019-4028 ◽  
Author(s):  
Hideo Asada ◽  
Vera Klaus-Kovtun ◽  
Hana Golding ◽  
Stephen I. Katz ◽  
Andrew Blauvelt
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dendritic Cells ◽  
Mononuclear Cells ◽  
Human Herpesvirus ◽  
Interleukin 4 ◽  
Human Herpesvirus 6 ◽  
Aids Patients ◽  
Peripheral Blood Mononuclear ◽  
Immunodeficiency Virus ◽  
Herpesvirus 6

ABSTRACT 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.

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