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Human Herpesvirus 6: An Emerging Pathogen

Gabriella Campadelli-Fiume, Prisco Mirandola, and Laura Menotti
University of Bologna, Bologna, Italy


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Figure 1. Schematic representation of HHV-6 and HHV-7 genomes. The genomes are colinear. Homologies are 46.6% to 84.9%. Red blocks represent the herpesvirus core genes, numbered from I to VII. Yellow blocks represent ß-herpesvirus subfamily-specific genes (from U2 to U14). Green blocks indicate genes present only in the Roseolovirus genus, i.e., in HHV-6 and HHV-7. Only three ORFs (U22, U83 and U94) are present in HHV-6 and absent from HHV-7 (modified from [15]).


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Figure 2. Stages of the natural history of HHV-6 infection: I. Primary infection occurs in infants, may result in exanthem subitum (rash on the child's chest), and spreads to organs. Question marks denote sites where HHV-6 spread is likely but not proven. II. In healthy infants and adults, HHV-6 is present in a latent or persistent form in lymph nodes and is produced asymptomatically in salivary glands and shed in saliva, the most probable route of transmission. III. HHV-6 infection/reactivation occurs in persons undergoing therapeutic immunosuppression after organ transplant or in AIDS patients.


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Figure 3. Expression of human herpesvirus 6B (HHV-6B) and HHV-7 antigens in serial sections of Kaposi sarcoma specimens. Panels A-C: In Kaposi sarcoma environment, cells can be doubly infected by HHV-6B and HHV-7: (A) Staining with monoclonal antibody 5E1 to HHV-7-specific antigen pp85; (B) Staining with monoclonal antibody to HHV-6B-specific antigen p101; (C) Overlaid serial sections show colocalization of HHV-6B and HHV-7 (71).

 

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This page last reviewed July 1, 1999

Emerging Infectious Diseases Journal
National Center for Infectious Diseases
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