HIV-1 Tat enhances Kaposi sarcoma-associated herpesvirus (KSHV) infectivity.
The high frequency of Kaposi sarcoma (KS) in immunodeficiency states, particularly in patients with AIDS, has been attributed to increased replication of KS-associated herpesvirus (KSHV), a necessary cofactor for KS development. However, experimental KSHV infection of endothelial lineage cells that compose KS lesions has been difficult even in the absence of immune cells. Here we show that HIV-1 Tat protein can directly promote KSHV transmission. Full-length HIV-1 Tat and a 13-amino-acid peptide corresponding to the basic region of Tat specifically enhances the entry of KSHV into endothelial and other cells, presenting evidence for an active role of HIV-1 in the development of KSHV-associated diseases. These results can explain why AIDS-KS is more frequent and clinically more aggressive than KS in other immunodeficiency states.
Aoki
Yoshiyasu
Y
Experimental Transplantation and Immunology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-1907, USA. aokiy@mail.nih.gov
Tosato
Giovanna
G
D000595:Amino Acid Sequence; D002460:Cell Line; D015756:Genes, tat; D015497:HIV-1 / Q000235:genetics*; D006566:Herpesviridae Infections / Q000235:genetics*; D019288:Herpesvirus 8, Human / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D007668:Kidney; D008969:Molecular Sequence Data; D010446:Peptide Fragments; D012514:Sarcoma, Kaposi / Q000235:genetics*; D014779:Virus Replication
D010446:Peptide Fragments