RESUMO
Inguinal lymph nodes from 24 human immunodeficiency virus (HIV) type 1-infected subjects without Kaposi sarcoma-associated herpesvirus (KSHV)-associated diseases were examined for KSHV infection. KSHV-infected cells were detected at a very low frequency in the lymph nodes of 7 subjects (median frequency, 2 infected cells/10(7) lymph node cells). Latent, but not lytic, KSHV gene expression was detected and KSHV-infected cells were located in B cell-rich areas of lymph node follicles. These findings provide evidence that, in the absence of KSHV-associated diseases, latent infection of lymph node cells provides a mechanism for the persistence of KSHV in KSHV/HIV-1-coinfected persons.
Assuntos
Linfócitos B/virologia , Infecções por HIV/complicações , Herpesvirus Humano 8/fisiologia , Linfonodos/citologia , Sarcoma de Kaposi/complicações , Latência Viral , Adulto , Reservatórios de Doenças , Feminino , HIV-1/fisiologia , Humanos , Linfonodos/virologia , Masculino , Pessoa de Meia-Idade , Sarcoma de Kaposi/virologiaRESUMO
The effects of hematopoietic stem cell (HSC) mobilization on Kaposi's sarcoma-associated herpesvirus (KSHV) were evaluated in three KSHV and human immunodeficiency virus type 1 co-infected subjects. KSHV DNA was not detected in purified CD34+ cell preparations from the period of filgrastim treatment. However, two of 3 subjects had transiently increased cell-free plasma KSHV DNA during filgrastim treatment. Peak plasma KSHV DNA (2,600 and 4,300 copies/mL) occurred on day 4 and declined to below the limit of detection by day 7. These findings suggest that, although CD34+ cell preparations do not have evidence of KSHV infection, HSC mobilization may stimulate KSHV replication in other cellular compartments that contribute to KSHV viremia.
