Human herpesvirus 8 load and progression of AIDS-related Kaposi sarcoma lesions (original) (raw)
Global Dermatology, 2016
Introduction: Epidemic AIDS-associated Kaposi´s sarcoma (KS) is the most aggressive form of this neoplasm and is strongly associated with the reactivation of human herpesvirus type 8 (HHV-8), particularly among men who have sex with men. Objectives: To evaluate the presence of HHV-8 DNA in the biopsy smears of 31 patients with different clinical forms of AIDS-associated KS. Materials and methods: Epidemiologic, clinic, immunologic and virologic characteristics of 31 HIV infected patients with KS were included in this descriptively and retrospectively analysis from 2010 to 2013. KS was classified in four clinical forms including only cutaneous lesions, only mucosal involvement, mucocutaneous compromise and disseminated disease. The detection of DNA HHV-8 was performed by polymerase chain reaction (PCR) in all biopsy smears by tissue disruption to perform the DNA extraction, DNA purification by spectrophotometry analysis and DNA amplification with specific oligonucleated primers. Results: Thirty patients were male, the median of age was 34 years and the most frequent risk factor for HIV infection was unprotected sexual contact (90%). The median of time between HIV infections to neoplasm diagnosis was 6 years. In 11 patients (35%) KS was the first defining illness. The median of CD4 T cell count at the time of neoplasm diagnosis was 39 cell/μL. The majority of patients (84%) were not receiving highly active antiretroviral therapy (HAART). Clinical forms includes 12 patients with cutaneous KS, 8 patients with mucosal KS, 7 patients with disseminated disease and 4 patients with mucocutaneous involvement. PCR HHV-8 was positive in 24 (77%) biopsy smears. When we analyzed this group the median of age was 34 years, the median of time between HIV infection to neoplasm diagnosis was 9 years, the median the median of CD4 T cell count was 39 cell/μL and only 5 patients were receiving HAART at the time of diagnosis. No significant difference was observed between the HHV-8 positive and negative probable due to the small size of the cohort. Conclusion: Although HHV-8 DNA was detected in a high number of patients in these series, it is possible that other mechanisms may be involved in the pathogenesis of AIDS-associated KS.
PLoS ONE, 2009
Introduction: Kaposi sarcoma (KS) is the leading cause of cancer in Uganda and occurs in people with and without HIV. Human herpesvirus-8 (HHV-8) replication is important both in transmission of HHV-8 and progression to KS. We characterized the sites and frequency of HHV-8 detection in Ugandans with and without HIV and KS. Methods: Participants were enrolled into one of four groups on the basis of HIV and KS status (HIV negative/KS negative, HIV positive/KS negative, HIV negative/KS positive, and HIV positive/KS positive). Participants collected oral swabs daily and clinicians collected oral swabs, anogenital swabs, and plasma samples weekly over 4 weeks. HHV-8 DNA at each site was quantified by polymerase chain reaction (PCR).
Journal of Infectious Diseases, 1997
Polymerase chain reaction (PCR) was used to examine human herpesvirus 8 (HHV-8) DNA from Kaposi's sarcoma (KS) lesions, normal skin, and peripheral blood mononuclear cells (PBMC) from human immunodeficiency virus (HIV) -infected patients who did or did not have KS. Of 9 KS biopsies, 8 were positive for five HHV-8 open-reading frames and ranged from 1 viral genome per 2.5 -12.7 cells. Two putative replicative gene RNAs were detected by reverse transcription -PCR at low levels in 1 KS lesion. HHV-8 DNA was detected in 4 of 8 PBMC samples from patients with KS and in 2 of 18 PBMC samples from patients without KS. Sera were tested for reactivity with BCBL-1 cells (HHV-8 positive): High immunofluorescence antibody titers against HHV-8 lytic and latent antigens were detected in samples from KS-positive patients, and ú20 polypeptides from induced BCBL-1 cells were recognized. Sera from 6 of 18 patients without KS showed low levels of antibodies against HHV-8 lytic and latent antigens.
JNCI Journal of the National Cancer Institute, 1999
Background: The incidence of Kaposi's sarcoma (KS) is increased severalfold in individuals infected with human immunodeficiency virus-1 (HIV). Human herpesvirus 8 (HHV8) has also been implicated in KS. We investigated several factors that may determine the onset of KS, particularly HHV8 infection in individuals after becoming seropositive for HIV. Methods: We studied 366 individuals belonging to different HIVexposure categories (i.e., homosexual activity, intravenous drug use, and heterosexual contact) for whom a negative HIV serologic test and then a positive HIV serologic test were available within a 2-year period. HHV8 antibody testing was performed by use of an immunofluorescence assay on the first serum sample available after the first positive HIV test. Actuarial rates of progression of KS and of other acquired immunodeficiency syndrome (AIDS)-defining diseases were estimated by use of time-to-event statistical methods. All statistical tests were twosided. Results: Twenty-one of the 366 study participants developed AIDSrelated KS, and 83 developed AIDS without KS. One hundred forty (38.3%) participants had detectable anti-HHV8 antibodies. The actuarial progression rate to KS among persons co-infected with HIV/HHV8 was nearly 30% by 10 years after HIV seroconversion. Increasing HHV8 antibody titers
Journal of Medical Virology, 2010
The patterns of antibodies against latent and lytic antigens of human herpesvirus 8 (HHV-8) were assessed using immunofluorescence assays of samples from 155 persons seropositive for HHV-8 seen at public health centers and 24 patients with Kaposi's sarcoma (KS) from Mozambique. Of the 155 persons without KS, 48 (31%) had antibodies against latent antigens only, 29 (18.7%) had antibodies against lytic antigens only, and 78 (50.3%) had antibodies against both types of antigen. The HHV-8 antibody titer tended to increase with age until age 40, after which it began to decrease. High titers of antibodies against latent and lytic antigens of HHV-8 were detected mostly in persons co-infected with HIV, and these increased titers could have a predictive value. All patients with KS except four patients who were seronegative for HHV-8 had elevated titers of HHV-8 antibodies, predominantly against latent antigens. The data suggest the potential for an increase in the development of KS in this endemic area for HHV-8.