Detection of Kaposi´s sarcoma-associated human herpes virus type 8 DNA in biopsy smears of human

Because preclinical models have indicated potential synergy between antiangiogenic and cytotoxic therapies, Little and colleagues[29] at the NCI initiated a phase 2 clinical trial of liposomal doxorubicin (20 mg/m2 IV every 3 weeks) plus IL-12 (300 ng/kg subcutaneously twice weekly) for 18 weeks. There were 30 HHV-8 seropositive women; their IgG antibody titer against HHV-8 lytic antigens ranged from 1:100 to 1:6400 (). Available assays to detect HHV-8 antibodies make use of use latent or lytic viral proteins expressed in infected cells, whole virus particles, and recombinant proteins. Assuming that, as in cultured PEL cell lines, infected cells harbor ∼50 copies of episomal KSHV DNA per cell, we estimate that this level of viral DNA would correspond to infection of ∼1 cell in 1,000 in the implant (see ). In conclusion, HHV-8 sequences were rarely detected in CV secretions and PBMC samples from HIV-1—seropositive and seronegative women. All literature searches are restricted to studies in humans. This relatively high rate could be explained by the fact that our patients came from central and southern Italy, which have a higher-than-average rate of HHV-8 infection and where classical KS is endemic (1, 6, 23).

The patient seroconverted on lytic IFA 2 months after transplantation. Another latent viral protein, LANA2 has a possible role in developing resistance to the drug paclitaxel by binding to the polymerized microtubules, decreasing their stability and interfering with the binding of the drug to the tubules [33]. BCBL-1 DNA with known HHV-8 copy numbers, as determined by real-time PCR, was added to equivalent amounts of donor DNA, and the limit of detection in breast milk and saliva was determined by PCR amplification of the ORF26 gene. (B) Time course of infection. Overall, the seroprevalence of HHV-8 (according to either LANA or lyticantigen IFA) was 79.1% in Amerindians and 6.1% in non-Amerindians (SR, 12.63 [95% CI, 7.1–22.4]). If a man was HIV-1 infected, the OR that his wife had HIV-1 infection was 13.5 (95% CI, 7.0–26.2; P < .001). There were 117 households that had incomplete data and record completion at enrollment, thus information from 251 households was available for analysis.

A, B, C, D, and E are the 5 molecular HHV‐8 subtypes. The medium was changed after the cells were allowed to adhere overnight. In contrast, we detected HHV-8 DNA in prostate by solution-based PCR in five of the nine seropositive men, including the one HHV-8-seropositive, HIV-seronegative man. Ntuba, N. Fifteen of 78 (19%) chimpanzee samples, corresponding to 6 of 20 individuals (30%) (Table 2), were positive for CMV (Pan troglodyte CMV [PtroCMV]) (Table 3). Punctuate nuclear staining was considered positive for antibodies against LANA in untreated cells. For TIME cell inductions, the medium was subsequently replaced with fresh medium containing TPA or TPA with phosphonoacetic acid (PAA).

Results of IgG ELISA obtained with serum pools from Kaposi’s sarcoma patients and blood donors and latent+lytic+, latent−lytic+, and laten− lytic− serum pools are displayed as line plots (mean results of 3 pools for each patient group). The linkage analysis was based on the model generated by segregation analysis, which provided clear evidence for a recessive major gene conferring a strong predisposition to HHV-8 infection in children under the age of 10 years. For EBV protein analysis, a mouse monoclonal antibody against the latent membrane protein 1 at a dilution of 1:50 (DAKO Cytomation) was used. We used data from the remaining 1179 participants in the present study. Moreover, the adoption of HHV-8 screening is supported by evidence that prophylaxis with antiherpes drugs (such as foscarnet and ganciclovir) may protect against the development of KS [3]. A description of the 4 different types of KS is as follows and can be found in Table : classical, endemic, iatrogenic/transplant, and AIDS-associated/epidemic KS. Human herpesvirus type 8 (HHV-8), also called “Kaposi sarcoma–associated herpesvirus” (KSHV), is the etiologic agent of all forms of Kaposi sarcoma (KS) [1, 2], primary effusion lymphoma [3], and the HIV-associated plasmablastic cell variant of multicentric Castleman disease [4, 5].

All participants had blood drawn, and since the original study, the sera have been stored at –20 °C. Before the AIDS era, it was known as a rare tumor-like lesion of elderly men from the Mediterranean region and geographic pockets of equatorial Africa. In 11 patients (35%) KS was the first defining illness. This and further aspects of this process are discussed more fully in the text. We developed a consensus primer PCR method for amplification of a region of the herpesviral DNA-directed DNA polymerase. An enzyme-linked immunosorbent assay (ELISA) utilizing KSHV ORF65 recombinant protein was employed to analyze the antibody response to KSHV ORF65 in sera from 122 healthy physical examination people, 107 intravenous drug users, 135 non-intravenous drug users, 211 hepatitis B (HBV) patients infected via blood transmission, 107 kidney transplant recipients, and 72 female sex workers in Zhejiang Province in Southeast China.

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