Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have developed a quantitative real-time PCR (TaqMan) assay aimed at measuring the cellular human herpesvirus 8 (HHV-8) DNA load in various clinical samples. Standard curves were obtained by serial dilutions of a control plasmid containing both HHV-8 (ORF73 gene) and the cellular target (human albumin gene). The assay appeared to be very sensitive (100% detection rate for at least 10 copies per well) and specific and was easily reproducible (less than 3% intra-assay variability, 5% interassay variability). This method allowed us to quantify precisely the average HHV-8 copy number per cell in various persistently HHV-8-infected cell lines (BBG-1 cells, n = 200; BC-1 cells, n = 59; BCBL-1 cells, n = 70). A retrospective study was also conducted to assess the HHV-8 DNA load in 12 human immunodeficiency virus-infected patients with either Kaposi's sarcoma (KS; seven patients monitored over a 3-month period) or multicentric Castleman's disease (MCD; five patients). The HHV-8 DNA load ranged from 0 to 9,171 copies/10(6) cells in low-risk KS patients (T0, I0, S0 according to the classification of the AIDS Clinical Trials group). We also measured the viral loads in MCD patients either during symptomatic periods or during remission. The results are in agreement with previously published data, with high viral loads correlating with clinical symptoms (1.3 x 10(6) copies/10(6) cells) and low viral loads correlating with asymptomatic periods (less than 5,000 copies/10(6) cells).
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PMID:Quantitative analysis of human herpesvirus 8 viral load using a real-time PCR assay. 1074 15

The human herpes virus 8 (HHV8) or Kaposi's sarcoma-associated herpes virus (KSHV) is present in all Kaposi's sarcoma, and the detection of the virus using polymerase chain reaction or in situ hybridization is a highly sensitive and specific diagnostic test for the diagnosis of this neoplasm. HHV8 is furthermore invariably present in primary effusion lymphoma (PEL) and has also been detected in patients with acquired immunodeficiency syndrome (AIDS)-associated multicentric Castleman's disease (MCD) as well as, to a lesser extent, in non-AIDS MCD. In contrast to Kaposi's sarcoma, in which the tumor cells show primarily latent HHV8 infection, a higher rate of lytically infected cells can be observed in MCD. Epidemiological surveys indicate that the seroprevalence for HHV8 parallels the risk of developing Kaposi's sarcoma--5-10% in the general population of the Western world but ranging up to 20-70% in homosexual human immunodeficiency virus (HIV)-infected patients, and the infection precedes the development of Kaposis's sarcoma. Finally, HHV8 has been reported in a number of other diseases, especially in multiple myeloma. However, the highly controversial role of HHV8 in these lesions has to be clarified. Based on the data available today, HHV8 can be assigned as a new human virus, associated with tumors.
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PMID:Human herpes virus 8: a new virus discloses its face. 1078 77

Human herpesvirus 8 (HHV-8) is a gamma2-herpesvirus consistently identified in Kaposi's sarcoma (KS), primary effusion lymphoma, and multicentric Castleman's disease. Although HHV-8 infection appears to be necessary, it may not be sufficient for development of KS without the involvement of other cofactors. One potentially important cofactor is HIV-1. HIV-1-infected cells produce HIV-1-related proteins and cytokines, both of which have been shown to promote growth of KS cells in vitro. Though HIV-1 is not absolutely necessary for KS development, KS is the most frequent neoplasm in AIDS patients, and AIDS-KS is recognized as a particularly aggressive form of the disease. To determine whether HIV-1 could participate in the pathogenesis of KS by modulating HHV-8 replication (rather than by inducing immunodeficiency), HIV-1-infected T cells were cocultured with the HHV-8-infected cell line, BCBL-1. The results demonstrate soluble factors produced by or in response to HIV-1-infected T cells induced HHV-8 replication, as determined by production of lytic phase mRNA transcripts, viral proteins, and detection of progeny virions. By focusing on cytokines produced in the coculture system, several cytokines known to be important in growth and proliferation of KS cells in vitro, particularly Oncostatin M, hepatocyte growth factor/scatter factor, and interferon-gamma, were found to induce HHV-8 lytic replication when added individually to BCBL-1 cells. These results suggest specific cytokines can play an important role in the initiation and progression of KS through reactivation of HHV-8. Thus, HIV-1 may participate more directly than previously recognized in KS by promoting HHV-8 replication and, hence, increasing local HHV-8 viral load.
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PMID:Induction of HHV-8 lytic cycle replication by inflammatory cytokines produced by HIV-1-infected T cells. 1085 19

Kaposi's sarcoma-associated herpes virus (KSHV), also known as human herpes virus-8 (HHV-8), is a recently described gamma-herpes virus that has been etiologically linked to two different acquired immunodeficiency syndrome (AIDS)-related malignancies by strong epidemiologic and pathologic evidence. Infection been shown to precede and predict the development of Kapasi's sarcoma (KS) in human immunodeficiency virus (HIV)-infected patients, and viral DNA has been found in KS lesions of all types and stages. Furthermore, KSHV is a lymphotropic virus and is present in nearly all cases of primary effusion lymphoma, a rare malignancy disproportionately affecting HIV-infected individuals. KSHV is also thought to dramatically affect the incidence, type, and course of multicentric Castleman's disease, another lymphoproliferative disorder over-represented in people with AIDS. KSHV encodes many potentially oncogenic products, including several apparently pirated from the human genome. These include various chemokines, cell cycle regulatory proteins, and survival and proliferation factors. Knowledge is rapidly accumulating concerning the viral pathogenic mechanisms and host cofactors necessary for KSHV-mediated disease.
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PMID:Kaposi's sarcoma-associated herpes virus and acquired immunodeficiency syndrome-related malignancy. 1095 Mar 67

Current genotyping systems for Human herpesvirus 8 (HHV-8) are based on the highly variable gene encoding the K1 glycoprotein. Most strains collected worldwide cluster into two subtypes (I/A and II/C). Sequenced African strains have belonged to subtypes I/A and IV/B. Members of all three of these subtypes can have either the M or P allele at the right-hand side (RHS) of the genome. Strains obtained predominantly from aboriginal or relatively isolated populations have formed clades that branch at a distance from subtypes I/A and II/C, all being of the RHS P allele. The characterization is reported here of 16 Japanese, two Kuwaiti and five Argentine HHV-8 strains obtained from human immunodeficiency virus-infected and non-infected patients with Kaposi's sarcoma (KS), primary effusion lymphoma, multicentric Castleman's disease or renal transplants. K1 sequences of five Japanese, one Kuwaiti and two Argentine strains were identified as subtype I/A and eight Japanese, one Kuwaiti and three Argentine strains were subtype II/C. Three strains from elderly classic KS patients originally from Hokkaido, a northern Japanese island, were relatively closely related to strains of subtypes III/D and E. Consistent with previous observations, both the M and P alleles were identified at the RHS of subgroup I/A and II/C genomes; only the P allele was detected among the three Hokkaido strains. Distances among the Hokkaido strains were similar to the distance between subtypes I/A and II/C, suggesting that the Hokkaido strains may represent two distinct subtypes and that, as more strains are analysed, the currently recognized III/D subgroups will probably emerge as independent subtypes.
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PMID:Molecular characterization of strains of Human herpesvirus 8 from Japan, Argentina and Kuwait. 1117 90

Kaposi's sarcoma (KS) occurs in Europe and the Mediterranean countries (classic KS) and Africa (endemic KS), immunosuppressed patients (iatrogenic or post-transplant KS) and those with acquired immune deficiency syndrome (AIDS), especially among those who acquired human immunodeficiency virus sexually (AIDS-KS). KS-associated herpesvirus (KSHV or HHV-8) is unusual among herpesviruses in having a restricted geographical distribution. Like KS, which it induces in immunosuppressed or elderly people, the virus is prevalent in Africa, in Mediterranean countries, among Jews and Arabs and certain Amerindians. Distinct KSHV genotypes occur in different parts of the world, but have not been identified as having a differential pathogenesis. KSHV is aetiologically linked to three distinct neoplasms: (i) KS, (ii) primary effusion lymphoma, and (iii) plasmablastic multicentric Castleman's disease. The histogenesis, clonality and pathology of the tumours are described, together with the epidemiology and possible modes of transmission of the virus.
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PMID:Epidemiology and pathogenesis of Kaposi's sarcoma-associated herpesvirus. 1131 14

Previous serological or molecular studies by means of the polymerase chain reaction have failed to show an association between classic Hodgkin's disease (HD) and human herpesvirus 8 (HHV-8). Using immunohistochemistry, this study re-examines (with anti-LNA1 antibody) the possible association of HHV-8 with HD, particularly in human immunodeficiency virus (HIV) infected patients. HHV-8 was not detected in the Reed Sternberg cells of the cases examined (33 HIV negative and 17 HIV positive), thus confirming the lack of involvement of HHV-8 in HD. Interestingly, a case of HHV-8 positive multicentric Castleman's disease was associated with Epstein-Barr virus positive HD in the same lymph node, which was probably a fortuitous occurrence.
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PMID:Simultaneous occurrence of Epstein-Barr virus associated Hodgkin's disease and HHV-8 related multicentric Castleman's disease: a fortuitous event? 1157 29

Kaposi's sarcoma-associated herpesvirus (KSHV) is a gammaherpesvirus etiologically linked to primary effusion lymphoma (PEL), to a subset of multicentric Castleman's disease and to Kaposi's sarcoma (KS), the most common neoplasm associated with AIDS. Among KSHV-infected individuals, the risk of KS is much higher in those with human immunodeficiency-1 (HIV-1) infection than among those with other types of immunosuppression, suggesting a direct action of HIV-1 on KSHV replication. We show in our report that BC-3 cells, a chronically KSHV-infected B-cell line of a PEL origin, are permissive to HIV-1, offering a new tool for studying the interactions between these 2 viruses. In these cells, HIV-1 infection leads to reactivation of latent KSHV genomes, as demonstrated by the expression of KSHV lytic viral mRNAs. Although recombinant HIV-1 gp120 fails to enhance herpesvirus expression, transient transfection of the HIV-1 trans-activator Tat suffices to reactivate latent KSHV. By showing that HIV-1 infection directly reactivates latent KSHV, our results suggest a direct role of HIV-1 in the onset of KS in coinfected individuals.
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PMID:HIV-1 infection of primary effusion lymphoma cell line triggers Kaposi's sarcoma-associated herpesvirus (KSHV) reactivation. 1185 56

Human herpesvirus type 8 (HHV-8; Kaposi's sarcoma-associated herpesvirus) is frequently identified in tumor tissue obtained from human immunodeficiency virus (HIV)-infected patients with Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), or multicentric Castleman's disease. The association between HHV-8 and acquired immunodeficiency syndrome (AIDS)-associated solid lymphomas is less clear. Herein, I describe the case of a man with a CD4+ count of 30 cells/microL, and HIV viral load of 90,000 copies/mL, multi-drug resistant HIV infection, and limited stage KS. Biopsy of a progressive dorsal foot rash revealed a dense, deep, lymphoid infiltrate that extended into papillary dermis but without epidermotrophism. Microscopy showed a homogeneous population of anaplastic large B cells that stained positive for CD20 (L26), CD30, and lambda light chain. In situ hybridization of tumor tissue identified Epstein-Barr virus (EBV)-encoded RNA, and polymerase chain reaction amplification yielded HHV-8-specific gene products. Staging studies did not reveal lymphoma elsewhere, and the patient began chemotherapy, but died from septic complications. Autopsy was notable only for the presence of a consolidative pneumonia. Although extranodal presentations are common in the setting of immunodeficiency, reports of AIDS-associated lymphoma presenting as a nonepidermotrophic foot lesion are rare. Such a presentation serves to broaden the differential of skin and foot lesions in the setting of HIV infection. More importantly, this case provides further support that HHV-8 can be associated with solid lymphomas that have an anaplastic large cell morphology.
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PMID:HHV-8- and EBV-associated nonepidermotrophic large B-cell lymphoma presenting as a foot rash in a man with AIDS. 1201 67

Kaposi's sarcoma-associated herpesvirus (KSHV) is found in Kaposi's sarcoma (KS), multicentric Castleman's disease, and primary effusion lymphomas. To prospectively evaluate KSHV load as a biomarker for KS clinical status and prognosis in a cohort of men with AIDS-related KS, 2 quantitative polymerase chain reaction (PCR) assays were developed and tested to determine KSHV peripheral blood mononuclear cell (PBMC) virus loads. Most patients (13/15) with good-prognosis KS had < or =1.5 log KSHV copies/10(5) PBMC by both quantitative competitive (QC) and real-time Applied Biosystems (ABI) PCR. Both assays provided 94% specificity for identifying the 16 patients without KS progression during 20 months of follow-up. QC-PCR and ABI-PCR exhibited 100% and 80% levels of diagnostic sensitivity, respectively, for identifying the 5 patients whose KS progressed. Neither dichotomized human immunodeficiency virus loads nor dichotomized CD4 counts predicted either KS progression or KS clinical stage (all positive predictive values < 30%). These results are evidence that the quantity of circulating KSHV in KS patients is biologically meaningful and is measurable with sufficient accuracy to provide clinically useful information.
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PMID:Elevated virus loads of Kaposi's sarcoma-associated human herpesvirus 8 predict Kaposi's sarcoma disease progression, but elevated levels of human immunodeficiency virus type 1 do not. 1208 19


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