scholarly journals Complement receptor 2 mediates enhancement of human immunodeficiency virus 1 infection in Epstein-Barr virus-carrying B cells.

1990 ◽  
Vol 171 (5) ◽  
pp. 1791-1796 ◽  
Author(s):  
M Tremblay ◽  
S Meloche ◽  
R P Sekaly ◽  
M A Wainberg
Keyword(s):  
B Cells ◽  
Viral Entry ◽  
Progeny Virus ◽  
Complement Receptor ◽  
Human Complement ◽  
Barr Virus ◽  
Complement Receptor 2 ◽  
Immunodeficiency Virus ◽  
Epstein Barr ◽  
Hiv 1

Although the CD4 glycoprotein is the primary receptor for HIV-1, recent reports have suggested that other molecules might be involved in the enhancement of HIV-1 infection. We investigated the possible role of the complement receptor 2 in enhancement of HIV-1 infection in CD4+ EBV-containing B cells by infecting such cells in the presence of sera from HIV sero-positive donors, with or without added human complement. A marked increase in production of viral p24 and infectious progeny virus was observed only when infection had been carried out in the presence of human complement. The addition of mAb to the human complement receptor 2 completely inhibited this enhancement. This mechanism was CD4 dependent, suggesting a cooperative effect between these two ligands in the potentiation of viral entry.

Expression profile of MUM1/IRF4, BCL-6, and CD138/syndecan-1 defines novel histogenetic subsets of human immunodeficiency virus–related lymphomas

Blood ◽  
2001 ◽  
Vol 97 (3) ◽  
pp. 744-751 ◽  
Author(s):  
Antonino Carbone ◽  
Annunziata Gloghini ◽  
Luigi M. Larocca ◽  
Daniela Capello ◽  
Francesco Pierconti ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
B Cells ◽  
B Cell ◽  
Primary Effusion Lymphoma ◽  
Large Fraction ◽  
Large Cell ◽  
Barr Virus ◽  
Immunoblastic Lymphoma ◽  
Immunodeficiency Virus ◽  
Epstein Barr

Abstract This study was aimed at defining the histogenesis of the pathologic spectrum of lymphoma arising in the context of human immunodeficiency virus (HIV) infection. Toward this aim, 87 AIDS-related non-Hodgkin lymphomas (AIDS-NHL) and 16 Hodgkin lymphomas arising in HIV+ patients (HIV-HL) were comparatively analyzed for the expression pattern of several B-cell histogenetic markers, including BCL-6 (expressed by centroblasts and centrocytes), MUM1/IRF4 (expressed by late centrocytes and post–germinal center [GC] B cells), and CD138/syn-1 (expressed by post-GC B cells). Expression of MUM1, BCL-6, and syn-1 segregated 3 major phenotypic patterns among AIDS-NHL and HIV-HL: (1) the BCL-6+/MUM1−/syn-1− pattern, selectively clustering with a large fraction of AIDS-Burkitt lymphoma (17 of 19) and of systemic AIDS–diffuse large cell lymphoma (12 of 16); (2) the BCL-6−/MUM1+/syn-1−pattern, associated with a fraction of AIDS-immunoblastic lymphoma (8 of 24); and (3) the BCL-6−/MUM1+/syn-1+ pattern, associated with systemic and primary central nervous system immunoblastic lymphoma (14 of 24) and with primary effusion lymphoma (10 of 10), plasmablastic lymphoma of the oral cavity (7 of 7), and HIV-HL (15 of 16). Analysis of nonneoplastic lymph nodes showed that the 3 phenotypic patterns detected in AIDS-NHL and HIV-HL correspond to distinct stages of physiologic B-cell development—centroblasts (BCL-6+/MUM1−/syn-1−), late GC/early post-GC B cells (BCL-6−/MUM1+/syn-1−), and post-GC B cells (BCL-6−/MUM1+/syn-1+). Expression of the Epstein-Barr virus-encoded latent membrane protein-1 clustered with the BCL-6−/MUM1+/syn-1+profile throughout the clinicopathologic spectrum of AIDS-NHL and HIV-HL. Overall, these results define novel histogenetic subsets of AIDS-NHL and HIV-HL and may provide novel tools for refining the diagnosis of these disorders.

Human immunodeficiency virus type 1 Tat protein modulates cell cycle and apoptosis in Epstein–Barr virus-immortalized B cells

2004 ◽  
Vol 295 (2) ◽  
pp. 539-548 ◽  
Author(s):  
Eva Colombrino ◽  
Elisabetta Rossi ◽  
Gianna Ballon ◽  
Liliana Terrin ◽  
Stefano Indraccolo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Human Immunodeficiency Virus ◽  
B Cells ◽  
Human Immunodeficiency Virus Type ◽  
Epstein Barr Virus ◽  
Tat Protein ◽  
Barr Virus ◽  
Immunodeficiency Virus ◽  
Epstein Barr

scholarly journals Quantitative analysis of the human immunodeficiency virus type 1 (HIV-1)-specific cytotoxic T lymphocyte (CTL) response at different stages of HIV-1 infection: differential CTL responses to HIV-1 and Epstein-Barr virus in late disease.

1993 ◽  
Vol 177 (2) ◽  
pp. 249-256 ◽  
Author(s):  
A Carmichael ◽  
X Jin ◽  
P Sissons ◽  
L Borysiewicz
Keyword(s):  
Structural Gene ◽  
Gene Products ◽  
Ctl Response ◽  
Barr Virus ◽  
Immunodeficiency Virus ◽  
Persistent Virus ◽  
Epstein Barr ◽  
Cd4 Lymphocyte ◽  
Hiv 1

Major histocompatibility complex (MHC)-restricted cytotoxic T lymphocytes (CTL) are part of the cellular immune response to human persistent virus infections. Measurements of the frequency and specificity of human immunodeficiency virus type 1 (HIV-1)-specific CTL and their variation with time may indicate their relative importance in modulating the progression of HIV-1 infection. We have used limiting dilution analysis (LDA) to derive quantitative estimates of the frequency of HIV-1-specific CTL precursors in a cross-sectional study of 23 patients at different clinical stages of HIV-1 infection and to compare these with the frequency of CTL precursors specific for another persistent virus (Epstein-Barr virus [EBV]) in the same patients. Peripheral blood mononuclear cells (PBMC) were stimulated in vitro with autologous HIV-1-infected lymphoblasts and assayed for cytotoxicity in 51Cr release assays against autologous and MHC-mismatched lymphoblastoid B cells infected with recombinant vaccinia viruses expressing the three HIV-1 structural gene products. The frequency of MHC-restricted precursors was high in asymptomatic HIV-1-infected patients (env-specific CTL precursors up to 73/10(6) PBMC; gag-specific CTL precursors up to 488/10(6) PBMC), although the relative frequency against the different structural gene products varied from patient to patient. The HIV-1-specific CTL precursor frequency was reduced in patients who had more severe (< 400/microliters) CD4+ lymphocyte depletion, while in the majority of such patients the frequency of CTL precursors against EBV was maintained at levels observed in healthy controls. Direct CTL activity in unstimulated PBMC was observed in three of nine patients but no correlation was found between the presence of an activated CTL response and the magnitude of the CTL response detected after stimulation in LDA. Thus, CTL precursors were detected against all three HIV-1 structural gene products in patients with CD4+ lymphocyte counts > 400/microliters, at frequencies that are high compared with those reported for other persistent viruses. A CTL response directed against multiple protein antigens of HIV-1 may protect the patient against epitope variation. The fact that the EBV-specific CTL precursor frequencies were maintained in advanced HIV-1 infection suggests that there may be selective impairment of the HIV-1-specific CTL response associated with disease progression.

scholarly journals Molecular Profile of Epstein-Barr Virus in Human Immunodeficiency Virus Type 1–Related Lymphadenopathies and Lymphomas

Blood ◽  
1997 ◽  
Vol 90 (1) ◽  
pp. 313-322 ◽  
Author(s):  
Lucia Ometto ◽  
Chiara Menin ◽  
Sara Masiero ◽  
Laura Bonaldi ◽  
Annarosa Del Mistro ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Epstein Barr Virus ◽  
Large Cell ◽  
Molecular Profile ◽  
Barr Virus ◽  
Immunodeficiency Virus ◽  
Epstein Barr ◽  
Hiv 1

Abstract Human immunodeficiency virus type 1 (HIV-1)–infected patients develop a spectrum of lymphoproliferative disorders ranging from nonneoplastic lymphadenopathies to B-cell lymphomas. Although evidence suggests that Epstein-Barr virus (EBV) might be involved, its molecular profile and expression pattern in HIV-1–related lymphoproliferations remain to be defined. Using polymerase chain reaction–based techniques, we studied EBV types and variants in 28 lymphadenopathy lesions and in 20 lymphomas (15 large cell and 5 Burkitt-like). EBV was detected in 89% of lymphadenopathies and in 80% of lymphomas; viral DNA content was significantly higher in the latter. EBNA2 and LMP1 gene analysis indicated that half of the EBV+ lymphadenopathies were coinfected with both EBV type 1 and 2 strains and/or multiple type 1 variants. Conversely, all but one lymphoma carried a single viral variant, consistently type 1 in large cell lymphomas, and type 2 in Burkitt-like tumors. Most lymphomas, but no lymphadenopathies, showed monoclonal Ig heavy-chain rearrangement. Analysis of 5 large cell lymphomas and 9 lymphadenopathies for EBV transcripts identified LMP1 mRNA in most samples, and the EBNA2 transcript in all tumors. These findings provide evidence of a heterogeneous EBV population in lymphadenopathy lesions, strengthen the notion that lymphomas arise from clonal expansion of EBV+ cells, and suggest different roles for EBV types 1 and 2 in HIV-1–related lymphoproliferations.

scholarly journals B cells engineered to express pathogen-specific antibodies using CRISPR/Cas9 protect against infection

2019 ◽  
Author(s):  
Howell F Moffett ◽  
Carson K Harms ◽  
Kristin S Fitzpatrick ◽  
Marti R Tooley ◽  
Jim Boonyaratankornkit ◽  
...  
Keyword(s):  
B Cells ◽  
Regulatory Elements ◽  
Barr Virus ◽  
Immunodeficiency Virus ◽  
Rsv Infection ◽  
Engineering Strategy ◽  
Epstein Barr ◽  
Syncytial Virus ◽  
Immunocompromised Hosts ◽  
Sterilizing Immunity

Effective vaccines inducing lifelong protection against many important infections such as respiratory syncytial virus (RSV), human immunodeficiency virus (HIV), influenza and Epstein-Barr virus (EBV) are not yet available despite decades of research. As an alternative to a protective vaccine we developed a genetic engineering strategy in which CRISPR/Cas9 was utilized to replace endogenously-encoded antibodies with antibodies protective against RSV, HIV, influenza or EBV in primary human or murine B cells. The engineered antibodies were expressed in up to 59% of primary B cells under the control of endogenous regulatory elements, which maintained normal antibody expression and secretion. Importantly, a single transfer of murine B cells engineered to express an antibody protective against RSV resulted in potent and durable protection against RSV infection in immunocompromised hosts. This approach offers the opportunity to achieve sterilizing immunity against pathogens for which traditional vaccination has failed to induce or maintain protective antibody responses.

scholarly journals CD27 and CD57 Expression Reveals Atypical Differentiation of Human Immunodeficiency Virus Type 1-Specific Memory CD8+ T Cells

2006 ◽  
Vol 14 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Aki Hoji ◽  
Nancy C. Connolly ◽  
William G. Buchanan ◽  
Charles R. Rinaldo
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Barr Virus ◽  
Specific Memory ◽  
Immunodeficiency Virus ◽  
Epstein Barr ◽  
Hiv 1

ABSTRACT The failure of human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T cells to control chronic HIV-1 infection could be due to the progressive loss of their capacities to undergo normal memory effector differentiation. We characterized and compared the expressions of CD27, CD28, CD57, and CD62L by Epstein-Barr virus (EBV)-, cytomegalovirus (CMV)-, and HIV-1-specific CD8+ T cells by six-color, eight-parameter flow cytometry. In contrast to the maturation of EBV- and CMV-specific memory CD8+ T cells, we found that HIV-1-specific CD8+ T cells did not display coordinated down-regulation of CD27 and up-regulation of CD57 and accumulated in an atypical CD27high CD57low subset. Moreover, the accumulation of CD27high CD57low HIV-1-specific CD8+ T cells was positively correlated with HIV-1 plasma viremia. The differentiation of HIV-1-specific CD8+ T cells to an effector subset is therefore impaired during chronic HIV-1 infection. This lack of normal CD8+ T-cell differentiation could contribute to the failure of cellular immune control of HIV-1 infection.

scholarly journals Integration of HIV in the Human Genome: Which Sites Are Preferential? A Genetic and Statistical Assessment

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Juliana Gonçalves ◽  
Elsa Moreira ◽  
Inês J. Sequeira ◽  
António S. Rodrigues ◽  
José Rueff ◽  
...  
Keyword(s):  
Human Genome ◽  
Nonparametric Tests ◽  
Fragile Sites ◽  
Jurkat Cells ◽  
Barr Virus ◽  
Immunodeficiency Virus ◽  
Chromosomal Fragile Sites ◽  
Epstein Barr ◽  
Hiv Integration ◽  
Hiv 1

Chromosomal fragile sites (FSs) are loci where gaps and breaks may occur and are preferential integration targets for some viruses, for example, Hepatitis B, Epstein-Barr virus, HPV16, HPV18, and MLV vectors. However, the integration of the human immunodeficiency virus (HIV) in Giemsa bands and in FSs is not yet completely clear. This study aimed to assess the integration preferences of HIV in FSs and in Giemsa bands using anin silicostudy. HIV integration positions from Jurkat cells were used and two nonparametric tests were applied to compare HIV integration in dark versus light bands and in FS versus non-FS (NFSs). The results show that light bands are preferential targets for integration of HIV-1 in Jurkat cells and also that it integrates with equal intensity in FSs and in NFSs. The data indicates that HIV displays different preferences for FSs compared to other viruses. The aim was to develop and apply an approach to predict the conditions and constraints of HIV insertion in the human genome which seems to adequately complement empirical data.

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