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.

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 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.

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 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 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

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.

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