DNA Electrochemical Biosensor for the Detection of Short DNA Sequences Related to the Human Immunodeficiency Virus

1996 ◽  
Vol 68 (15) ◽  
pp. 2629-2634 ◽  
Author(s):  
Joseph Wang ◽  
Xiaohua Cai ◽  
Gustavo Rivas ◽  
Haruki Shiraishi ◽  
Percio A. M. Farias ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dna Sequences ◽  
Electrochemical Biosensor ◽  
Dna Electrochemical Biosensor ◽  
Immunodeficiency Virus

Association of Primary Pleural Effusion Lymphoma of T-Cell Origin and Human Herpesvirus 8 in a Human Immunodeficiency Virus–Seronegative Man

2001 ◽  
Vol 125 (9) ◽  
pp. 1246-1248 ◽  
Author(s):  
Emmanuèle Lechapt-Zalcman ◽  
Dominique Challine ◽  
Marie-Hélène Delfau-Larue ◽  
Corinne Haioun ◽  
Dominique Desvaux ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Dna Sequences ◽  
Primary Effusion Lymphoma ◽  
Polymerase Chain Reaction Amplification ◽  
Human Herpesvirus ◽  
Body Cavity ◽  
Human Herpesvirus 8 ◽  
Herpesvirus 8 ◽  
Immunodeficiency Virus

Abstract We describe a case of an 87-year-old human immunodeficiency virus (HIV)–negative man who developed a primary pleural lymphoma without any identifiable tumor mass associated with human herpesvirus 8 (HHV-8) infection. A large T-cell lymphoma was diagnosed based on morphologic, immunophenotypic, and molecular findings. The HHV-8 DNA sequences were detected using specific polymerase chain reaction amplification in the lymphomatous effusion. Study of the patient's serum confirmed the HHV-8 infection. This case report displays the characteristic features of HHV-8–related body cavity-based lymphoma/primary effusion lymphoma previously reported in HIV-seronegative patients, except that it is of T-cell origin. Whether this case may be included or not within the primary effusion lymphoma entity, the association of a pleural T-cell non-Hodgkin lymphoma with HHV-8 infection raises the question of the possible occurrence of T cells as the target of malignant transformation associated with HHV-8 infection.

Ultrasensitive DNA electrochemical biosensor based on MnTBAP biomimetic catalyzed AGET ATRP signal amplification reaction

2020 ◽  
Vol 56 (49) ◽  
pp. 6636-6639
Author(s):  
Haobo Sun ◽  
Yunliang Qiu ◽  
Yajie Lu ◽  
Jinming Kong ◽  
Xueji Zhang
Keyword(s):  
Dna Sequences ◽  
Signal Amplification ◽  
Electrochemical Biosensor ◽  
Aget Atrp ◽  
Dna Electrochemical Biosensor ◽  
Amplification Reaction

In this paper, an ultrasensitive, highly selective and green electrochemical biosensor for quantifying DNA sequences (aM DNA) based on a MnTBAP catalyst for AGET ATRP reaction is proposed.

scholarly journals A quantitative analysis of the FIV and HIV genome using bioinformatics software

2022 ◽  
Author(s):  
Charlotte Siu ◽  
Xiao Wen Cheng ◽  
Meredith Horn
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dna Sequences ◽  
Illumina Miseq ◽  
Hiv Treatment ◽  
Behavioral Differences ◽  
Percent Identity ◽  
Immunodeficiency Virus ◽  
Bioinformatics Software ◽  
Human Kinds

Among viruses, the human immunodeficiency virus (HIV) presented the greatest challenge to human kinds. the HIV and FIV gag genome was sequenced using the Illumina MiSeq Benchtop next-generation sequencer.The DNA sequences obtained were then run through the LALIGN bioinformatics software to compute the E value, bit score, waterman eggert score, percent identity,which are four important indicators of how similar the sequences are. The E value was 3.1 x 10 ^-9, the percent identity was 54.4 percent and the bit score was 51.9. It was also sensed that base 1600 to 1990 in HIV and base 800 to 910 in FIV have a higher than normal similarity. This reflects that while the DNA sequences of the gag region of both the HIV and FIV genome are rather similar and it is unlikely that this similarity is due to random chance, there are a noticeable amount of differences. A better understanding of the level of similarity and differences in the gag region of the genome sequence would facilitate our understanding of structural and cellular behavioral differences between FIV and HIV, and in the long term it prevides new explanations to differences observed in previous studies, or even facilitate the development of an effective HIV treatment.

scholarly journals Human herpesvirus-8 DNA sequences in human immunodeficiency virus- negative angioimmunoblastic lymphadenopathy and benign lymphadenopathy with giant germinal center hyperplasia and increased vascularity

Blood ◽  
1996 ◽  
Vol 87 (9) ◽  
pp. 3903-3909 ◽  
Author(s):  
M Luppi ◽  
P Barozzi ◽  
A Maiorana ◽  
T Artusi ◽  
R Trovato ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dna Sequences ◽  
Germinal Center ◽  
Human Herpesvirus ◽  
Human Herpesvirus 8 ◽  
Angioimmunoblastic Lymphadenopathy ◽  
Herpesvirus 8 ◽  
Immunodeficiency Virus ◽  
Germinal Center Hyperplasia ◽  
Viral Sequences

Human herpesvirus-8 (HHV-8) DNA sequences have been reported to be strictly associated not only with various forms of Kaposi's sarcoma but also with an unusual subgroup of acquired immunodeficiency syndrome (AIDS)-related B-cell lymphomas. A possible relation of this putative virus also with multicentric Castleman's disease (MCD) has been recently suggested. We used polymerase chain reaction to look for the presence of HHV-8 sequences in a well characterized series of benign, atypical, and malignant lymphoid tissues from 45 Hodgkin's disease and 43 non-Hodgkin's lymphoma (NHL) cases, as well as from 5 MCD, 15 angioimmunoblastic lymphadenopathy (AILD), and 23 benign lymphadenopathy cases. Among the 38 AIDS-related lymphoid lesions, only 1 NHL and 1 persistent generalized lymphadenopathy (PGL) case were positive. Furthermore, among the 92 non-AIDS-related lymphoproliferative disorders, HHV-8 sequences were detected in 3 classic AILD cases and in 4 reactive lymphadenopathies. Six of 9 HHV-8 positive lymphoid lesions (1 NHL, 1 PGL, 1 AILD, and 3 reactive lymphadenopathy cases) were also positive for Epstein-Barr viral sequences. The four human immunodeficiency virus (HIV) negative lymphadenopathies positive for HHV-8 sequences showed an almost identical histology, characterized by a predominantly follicular lesion, with giant germinal center hyperplasia, and increased vascularity, resembling HIV-related lymphadenopathy and MCD. Our results, while providing the first evidence of the presence of HHV-8 sequences in AILD cases, suggest a possible association of these herpes viral sequences with a distinct histologic type of non-neoplastic lymphadenopathy, not associated with other common herpes infections.

scholarly journals Population Level Analysis of Human Immunodeficiency Virus Type 1 Hypermutation and Its Relationship with APOBEC3G and vif Genetic Variation

2006 ◽  
Vol 80 (18) ◽  
pp. 9259-9269 ◽  
Author(s):  
Craig Pace ◽  
Jean Keller ◽  
David Nolan ◽  
Ian James ◽  
Silvana Gaudieri ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Amino Acid ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Dna Sequences ◽  
Population Level ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
Level Analysis

ABSTRACT APOBEC3G and APOBEC3F restrict human immunodeficiency virus type 1 (HIV-1) replication in vitro through the induction of G→A hypermutation; however, the relevance of this host antiviral strategy to clinical HIV-1 is currently not known. Here, we describe a population level analysis of HIV-1 hypermutation in near-full-length clade B proviral DNA sequences (n = 127). G→A hypermutation conforming to expected APOBEC3G polynucleotide sequence preferences was inferred in 9.4% (n = 12) of the HIV-1 sequences, with a further 2.4% (n = 3) conforming to APOBEC3F, and was independently associated with reduced pretreatment viremia (reduction of 0.7 log10 copies/ml; P = 0.001). Defective vif was strongly associated with HIV-1 hypermutation, with additional evidence for a contribution of vif amino acid polymorphism at residues important for APOBEC3G-vif interactions. A concurrent analysis of APOBEC3G polymorphism revealed this gene to be highly conserved at the amino acid level, although an intronic allele (6,892 C) was marginally associated with HIV-1 hypermutation. These data indicate that APOBEC3G-induced HIV-1 hypermutation represents a potent host antiviral factor in vivo and that the APOBEC3G-vif interaction may represent a valuable therapeutic target.

scholarly journals Kaposi's Sarcoma Herpesvirus-Like DNA Sequences in the Saliva of Individuals Infected with Human Immunodeficiency Virus

1996 ◽  
Vol 23 (2) ◽  
pp. 406-407 ◽  
Author(s):  
I. Boldogh ◽  
P. Szaniszlo ◽  
W. A. Bresnahan ◽  
C. M. Flaitz ◽  
M. C. Nichols ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dna Sequences ◽  
Kaposi's Sarcoma ◽  
Kaposi’S Sarcoma ◽  
Immunodeficiency Virus

scholarly journals Photochemical inactivation of cell-associated human immunodeficiency virus in platelet concentrates

Blood ◽  
1993 ◽  
Vol 82 (1) ◽  
pp. 292-297 ◽  
Author(s):  
L Lin ◽  
H Londe ◽  
CV Hanson ◽  
G Wiesehahn ◽  
S Isaacs ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dna Adducts ◽  
Dna Sequences ◽  
Uv Light ◽  
Platelet Concentrates ◽  
Long Wavelength ◽  
Hla Dq ◽  
Immunodeficiency Virus ◽  
Cellular Dna ◽  
Hiv 1

Photochemical decontamination (PCD) of platelet concentrates, with adequate preservation of platelet function, has been shown using 8- methoxypsoralen (8-MOP) and long wavelength UV light (UVA). To further evaluate this technique, models for the inactivation of pathogenic human cell-associated viruses and integrated proviral sequences are required. We have assessed the ability of the PCD technique to inactivate cell-associated human immunodeficiency virus 1 (HIV-1) in platelet concentrates. We correlated PCD inhibition of HIV-1 infectivity with 8-MOP-DNA adduct formation in contaminating nucleated cells, and measured the inhibition of polymerase chain reaction (PCR)- mediated amplification of cellular DNA sequences as a surrogate for inactivation of integrated proviral nucleic acid sequences. After PCD treatment (8-MOP 300 micrograms/mL, UVA 17 mW/cm2) for 60 minutes, 0.5 x 10(6) plaque-forming units (PFU)/mL of cell-associated HIV-1 were inactivated and no virus was detectable by infectivity assay. After 60 minutes of PCD, 15 8-MOP-DNA adducts per 1,000 bp were formed, while in the absence of UVA, no adducts were formed. PCR-mediated amplification of a 242-bp cellular DNA sequence (HLA-DQ-alpha) was inhibited when greater than eight psoralen-DNA adducts per 1,000 bp were present. These studies indicate that high titers of cell-associated HIV-1 in platelet concentrates were inactivated by PCD, and the numbers of 8-MOP- DNA adducts in nucleated cells were sufficient to inhibit amplification of DNA segments that encode for as few as 80 amino acids. Based on the frequency of 8-MOP-DNA adducts, for the 10-kb HIV-1 genome, the probability of an integrated genome without at least one 8-MOP adduct after 60 minutes of PCD was 10(-33).

scholarly journals Influence of molecular characteristics on clinical outcome in human immunodeficiency virus-associated non-Hodgkin's lymphoma: identification of a subgroup with favorable clinical outcome

Blood ◽  
1995 ◽  
Vol 85 (7) ◽  
pp. 1727-1735 ◽  
Author(s):  
LD Kaplan ◽  
B Shiramizu ◽  
B Herndier ◽  
J Hahn ◽  
TC Meeker ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Clinical Outcome ◽  
Dna Sequences ◽  
Cd4 Count ◽  
Hodgkin's Lymphoma ◽  
Molecular Characteristics ◽  
Gene Rearrangements ◽  
Molecular Features ◽  
Immunodeficiency Virus ◽  
Ebv Dna

The relationship between clinical and molecular characteristics of 45 treated individuals with histologically-documented human immunodeficiency virus (HIV)-associated B-cell non-Hodgkin's lymphoma was examined to determine whether differences in molecular features of lymphoma were associated with differences in clinical outcome. Tissue specimens from these tumors were evaluated for evidence of Ig heavy-chain gene rearrangements using both Southern blot analysis and reverse transcriptase polymerase chain reaction (RT-PCR). Lymphomas were also evaluated for the presence of Epstein-Barr virus (EBV) DNA sequences and c-myc gene rearrangements. Twenty-five lymphomas were characterized as polyclonal and 20 as monoclonal. PCR amplification of expressed Ig variable (V)-region genes confirmed polyclonality in three extensively studied polyclonal lymphomas. The median CD4 count was significantly higher in the group with polyclonal disease (277/microL) than in the group with monoclonal disease (123/microL), P = .04. The complete response rate to therapy was significantly higher in patients with polyclonal disease (78%) and CD4 greater than 200/microL (81%) than in those with monoclonal disease (31%) and CD4 less than 200/microL (33%). CD4 count, clonality, and presence of EBV DNA sequences were the most important predictors of survival. Both Kaplan-Meier and Cox proportional hazards analyses showed a markedly prolonged survival in those patients with both CD4 > or = 200/microL and polyclonal disease. Histologically the polyclonal lymphomas were high grade in appearance and contained prominent macrophages. All seven surviving patients were in this group. Median survival for those individuals whose tumors contained EBV sequences was only 3.2 months (range, 0.4 to 19.5), whereas those with EBV-tumors survived for a median of 9.0 months (range, 0.7 to 65.2), P = .0007. These data indicate that molecular features of HIV-associated lymphomas may be important predictors of clinical outcome. These characteristics define a distinct subset of patients with polyclonal EBV-tumors and CD4 counts greater than 200/microL that appear to have a less aggressive clinical course.

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