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Featured researches published by Dexi Chen.


Mutation Research | 2009

Mitochondrial DNA base excision repair and mitochondrial DNA mutation in human hepatic HuH-7 cells exposed to stavudine.

Yasong Wu; Ning Li; Tong Zhang; Hao Wu; Chun Huang; Dexi Chen

The mitochondrial toxicity of nucleoside reverse transcriptase inhibitors (NRTIs) is due to the inhibition of mitochondrial DNA (mtDNA) polymerase gamma (Pol gamma), resulting in a blockade of mtDNA replication and subsequent disruption of cellular energetics. Because mtDNA Pol gamma is not only involved in mtDNA replication but also responsible for mtDNA repair, we hypothesize that mitochondrial oxidative stress leads to changes in the balance between mtDNA repair and mutation following stavudine (d4T) treatment. However, the mechanisms underlying how changes in mtDNA base excision repair (mtBER) lead to mtDNA mutation remain unclear. To test this hypothesis, total mitochondrial repair capability, different steps of mtBER, mtDNA mutations in D-loop, and oxidative stress were all assessed in cultured HuH-7 human hepatoblast cells treated with d4T for 2 weeks. Assessment by denaturing Southern blotting and quantitative PCR revealed that d4T significantly reduced in vivo repair of H(2)O(2) damaged mtDNA in HuH-7 cells. d4T reduced total in vitro mtBER and DNA Pol gamma capability, but did not affect mtDNA oxoguanine glycosylase and apurinic/apyrimidinic endonuclease activity in HuH-7 cells. In addition, d4T treatment is associated with a significant increase in the frequency of mtDNA mutations in HuH-7 cells. In conclusion, d4T treatment reduces mtBER and contributes mechanistically to NRTI-induced mtDNA mutation. These events may potentially be associated with some diseases linked to mtDNA mutation.


PLOS ONE | 2012

High CCR5 density on central memory CD4+ T cells in acute HIV-1 infection is mostly associated with rapid disease progression.

Xue Yang; Yanmei Jiao; Rui Wang; Yunxia Ji; Hongwei Zhang; Yonghong Zhang; Dexi Chen; Tong Zhang; Hao Wu

CD4+ central memory T cells play a critical role in the pathogenesis of simian immunodeficiency virus disease, and the CCR5 density on the surface of CD4 T cells is an important factor in human immunodeficiency virus (HIV)-1 disease progression. We hypothesized that quantifying central memory cells and CCR5 expression in the early stages of HIV-infection could provide useful prognostic information. We enrolled two different groups of acute HIV-infected subjects. One group progressed to CD4 T cell numbers below 250 cells/µl within 2 years (CD4 Low group), while the other group maintained CD4 cell counts above 450 cells/µl over 2 years (CD4 High group). We compared the CCR5 levels and percentage of CD4 subsets between the two groups during the 1st year of HIV infection. We found no differences between the two groups regarding the percentage of naïve, central memory and effector memory subsets of CD4 cells during the 1st year of HIV-1 infection. CCR5 levels on CD4+ CM subset was higher in the CD4 Low group compared with the CD4 High group during the 1st year of HIV-1 infection. High CCR5 levels on CD4 central memory cells in acute HIV infection are mostly associated with rapid disease progression. Our data suggest that low CCR5 expression on CD4 central memory cells protects CD4 cells from direct virus infection and favors the preservation of CD4+ T cell homeostasis.


Viral Immunology | 2012

Primary CXCR4 Co-receptor Use in Acute HIV Infection Leads to Rapid Disease Progression in the AE Subtype

Yanmei Jiao; Yingxue Song; Buxin Kou; Rui Wang; Zhiying Liu; Xiaojie Huang; Dexi Chen; Tong Zhang; Hao Wu

This is a comparative study of HIV co-receptor usage in the early stages of HIV infection between two distinct patient groups, one with a low CD4 count (group 1), and the other with a high CD4 count (group 2). Group 1 progressed to a CD4 count below 200 cells/μL within 2 y, while group 2 had a CD4 count above 500 cells/μL within 2 y. Viral RNA was extracted from the plasma of these patients, and the C2-V5 region of the HIV-1 env genes were cloned and sequenced. The co-receptor usage was predicated based on V3 loop amino acid sequences using Geno2pheno and PSSM programs. Our results indicate that in acute HIV infection of rapid progressors (low CD4 count; group 1), the primary co-receptor usage is CXCR4, while in the high CD4 count group (group 2), the co-receptor usage is predominantly CCR5. One-year follow-up data from these patients showed no obvious change in HIV co-receptor usage in either group. Sequence analysis of patients from both study groups showed prevalence of the AE subtype, and therefore we can speculate that the CXCR4 co-receptor may be the primary HIV-1 co-receptor used in the HIV-1 AE subtype, and may be responsible for rapid HIV-1 disease progression in the MSM cohort.


Virology Journal | 2010

Keratin 18 phosphorylation as a progression marker of chronic hepatitis B

Ying Shi; Shihui Sun; Yali Liu; Junfeng Li; Tong Zhang; Hao Wu; Xinyue Chen; Dexi Chen; Yusen Zhou

BackgroundThe intermediate filament proteins keratins 18 (K18) and 8 (K8) polymerize to form the cytoskeletal network in the mature hepatocytes. It has been shown that the phosphorylation of K18 at two serine residues, 33 and 52, correlates with the progression of hepatitis C, but little is known of chronic hepatitis B (CHB). In this study, we examined K18 phosphorylation in relation to CHB.ResultsSite-specific phosphorylation of K18 was determined in livers of twelve healthy donors, and non-cirrhosis (n = 40) and cirrhosis (n = 21) patients. On average, progressively higher level of Ser52 phosphorylation was observed in non-cirrhotic and cirrhotic livers, while elevated Ser33 phosphorylation was detected in both livers but no significant difference. Progressive increase of Ser33 and Ser52 phosphorylation correlated with the elevation of both histological lesions and enzymatic activities of alanine aminotransferase in non-cirrhotic livers. In the hepatocytes of an inactive HBV carrier, strong signals of Ser33 phosphorylation were co-localized with viral infection, while only basal level of Ser52 phosphorylation was detected in infected cells.ConclusionAssuming all obtained data, our data suggest that K18 phosphorylation is a progression marker for CHB.


DNA Repair | 2010

A new approach utilizing real-time qPCR to detect in vitro base excision repair.

Honghai Zhang; Yunjin Zang; Yu Sun; Ronghua Jin; Hao Wu; Meixia Wang; Ning Li; Dexi Chen

DNA lesions in mammalian cells may be induced by reactive oxygen species, alkylation, and ionizing radiation. This damage can then be repaired via the base excision repair (BER) pathway, which includes single strand break repair (SSBR). Thus, the BER (SSBR) pathway plays a critical role in maintaining genomic integrity, and may help us to better understand the mechanisms of aging, tumor formation, and degenerative diseases. AP site (apurinic/apyrimidinic site) or damaged base excision, nucleotide insertion and ligation are included in the BER (SSBR) pathway, which are facilitated by different enzymes at each step. Most previous in vitro BER studies have used modified radiolabeled (32)P oligonucleotide substrates. Which is a very conventional method for in vitro BER assay. However, the use of radioactive isotope material was limited in various laboratories which are unable to handle radioactive hazard. In this study, we developed a novel technique using real-time quantitative PCR (qPCR) to quantify BER activity in in vitro assays. Single strand breaks, DNA ligase activity, and glycosylase activity were detected to establish the feasibility and advantages of this qPCR technique for in vitro BER profiling.


PLOS ONE | 2013

Association of Preexisting Drug-Resistance Mutations and Treatment Failure in Hepatitis B Patients

Jie Ma; Yingchun Zhang; Xinyue Chen; Yi Jin; Dexi Chen; Yun Wu; Jing Cui; Haitao Wang; Jia Liu; Ning Li; Feng Gao

The role of preexisting minority drug-resistance mutations in treatment failure has not been fully understood in chronic hepatitis B patients. To understand mechanisms of drug resistance, we analyzed drug-resistance mutations in 46 treatment-failure patients and in 29 treatment-naïve patients and determined linkage patterns of the drug-resistance mutations in individual viral genomes using a highly sensitive parallel allele-specific sequencing (PASS) method. Lamivudine resistance (LAMr) mutations were predominant in treatment-failure patients, irrespective of the inclusion of LAM in the regimen. The primary LAMr mutations M204V and M204I were detected in 100% and 30% of the treatment-failure patients, respectively. Two secondary LAMr mutations (L180M and V173L) were also found in most treatment-failure patients (87% and 78%, respectively). The linkages containing these three mutations dominated the resistant viruses. Importantly, minority LAMr mutations present in <2% of the viral population were detected in 83% of the treatment-naïve patients. Moreover, the low-frequency same linked LAMr mutations (<0.15%) were detected in 24% of the treatment-naïve patients. Our results demonstrate that the selection of preexisting minority linked LAMr mutations may be an important mechanism for the rapid development of LAM resistance, caution the continuous use of LAM to treat drug-experienced and -naïve hepatitis B patients, and underline the importance of the detection of minority single and linked drug-resistance mutations before initiating antiviral therapy.


Epidemiology and Infection | 2012

Prevalence of GB virus type C viraemia in MSM with or without HIV-1 infection in Beijing, China.

Zhiying Liu; Lan Li; Zhiwei Chen; M. Xu; Tong Zhang; Yanmei Jiao; B. Sheng; Dexi Chen; Hao Wu

GB virus C (GBV-C) is frequently identified in patients co-infected with human immunodeficiency virus type 1 (HIV-1) due to the similar transmission routes. However, it remains unclear how these two viruses interact with each other and how one virus affects the replication of the other in the human body. In this study, we performed a case-control study to determine whether GBV-C viraemia could prevent the acquisition of HIV-1 infection, and a cohort study to determine the prevalence, genotypic characteristics and incidence of GBV-C infection in men who have sex with men (MSM) populations in Beijing, China. The prevalence of GBV-C infection in HIV-1-negative subjects was similar to that in HIV-1-positive subjects. Before HIV-1 acquisition, the prevalence of GBV-C was 17·7%, which increased to 27·2% at the acute stage and to 34% at the chronic stage. Genotype 3 was the major genotype of GBV-C in both groups. A significantly positive correlation was observed between the CD4+ T-cell counts and GBV-C viral loads at the acute stage of HIV infection. At the chronic stage (12 months later), this correlation was no longer significant, although it was still positive. Overall, this study demonstrated that pre-existing GBV-C viraemia could not prevent the acquisition of HIV-1 infection and transmission of HIV-1 significantly increased the prevalence of GBV-C viraemia.


Epidemiology and Infection | 2016

Detection of GB virus C genomic sequence in the cerebrospinal fluid of a HIV-infected patient in China: a case report and literature review.

Zhiying Liu; Yulin Zhang; F. Wei; M. Xu; Danlei Mou; Tong Zhang; Wei Li; Dexi Chen; Hao Wu

Hepatitis G virus or GB virus C (GBV-C) is a human virus of the Flaviviridae family that is structurally and epidemiologically closest to hepatitis C virus, but replicates primarily in lymphocytes. Co-infection with GBV-C has been reported to confer beneficial outcomes in some HIV-positive patients. Up to now, however, studies on GBV-C infection in the central nervous system (CNS) of HIV-infected patient have rarely been reported. Herein, we report on a 32-year-old HIV-1-infected patient with cerebral toxoplasmosis and fungal encephalitis. GBV-C viral loads were detected in CSF by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR), and the results showed that GBV-C viral load was 6·5 log copies/ml. We amplified and sequenced the E2 and 5-untranslated regions from the purified viral RNA from CSF by RT-PCR. Both sequences belong to genotype 3 and there were some minor nucleotide divergence among the E2 sequences from the CSF of the patient. These data suggest that GBV-C may be able to penetrate the blood-brain barrier and colonize the CNS of HIV-infected patients. However, the exact mechanisms and potential effect of the infected GBV-C in CNS on HIV-associated neuropathy needs to be further explored.


International Journal of Infectious Diseases | 2009

PP-146 Incidence and characterization of acute HIV-1 infection among high-risk self-identified men who have sex with men in Beijing, China

Xiaojie Huang; Haiying Li; Zhiying Liu; Caiping Guo; Yanqing Gao; Zaicun Li; Yan Fu; Tong Zhang; Dexi Chen; Xiao-Ning Xu; Hao Wu

A (mtTFA) and indirect role via up-regulation of the p53R2 expression2-4. Recently more than 6 kinds of P53 isoform have been reported and they played the different role in DNA repair pathways, cell-cycle checkpoints and cell apoptosis5. P53 and its different p53 isoforms play what kind of role in mitochondrial toxicity induced by NRTIs is unclear. In this study, we identified the role of wild type p53 and its isoforms (N40P53 and N133P53) in mitochondrial toxicity induced by AZT and oxidative stress. In this study we treated the A549 p53+/+, H1299 N40 P53+/+, H1299 N133P53+/+ and H1299 P53-/cell lines with 5 to 200 μM AZT for 12 hours for studying cell death and the expression of p53R2, p21 and bax via p53R2 (Bax, P21) pGL3-Luciferase reporter gene assay, real-time PCR and Western Blotting; treated cells with 30uμM AZT for 5 weeks, 10 weeks and 1μM H2O2 for 1 hour/week to study the mtDNA mutation, mtDNA deletion and mitochondrial toxicity. The cells were treated with p53R2 interference RNA to study the p53R2 how regulated the DNA Pol γ capability. The result showed that A549 p53+/+ cell death is more sensitive to high concentration of AZT. The increased cell death was detected from 120 uM of AZT and more that 80% cell were into apaotosis in 2000 μM AZT. But other three cell lines have strong tolerance to AZT toxicity. They are only less than 10% cell death in 2000 μM AZT. The results from report gene assay and real-time PCR assay suggested that wild type p53, N40 P53, N133P53 played different role in p53R2, P21 and Bax promoters. All of wild type and isoform P53 up-regulated the p53R2 expression, but isoform P53 played a domain negative regulation in Bax expression. The p21 expression was co-stimulated by wilde-type P53 and N40, N133P53. D-loop of mtDNA mutation and mtDNA quatitiy assay showed that A549 p53+/+ cell has lower mtDNA mutation rate and almost no mtDNA loss following 5 weeks AZT stress. N40 P53,N133P53 cells have lower mtDNA mutation too, but mtDNA loss is significant higher than that in A549 P53 +/+ cells. H1299 P53 null cells has higher mtDNA mutation rate and mtDNA loss than that in wild-type P53 and N40 P53, N133P53 isoform cells. Conclusion: Both wild type and N40 P53,N133P53 isoform p53 play protect role in AZT induced mitochondrial toxicity. The P53R2 would be involved in the centrol molecular pathway of p53 reduced mtDNA mutation and mtDNA loss induced by AZT


International Journal of Infectious Diseases | 2011

OL-065 Clinical application and study of a HIV-1 diagnosis assay with PCR

Lili Dai; Dexi Chen; Ying Shi; F.L. Wei; Tong Zhang

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Hao Wu

Capital Medical University

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Tong Zhang

Capital Medical University

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Xinyue Chen

Capital Medical University

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Ying Shi

Capital Medical University

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Yu Sun

Capital Medical University

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Zhiying Liu

Capital Medical University

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Ning Li

Capital Medical University

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Yanmei Jiao

Capital Medical University

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Honghai Zhang

Capital Medical University

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Lili Dai

Capital Medical University

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