TRIM22 can activate the noncanonical NF-κB pathway by affecting IKKα.

Tripartite motif 22 (TRIM22) is involved in various cellular processes. It has been reported that TRIM22 can activate nuclear factor-κB (NF-κB) pathway, but the precise mechanism remains unclear. In this study, we explored the exact role of TRIM22 in activating the NF-κB pathway.

Associated changes in the transcription levels of IL-17A and tight junction-associated genes in the duodenal mucosa of rhesus macaques repeatedly exposed to simian/human immunodeficiency virus.

Background: Mucosal barrier dysfunction might play a key role in HIV/AIDS, yet the early effects of HIV-1 on intestinal mucosal barrier, especially tight junctions (TJ) have not been well addressed.

Aims: To investigate the effects of acute HIV-1 infection on the expression of intestinal IL-17A and TJ-associated genes using an NHP-AIDS model.

Methods: TaqMan probe real-time RT-PCR methods were established and claudin-1, claudin-3, occludin and zonula occluden-1 (ZO-1) mRNA levels in the duodenal biopsies of rhesus macaques collected before and after rectal exposures to SHIV-SF162P4 were examined and compared with that of IL-17A, IL-6, TGF-β, RORγt, T-bet, Foxp-3 and GATA-3.

DNA methyltransferases 1 and 3B are required for hepatitis C virus infection in cell culture.

DNA methyltransferases (DNMTs) are responsible for establishing and maintaining DNA methylation, which are dysregulated in hepatitis C virus (HCV)-associated hepatocellular carcinoma (HCC). In this report, using lentivirus-mediated shRNA interference technology, we identified DNMT1 and DNMT3B as host factors involved in HCV propagation. Our results demonstrated that down-regulation of DNMT1 or DNMT3B expression in Huh7.

Characterization of TRIM62 as a RING finger E3 ubiquitin ligase and its subcellular localization.

TRIM62, also named DEAR1, is a member of the TRIM/RBCC family, which includes proteins with conserved RING finger, B-box and coiled-coil domains. Several reports have identified a role for this family in cancer, retroviral infection and innate immunity. In this study, the E3 ubiquitin ligase activity and subcellular localization of TRIM62 were characterized.

(-)-Epigallocatechin-3-gallate inhibits the replication cycle of hepatitis C virus.

(-)-Epigallocatechin-3-gallate (EGCG) is the most abundant catechin in green tea. In this study, we found that hepatitis C virus (HCV) infection was significantly suppressed by EGCG in an HCV cell culture (HCVcc) system using a JFH1-GFP chimeric virus, with a 50 % effective concentration (EC(50)) of 17.9 μM.

Emerging trends of drug-resistant HIV-1 among drug-treated patients in former blood donors in Hubei, China: a three-year surveillance from 2004 to 2006.

This study aimed to evaluate emerging trends of drug resistance to nucleoside reverse transcriptase inhibitors (NRTIs) and nonnucleoside reverse transcriptase inhibitors (NNRTIs) among 290 former blood donor HIV-1 infected patients in Hubei, China, from 2004 to 2006, all of whom had received anti-HIV-1 therapy. The presence of NRTI- and NNRTI-associated mutations were established by sequencing; genotypic and predicted phenotypic drug resistance were evaluated using HIVdb Program version 5.0.

Rhesus monkey TRIM5α has distinct HIV-1 restriction activity among different mammalian cell lines.

Rhesus monkey TRIM5α (TRIM5α(rh)), a member of the tripartite motif (TRIM) family, was identified as the main restriction factor responsible for resistance of old world monkey cells to HIV-1 infection. However, the precise mechanism of HIV-1 infection inhibition by TRIM5α remains elusive and appears to be related to some cellular cofactors. Here we reported that TRIM5α(rh) can significantly reduce the infection efficiency of VSV-G pseudotyped HIV-1/MA-YFP virus in human epithelial carcinoma (HeLa) cells, moderately reduce in porcine kidney (PK-15) cells and have no effect on the pseudotyped virus infection in Madin-Darby canine kidney (MDCK) cells.

Rhesus monkey TRIM5α represses HIV-1 LTR promoter activity by negatively regulating TAK1/TAB1/TAB2/TAB3-complex-mediated NF-κB activation.

TRIM5α has been identified as the main restriction factor responsible for resistance of Old World monkey cells to HIV-1 infection. The precise mechanism of viral inhibition by TRIM5α remains elusive but appears to occur in multiple ways. Here, we report that rhesus monkey TRIM5α (TRIM5α(rh)) can represses HIV-1 LTR promoter activity by negatively regulating TAK1/TAB1/TAB2/TAB3-complex-mediated NF-κB activation when TRIM5α(rh) is overexpressed.

Down-regulation of HIV-1 infection by inhibition of the MAPK signaling pathway.

The human immunodeficiency virus type 1 (HIV-1) can interact with and exploit the host cellular machinery to replicate and propagate itself. Numerous studies have shown that the Mitogen-activated protein kinase (MAPK) signal pathway can positively regulate the replication of HIV-1, but exactly how each MAPK pathway affects HIV-1 infection and replication is not understood. In this study, we used the Extracellular signal-regulated kinase (ERK) pathway inhibitor, PD98059, the Jun N-terminal kinase (JNK) pathway inhibitor, SP600125, and the p38 pathway inhibitor, SB203580, to investigate the roles of these pathways in HIV-1 replication.

Activity of superior interferon α against HIV-1 in severe combined immunodeficient mice reconstituted with human peripheral blood leukocytes.

Background: Interferon (IFN) can inhibit human immunodeficiency virus type 1 (HIV-1) replication in vitro and in clinic. However, IFN therapy for HIV infection was limited by its moderate antiviral efficacy and its frequent adverse effects. In the present study we evaluated the anti-HIV efficacy of a novel synthesized superior interferon α (sIFNα).

Complex positive selection pressures drive the evolution of HIV-1 with different co-receptor tropisms.

HIV-1 co-receptor tropism is central for understanding the transmission and pathogenesis of HIV-1 infection. We performed a genome-wide comparison between the adaptive evolution of R5 and X4 variants from HIV-1 subtypes B and C. The results showed that R5 and X4 variants experienced differential evolutionary patterns and different HIV-1 genes encountered various positive selection pressures, suggesting that complex selection pressures are driving HIV-1 evolution.

Human immunodeficiency virus-1 genotypic drug resistance among volunteer blood donors in Yunnan, China.

Background: Drug resistance profiles of human immunodeficiency virus-1 (HIV-1) in treatment-naïve infections have been reported in developed countries. However, little is known in developing countries, including China, especially in treatment-naïve volunteer blood donors.

Study Design And Methods: Fifty-two HIV-1-positive samples of blood donors were collected from 2005 to 2006 in Yunnan, China.

One-step label-free optical genosensing system for sequence-specific DNA related to the human immunodeficiency virus based on the measurements of light scattering signals of gold nanorods.

A one-step label-free optical genosensing method has been developed in this contribution by taking short DNA target with its sequence related to the human immunodeficiency virus type 1 (HIV-1) as an example. By employing anisotropic nonspherical and positively charged gold nanorods (Au-NRs) as the recognition platform, which show high stability against aggregation under high ionic strength conditions without any additional stable reagent, we found that the addition of target DNA to the mixture of nonmodified Au-NRs suspension and label-free probe DNA in high ionic strength buffer leads to a color change from red to light purple in less than 5 min, displaying strong plasmon resonance light scattering (PRLS) signals. Mechanism investigations showed that the strong PRLS signals should be ascribed to the aggregation of Au-NRs induced by the formed double-stranded oligonucleotides (dsDNA) from the hybridization of target DNA with probe DNA.

[Study on genotypic resistance mutations to antiretroviral drugs on HIV strains of treated and treatment-naive HIV-1 infectious patients in Hubei province].

Objective: To study the drug resistance status on HIV-1 patients who had been treated with highly active antiretroviral therapy (HAART) and those treatment-naive ones in Hubei province.

Methods: Nested polymerase chain reaction (PCR) was used to amplify 2 kb DNA fragment in HIV pol gene from peripheral blood of the HIV infected patients and the PCR products were sequenced. The sequences were compared to the Stanford HIV drug resistance database.

[Comparative proteome analysis of human papillomavirus-infected cervical specimens and the difference between the high- and low-risk genotypes of human papillomavirus].

Objective: To perform an comparative proteome analysis of human papillomavirus-infected cervical specimens and to investigate different expressions between high- and low-risk genotypes.

Methods: The cervical specimens were divided into two groups (cervical intraepithelial neoplasia group and condyloma acuminatum group) according to their genotypes. Using comparative proteome technology, high-risk human papillomavirus-infected cervical intraepithelial neoplasia, low-risk human papillomavirus-infected condyloma acuminatum, and normal cervical intraepithelial tissue were compared.

Snapshot of HIV pathogenesis in China.

Several reviews have focused on the nature of HIV infection and its spread in various geographical regions of China. In contrast, this review provides a comprehensive update on the prevalence of multiple HIV-1 subtypes, consequent emergence of recombinant and novel forms of HIV-1 in China, and the implications this may have on HIV diversity and the development of effective vaccines. In addition it also examines the dissemination of primary drug resistance in therapy naïve patients, as well as co-infections with two other important viruses-hepatitis B and C.