Hepatitis: Jia H

Chen T, Jia H, Li J, Chen X, Zhou H, Tian H. · Department of Endocrinology and Metabolism, West China Hospital of Sichuan University, Chengdu, China. · Transpl Int. · Pubmed #19207185 No free full text.

Abstract: New onset diabetes mellitus (NODM) postliver transplantation (LT) is very common and may negatively affect patient and graft survival, but its causative mechanism is still unclear. This study was to analyze the connection between Hepatitis C virus (HCV) infection and NODM after LT by systematically reviewing published medical literature. We electronically searched databases of MEDLINE, EMBASE and the Cochrane Library from January 1980 to January 2008. Only retrospective studies could be identified. Seven of them were subjected to the meta-analysis. Analysis was performed by using revman 4.2 software. We found that HCV increased the prevalence of NODM [OR 2.46; 95%CI (1.44, 4.19)]. Then, we further analyzed the association between HCV and persistent-NODM (P-NODM) after LT. The result showed that prevalence of P-NODM was higher in HCV-positive group than in HCV-negative group with marginally statistical significance [OR = 1.39; 95%CI (1.06, 1.83)]. The present meta-analysis based on retrospective studies suggested a significant relationship between HCV and NODM after LT, and it seems that HCV infection might also increase the prevalence of P-NODM. Multicenter, large sized prospective studies are still needed to further confirm these results.

Switzer WM, Salemi M, Qari SH, Jia H, Gray RR, Katzourakis A, Marriott SJ, Pryor KN, Wolfe ND, Burke DS, Folks TM, Heneine W. · Laboratory Branch, Division of HIV/AIDS Prevention, National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA. · Retrovirology. · Pubmed #19187529 links to  free full text

Abstract: BACKGROUND: Human T-lymphotropic virus type 4 (HTLV-4) is a new deltaretrovirus recently identified in a primate hunter in Cameroon. Limited sequence analysis previously showed that HTLV-4 may be distinct from HTLV-1, HTLV-2, and HTLV-3, and their simian counterparts, STLV-1, STLV-2, and STLV-3, respectively. Analysis of full-length genomes can provide basic information on the evolutionary history and replication and pathogenic potential of new viruses. RESULTS: We report here the first complete HTLV-4 sequence obtained by PCR-based genome walking using uncultured peripheral blood lymphocyte DNA from an HTLV-4-infected person. The HTLV-4(1863LE) genome is 8791-bp long and is equidistant from HTLV-1, HTLV-2, and HTLV-3 sharing only 62-71% nucleotide identity. HTLV-4 has a prototypic genomic structure with all enzymatic, regulatory, and structural proteins preserved. Like STLV-2, STLV-3, and HTLV-3, HTLV-4 is missing a third 21-bp transcription element found in the long terminal repeats of HTLV-1 and HTLV-2 but instead contains unique c-Myb and pre B-cell leukemic transcription factor binding sites. Like HTLV-2, the PDZ motif important for cellular signal transduction and transformation in HTLV-1 and HTLV-3 is missing in the C-terminus of the HTLV-4 Tax protein. A basic leucine zipper (b-ZIP) region located in the antisense strand of HTLV-1 and believed to play a role in viral replication and oncogenesis, was also found in the complementary strand of HTLV-4. Detailed phylogenetic analysis shows that HTLV-4 is clearly a monophyletic viral group. Dating using a relaxed molecular clock inferred that the most recent common ancestor of HTLV-4 and HTLV-2/STLV-2 occurred 49,800 to 378,000 years ago making this the oldest known PTLV lineage. Interestingly, this period coincides with the emergence of Homo sapiens sapiens during the Middle Pleistocene suggesting that early humans may have been susceptible hosts for the ancestral HTLV-4. CONCLUSION: The inferred ancient origin of HTLV-4 coinciding with the appearance of Homo sapiens, the propensity of STLVs to cross-species into humans, the fact that HTLV-1 and -2 spread globally following migrations of ancient populations, all suggest that HTLV-4 may be prevalent. Expanded surveillance and clinical studies are needed to better define the epidemiology and public health importance of HTLV-4 infection.

Duong YT, Jia H, Lust JA, Garcia AD, Tiffany AJ, Heneine W, Switzer WM. · Laboratory Branch, Division of HIV/AIDS Prevention, National Center for HIV, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention, 1600 Clifton Road, Atlanta, GA 30333, USA. · AIDS Res Hum Retroviruses. · Pubmed #19102684 No free full text.

Abstract: Clonal disorders of large granular lymphocytes (LGL) result in leukemia due to the expansion of a discrete subset of either CD3(+) T cells or natural killer (NK) cells. It has been hypothesized that a viral antigen acts as the initial stimulus causing the expansion of these cells. The possible involvement of human T cell lymphotropic virus types 1 and 2 (HTLV-1 and HTLV-2) in this disease has been studied but no conclusive evidence has linked either virus with LGL leukemia. In this study, we examined whether HTLV-3 or HTLV-4, two newly identified HTLV groups discovered in Central Africa in primate hunters, is involved in LGL leukemia. We developed two specific real-time PCR quantitative assays that are highly sensitive, capable of detecting 10 copies of HTLV-3 or HTLV-4 pol sequences in a background of 1 microg of DNA from human peripheral blood lymphocytes (PBL). We tested PBL DNA samples from 40 LGL leukemia patients in the United States and found that all samples were negative for HTLV-3 or HTLV-4 infection. These results suggest that HTLV-3 and HTLV-4 are not the causative agent of LGL leukemia.

Huang Y, Chen Z, Jia H, Wu W, Zhong S, Zhou C. · Institute of Infectious Diseases, First Affiliated Hospital, Medical College, Zhejiang University, Qingchun Road 79, Hangzhou 310003, China. · Clin Immunol. · Pubmed #16531121 No free full text.

Abstract: We evaluated the potential of dendritic cells (DCs) engineered to express antigen of hepatitis B virus (HBV) in priming Th/Tc and HBV-specific CTL responses in mice. Recombinant adenovirus expressing hepatitis B surface antigen (HBsAg) (Ad-S) was constructed, and bone marrow-derived DCs were transduced with Ad-S or pulsed with HBsAg protein. Mice were injected with either Ad-S-transduced DCs or HBsAg-pulsed DCs or plasmid DNA encoding HBsAg twice at 3-week intervals. We showed that adenovirus infection had no further effect on the phenotype, the ability to induce IFN-gamma-producing Th1/Tc1 response or the T cell stimulatory capacity of already mature DCs in vitro. We also showed that immunization with Ad-S-transduced DCs effectively induced Tc1 cells and HBsAg-specific CTLs in vivo and down-regulated the circulating HBsAg and HBV DNA in HBV transgenic mice. Furthermore, these efficacies were stronger than that of HBsAg-pulsed DCs and plasmid DNA. Thus, DCs transduced with recombinant adenovirus may be a promising candidate for an effective CTL-based therapeutic vaccine against HBV.

Jia H, Du J, Zhu S, Ma Y, Cai H. · The Immunological Department, Institute of Infectious Diseases of the First Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou 310003, China. · Chin Med J (Engl). · Pubmed #12875732 links to  free full text

Abstract: OBJECTIVE: To discuss the roles of serum interleukin-18 (IL-18), interleukin-10 (IL-10) and soluble interleukin-2R (sIL-2R) in the pathogenesis of chronic hepatitis C and to observe the effects of interferon (IFN) on the above- mentioned serum cytokines. METHODS: The levels of above- mentioned cytokines were detected in 10 healthy individuals, 24 asymptomatic hepatitis virus C (HCV) carriers and 27 patients with chronic hepatitis C (before and after IFN treatment) using enzyme linked immunosorbent assay (ELISA). RESULTS: The levels of the cytokines in patients with chronic hepatitis C are higher than in healthy people (P < 0.05) and in asymptomatic HCV carriers (P < 0.05). The values of the cytokines show a significant positive correlation to ALT (P < 0.05). Levels of tested cytokines decreased observably after IFN treatment (P < 0.05). The grades of the serum levels for sIL-2R and IL-10 before IFN treatment (from high to low) were categorized accordingly: non-response group > partial- response group > complete- response group (P < 0.05). CONCLUSIONS: The tested cytokines co-participate in the pathogenesis of chronic hepatitis C, and can be used to evaluate the effect of IFN on the immune state of organisms. Furthermore, sIL-2R and IL-10 are important for predicting the anti-viral efficacy of IFN.