Hepatitis: Xie X

Xie X, Lan G, Peng L, Peng F, Wang Y, Fang C, Nie M. · Department of Urological Organ Transplantation, Center of Organ Transplantation, Second Xiangya Hospital, Central South University, Changsha 410011, China. · Zhong Nan Da Xue Xue Bao Yi Xue Ban. · Pubmed #19349683 links to  free full text

Abstract: OBJECTIVE: To explore the effect and safety of transplantation of kidneys from HBV-positive or HCV-positive donors. METHODS: From January 2002 to June 2006, 283 kidney transplantations were performed in Second Xiangya Hospital. Altogether 57 recipients were HBV-positive, including 31 from donors with viral B hepatitis (DB + /RB +), and 26 from donors with HBV-negative (DB - /RB +). Nineteen patients with hepatitis C virus underwent a kidney transplantation, including 6 who received kidneys from anti-HCV-positive donors (DC + /RC +) and 13 from seronegative donors (DC - /RC +). Recipient's liver function, acute rejection, graft survival, and patient survival had been observed for an average follow-up of 14 months. RESULTS: No significant difference was observed between the DB + /RB + group and DB - /RB + group, or the DC + /RC + group and DC - /RC + group in the rate of liver disfunction, acute rejection, graft survival, and patient survival. CONCLUSION: Kidney transplantations from HBV-positive or HCV-positive donors into the matched serology-positive recipients is safe in the short term, and the long-term results need further observation.

Fu Y, Pan M, Wang X, Xu Y, Xie X, Knowles NJ, Yang H, Zhang D. · College of Veterinary Medicine, China Agricultural University, Beijing 100193, People's Republic of China. · J Gen Virol. · Pubmed #19264607 No free full text.

Abstract: Duck astroviruses (DAstVs) are known to cause duck viral hepatitis; however, little is known regarding their molecular biology. Here, we report the complete sequence of a DAstV associated with a recent outbreak of fatal hepatitis in ducklings in China. Sequence analyses indicated that the genome of DAstV possessed a typical astrovirus organization and also exhibited two unique features. The polyadenylated genome comprised 7722 nt, which is the largest among astroviruses sequenced to date. The ORF2 of DAstV was not in the same reading frame as either ORF1a or ORF1b, which was distinct from all other astroviruses. Sequence comparisons and phylogenetic analyses revealed that DAstV was more closely related to turkey astrovirus (TAstV) type 2, TAstV-3 and TAstV/MN/01 (a possible new TAstV serotype) than to TAstV-1 or other astroviruses. These findings suggest that astroviruses may transmit across ducks and turkeys.

Li Z, Guo X, Hao W, Wu Y, Ji Y, Zhao Y, Liu F, Xie X. · Institute of Hepatitis Research, Beijing You'an Hospital, Capital Medical University, Beijing 100054, China. · Chin Med J (Engl). · Pubmed #12890366 links to  free full text

Abstract: OBJECTIVES: To observe the changes of serum interleukins (IL), T-lymphocyte subsets, and white blood cell (WBC) count in patients with severe acute respiratory syndrome (SARS), and to investigate the relationship between injured immune function, immune response and disturbed immune adjustment in SARS patients. METHODS: The levels of serum IL-2, IL-10, IL-12 and T-lymphocyte subset counts were measured in 35 clinically diagnosed SARS patients by using enzyme linked immunosorbant assay (ELISA). The relationship between the measured results and WBC count was further analyzed. RESULTS: The level of serum IL was increased to a great extent in the 35 SARS patients, and the levels of serum IL-2, IL-10 and IL-12 were 242.53 (92.69) pg/ml, 77.43 (63.37) pg/ml and 65.94 (43.21) pg/ml, respectively. The level of serum IL-2 increased markedly (P < 0.01). The peripheral blood CD(3)(+), CD(4)(+) and CD(8)(+) counts were lower than normal in 23 patients (67.7%), 26 patients (74.3%) and 15 patients (42.9%), respectively. The peripheral blood WBC counts were lower than 4.0 x 10(9)/L in 10 patients, and their CD(3)(+), CD(4)(+) and CD(8)(+) counts were 583.90 (315.58) x 10(6)/L, 272.00 (94.13) x 10(6)/L and 209.00 (72.21) x 10(6)/L, respectively. The peripheral blood WBC counts were (4.0 - 10.0) x 10(9)/L in 20 patients, and their CD(3)(+), CD(4)(+) and CD(8)(+) counts were 700.00 (502.96) x 10(6)/L, 347.00 (247.58) x 10(6)/L and 322.05 (228.47) x 10(6)/L, respectively. The peripheral blood WBC counts were higher than 10.0 x 10(9)/L in 5 patients, and their CD(3)(+), CD(4)(+) and CD(8)(+) counts were 1466.00 (630.86) x 10(6)/L, 783.00 (311.14) x 10(6)/L and 640.00 (294.40) x 10(6)/L, respectively. The decreased CD(3)(+), CD(4)(+) and CD(8)(+) counts were consistent with the decreased WBC counts. The level of IL in SARS patients was significantly higher than that in patients with chronic hepatitis B (P < 0.01). CONCLUSIONS: The level of serum IL is closely related to cell immunity in SARS patients. The level of serum IL is increased evidently while CD(3)(+), CD(4)(+) and CD(8)(+) counts decrease. Both serum IL and CD are associated with injury of immune function, and thus they could be regarded as a monitoring index for judging the condition of SARS patients and prescribing immune therapy.

Lasarte JJ, Corrales FJ, Casares N, López-Díaz de Cerio A, Qian C, Xie X, Borrás-Cuesta F, Prieto J. · Department of Internal Medicine, Medical School and University Clinic, University of Navarra, Pamplona, Spain. · J Immunol. · Pubmed #10228002 links to  free full text

Abstract: Joint immunization with two recombinant adenoviruses, one expressing hepatitis C virus (HCV) core and E1 proteins and another expressing IL-12 (RAdIL-12), strongly potentiates cellular immune response against HCV Ags in BALB/c mice when RAdIL-12 was used at doses of 1 x 105-1 x 107 plaque-forming units. However, cellular immunity against HCV Ags was abolished when higher doses (1 x 108 plaque-forming units) of RAdIL-12 were used. This immunosuppressive effect was associated with marked elevation of IFN-gamma and nitric oxide in the serum and increased cell apoptosis in the spleen. Administration of N-nitro-L -arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, to mice that received high doses of RAdIL-12 was lethal, whereas no apparent systemic toxicity by L -NAME was observed in those immunized with lower doses of the adenovirus. Interestingly, in mice immunized with recombinant adenovirus expressing core and E1 proteins of HCV in combination with RAdIL-12 at low doses (1 x 107 plaque-forming units), L -NAME inhibited T cell proliferation and CTL activity in response to HCV Ags and also production of Abs against adenoviral proteins. In conclusion, gene transfer of IL-12 can increase or abolish cell immunity against an Ag depending of the dose of the vector expressing the cytokine. IL-12 stimulates the synthesis of NO which is needed for the immunostimulating effects of IL-12, but apoptosis of T cells and immunosuppression ensues when IFN-gamma and NO are generated at very high concentrations.

Yao ZQ, Waggoner SN, Cruise MW, Hall C, Xie X, Oldach DW, Hahn YS. · Beirne Carter Center for Immunology Research, Department of Microbiology and Pathology, University of Virginia, Charlottesville, Virginia 22908, USA. · J Virol. · Pubmed #16873288 links to  free full text

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Yao ZQ, Waggoner SN, Cruise MW, Hall C, Xie X, Oldach DW, Hahn YS. · Beirne Carter Center for Immunology Research, Department of Microbiology and Pathology, University of Virginia, Charlottesville, VA 22908, USA. · J Virol. · Pubmed #16306613 links to  free full text

Abstract: T cells play an important role in the control of hepatitis C virus (HCV) infection. We have previously demonstrated that the HCV core inhibits T-cell responses through interaction with gC1qR. We show here that core proteins from chronic and resolved HCV patients differ in sequence, gC1qR-binding ability, and T-cell inhibition. Specifically, chronic core isolates bind to gC1qR more efficiently and inhibit T-cell proliferation as well as gamma interferon (IFN-gamma) production more profoundly than resolved core isolates. This inhibition is mediated by the disruption of STAT phosphorylation through the induction of SOCS molecules. Silencing either SOCS1 or SOCS3 by small interfering RNA dramatically augments the production of IFN-gamma in T cells, thereby abrogating the inhibitory effect of core. Additionally, the ability of core proteins from patients with chronic infections to induce SOCS proteins and suppress STAT activation greatly exceeds that of core proteins from patients with resolved infections. These results suggest that the HCV core/gC1qR-induced T-cell dysfunction involves the induction of SOCS, a powerful inhibitor of cytokine signaling, which represents a novel mechanism by which a virus usurps the host machinery for persistence.