Objective To investigate the correlation between EBV-LMP2-specific cell responses,EBV DNA copies and titers of IgA antibody to viral capsid antigen (IgA/VCA).Methods IgA/VCA antibody were tested with immune-enzyme method.Both of plasma and lymphocytes were respectively separated from IgA/VCA-positive individuals and patients with nasopharyngeal carcinoma (NPC) without treatment.EBV DNA copies and LMP2-specific cell responses were detected by interferon-gamma Elispots assay and fluorescent quantitative PCR method.Results IgA/VCA antibody in 80 of 1 233 individuals was positive in Cangwu county,and the positive rate is 6％.EBV-LMP2-specific cell responses and EBV DNA copies were detected in 72 of 80 IgA/VCA positive individuals and patients with NPC.EBV DNA copies in plasma were increased with rise of titers of IgA/VCA antibody,while EBV-LMP2-specific cell responses were declined.Conclusion EBV-LMP2-specific cell responses and EBV DNA copies are probably associated with titers of IgA/VCA antibody.

Objective We previously demonstrated that peroxiredoxin 3 (PRX3) was overexpressed in cervical cancer and the expression of PRX3 was positively associated to that of oncogenes E6/E7 of human papillomaviruses (HPV) type 16.The present study was conducted to investigate the link between HPV oncogenes and PRX3,which would be helpful to understanding the mechanism for cervical carcinogenesis.Methods Cervical epithelial cells were cultured and were transfected with recombinant pcDNA3.1 vector containing HPV16 E6/E7.The changes of PRX3 expression were detected by quantitative real time PCR and Western blotting.Results In the epithelial cells which stably expressed HPV16 E6/E7,the expression of PRX3 was significantly down-regulated at both mRNA and protein levels compared to that in the control cells.Conclusion Integration of high risk HPV DNA into the chromosomes of cervical epitheliums induced the change of the PRX3 expression,which might be involved in the initiation of cervical cancer.

Objective: The present study was conducted to investigate the response of peroxiredoxin 3 (PRX3) to oxidative stress induced by high-risk human papillomavirus (HPV). Methods: Sixty patients with cervical cancer were included and sixty patients with hysteromyoma were assigned as controls. Serum PRX3 was detected by enzyme-linked immunosorbent assay. The expression of PRX3 and oncoprotein E6 of HPV16 or HPV18 was examined in cervical cancer tissues by immunohistochemistry and in cervical cancer cells by Western blotting respectively. Results: Patients with invasive squamous cervical cancer showed higher level of serum PRX3 than control subjects with hysteromyoma. PRX3 expression was up-regulated and was positively associated with that of E6 of HPV16 or HPV18 in cervical cancer tissues. The correlation was confirmed in HPV-containing cervical cancer cell lines including CaSki, and HeLa. Conclusions Our result indicated a positive response of PRX3 to HPV-induced oxidative stress. Serum PRX3 might be a potential indicator of active amplification of high-risk HPV in cervical cancer cells.