RESUMEN
Abstract Background The mechanism underlying the coexistence of hepatitis B surface antigen and antibodies to HBsAg in chronic hepatitis B patients remains unknown. Aims This research aimed to determine the clinical and virological features of the rare pattern. Methods A total of 32 chronic hepatitis B patients infected by HBV genotype C were included: 15 carrying both HBsAg and anti-HBs (group I) and 17 solely positive for HBsAg (group II). S gene and reverse transcriptase region sequences were amplified, sequenced and compared with the reference sequences. Results The amino acid variability within major hydrophilic region, especially the “a” determinant region, and within reverse transcriptase for regions overlapping the major hydrophilic region in group I is significantly higher than those in group II. Mutation sI126S/T within the “a” determinant was the most frequent change, and only patients from group I had the sQ129R, sG130N, sF134I, sG145R amino acid changes, which are known to alter immunogenicity. Conclusions In chronic patients, the concurrent HBsAg/anti-HBs serological profile is associated with an increased aa variability in several key areas of HBV genome. Additional research on these genetic mutants are needed to clarify their biological significance for viral persistence.
Asunto(s)
Adulto , Femenino , Humanos , Masculino , Adulto Joven , Anticuerpos contra la Hepatitis B/sangre , Antígenos de Superficie de la Hepatitis B/sangre , Virus de la Hepatitis B/genética , Hepatitis B Crónica/genética , Hepatitis B Crónica/inmunología , ADN Polimerasa Dirigida por ARN/genética , Proteínas del Envoltorio Viral/genética , China , ADN Viral , Genotipo , Virus de la Hepatitis B/inmunología , Mutación , Reacción en Cadena de la Polimerasa , Análisis de Secuencia de ADNRESUMEN
Objective To study the of effets of hFRNK gene transfected by adenoviral vector on human colon cancer cell invasion induced by gastfin.Methods The subjects were divided into three groups:control,G17 and hFRNK group.The G17 group was treated with 100 umol/L gastrin 17 for 12 h to induce Col0320WT cells.As to hFRNK group,Colo320WT cells were infected by pAdhFRNK(MOI:100)for 48 h after transient transfection of pCR3.1-CAR for 48 h and subsequently treated with gastrinl7 for 12 h,and the control group was untreated Colo320WT cells.Expression of phosphorylated FAK(PY397)were assayed by western blot.FAK(PY397)at lamellipoda was observed with a confocal microscope.The influence of hFRNK on formation of signal complex of FAK-Src-p130Cas-Dockl80 was assayed with coimnlunoprecipitation and immunity blotting.Activity of Rac-GTPase was determined by pull down.Results Phosphorylated FAKTyr397 drastically increased with the induction of gastrin.Compared with that of G17 group,FAK (PY397)expression decreased and little FAK(PY397)was found at lamellipoda,at the same time,the signal complex of FAK-Src-p130Cas-Dockl80 did not form,and the activity of Rac decreased.Conclusion hFRNK gene may block gastrin-induced FAK phosphorylation,prevent formation of the signal complex,prevention and treatment of tumor invasion and metastasis.