ABSTRACT
Objective To discuss the morphological changes of neurons infected with street strain of rabies virus (RV),and to explore the mechanism of the neuronal dysfunction caused by RV.Methods Invivo,the C57/BL mice were randomly divided into experimental group(n=10)and control group(n=10).The mice in experimental group were inoculated intracranially at 30 μL RV suspension (10TCID50 ), and the mice in control group were inoculated with identical volume of cell maintenance medium.Anti-RV antibody was used to detect the RV antigen distribution in brain tissue of the mice.Invitro,the primary hippocampal neurons were cultured for 1 week and the cells were infected by RV.The proliferation of RV was detected by immunofluorescence method after infection for 72,96,and 120 h.Results The RV antigen was found in neurons and neuronal dendrites of hippocampus CA1 4 d after infection;however, the RV antigen was detected only in neuronal dendrites of hippocampus CA1 7 d after infection.The number of infected neurons was the most 120 h after infection,and the number of infected dendrites was decreased.Conclusion RV can infect and injure the neuronal dendrites of hippocampus CA1 region and lead to neuronal dysfunction of the mice.
ABSTRACT
To elucidate whether the mutations in X region of hepatitis B virus (HBV) might be responsible for the different clinical profiles in cases positive for antibody to hepatitis B e antigen. The nucleotide sequences of X gene regions in serum HBV were examined in 14 asymptomatic carriers (AsC) and 14 chronic active hepatitis (CAH) patients with antibody to hepatitis e antigen. The results showed that 12 of 14 AsCs (85.7%) had insertions, deletions or point mutations in nucleotide sequence of X region resulting in truncation of the X protein by creating frame shift mutation or a new stop codon, whereas no patient with CAH had those X gene mutations( P