[Polymorphism analysis of Plasmodium falciparum histidine-rich protein II and III].

OBJECTIVE: To analyze the polymorphism of Plasmodium falciparum histidine-rich protein (PfHRP) II and III. METHODS: Genomic DNA was isolated from blood samples of 20 patients infected with Plasmodium falciparum in Yunnan Province. Blood samples were tested by microscopy and RDTs. The Pfhrp2 and Pfhrp3 gene fragments were amplified by PCR and sequenced. The sequencing results were analyzed and compared using the bioinformatics software. RESULTS: 20 patients infected with Plasmodium falciparum tested by microscopy and RDTs. PCR showed that the Pfhrp2 gene was with 389~986 bp, and Pfhrp3 gene with 329-640 bp. All PfH-IRP II sequences started with type 1 repeat (AHHAHHVAD) and ended with the type 12 repeat (AHHAAAHHEAATH). The number of type 7 (AHHAAD), type 2 (AHHAHHAAD) and type 6 (AHHATD) within PfHRP II was more than the other types of repeats, as well as type 16 (AHHAAN) and type 17 (AHHDG) for PfHRP III. Type 11 repeat (AHN) was not found from the PfHRP II and PfHRP III sequences. CONCLUSION: There is an extensive diversity in Pfhrp2 and Pfhrp3 fragments in the individuals infected with P. falciparum in Yunnan. Some types of repeats are shared by PfHRP II and PfHRP III.

[Observation on dynamic changes of SEA specific antibody in sera of BALB/c mice infected with Schistosoma japonicum].

OBJECTIVE: To investigate the dynamic changes of SEA-induced specific IgG, IgM in sera of BALB/c mice infected with Schistosoma japonicum in 18 weeks. METHODS: After mice were infected with S. japonicum cercarial for 2 weeks, the sera were collected from 2 to 18 weeks post-infection. The serum levels of SEA-specific IgG and IgM antibodies were measured respectively by ELISA, and the different fractions of IgG and IgM antibodies were identified by the Western blotting method. RESULTS: The ELISA results showed that the serum levels of SEA-specific IgG increased 5, 6, 9, 11 week, after the infection, and SEA-specific IgM increased obviously 5, 9 weeks after the infection. The Western blotting results showed that 140, 180 kDa molecules were recognized by IgG antibodies in the mouse sera 4 weeks after the infection. The specific IgG antibodies of 43, 50 kDa antigens appeared 5 weeks after the infection. 60-130 kDa fractions were recognized by IgG in the sera 6 weeks post-infection, and 38, 73 kDa proteins were recognized by IgG in the sera 9 weeks post-infection. The IgG antibodies of 26, 32, 35, 80 kDa molecules appeared 11 weeks post-infection and reacted strongly 12 weeks post-infection. The IgM antibodies of 100, 140, 180 kDa molecules appeared 3 weeks after the infection, and 73 kDa protein was recognized by sera 6 weeks after the infection, but the reaction became strong 9 weeks after the infection. The 38, 43, 50 kDa proteins induced IgM antibodies in 9-week-infection sera and the reaction became stronger 9 weeks after the infection. CONCLUSIONS: There is a dynamic change in the levels of specific IgG and IgM antibodies induced by S. japonica SEA and the appearance of the antibodies is related to different infection stages. The 43, 50, 10, 140, 180 kDa antigens might have the potential value of early immunodiagnosis. The 73 kDa antigen shows high diagnostic value in both acute and chronic schistosomiasis. The 28, 32, 35, 38, 80 kDa antigens are not only the diagnostic molecules for chronic schistosomiasis, but they may also have therapeutic effects, and in addition, they may be the candidate vaccines of the disease.