Protective and Anti-Pathology Effects of Sm Fructose-1,6-Bisphosphate Aldolase-Based DNA Vaccine against Schistosoma mansoni by Changing Route of Injection

This study aimed to evaluate the efficacy of fructose-1,6-bis phosphate aldolase (SMALDO) DNA vaccination against Schistosoma mansoni infection using different routes of injection. The SMALDO has been cloned into the eukaryotic expression vector pcDNA3.1/V5-His TOPO-TA and was used in injecting Swiss albino mice intramuscularly (IM), subcutaneously (SC), or intraperitoneally (IP) (50 microg/mouse). Mice vaccinated with non-recombinant pcDNA3.1 served as controls. Each group was immunized 4 times at weeks 0, 2, 4, and 6. Two weeks after the last booster dose, all mice groups were infected with 80 S. mansoni cercariae via tail immersion. At week 8 post-infection, animals were sacrificed for assessment of parasitological and histopathological parameters. High anti-SMALDO IgG antibody titers were detected in sera of all vaccinated groups (P<0.01) compared to the control group. Both the IP and SC vaccination routes resulted in a significant reduction in worm burden (46.2% and 28.9%, respectively, P<0.01). This was accompanied by a significant reduction in hepatic and intestinal egg counts (41.7% and 40.2%, respectively, P<0.01) in the IP group only. The number of dead eggs was significantly increased in both IP and IM groups (P<0.01). IP vaccination recorded the highest significant reduction in granuloma number and diameter (54.7% and 29.2%, respectively, P<0.01) and significant increase in dead miracidia (P<0.01). In conclusion, changing the injection route of SMALDO DNA vaccination significantly influenced the efficacy of vaccination. SMALDO DNA vaccination via IP route could be a promising protective and anti-pathology vaccine candidate against S. mansoni infection.

Evaluation of some genetic factors influencing the phenotypic severity of beta thalassemia Egyptian patients

The objective of this study was to identify the influence of some genetic factors on the severity of Beta thalassemia. The study included 62 patients [27 Beta thalassemia major and 35 Beta thalassemia intermedia]. The patients were classified as major or intermedia on the basis of clinical examination, age of onset, rate of blood transfusion and hematological data. The search for mutations was done using polymerase chain reaction followed by reverse dot-biot technique. Severe mutations [B0] were found to cause Beta thalassemia major while milder mutations [B++] were noticed in Beta thalassemia intermedia patients. Amplification of a globin gene was successful in 57 Beta thalassemia patients. Alpha globin gene deletion was detected in 7% of the patients with a frequency of 9.4% for Beta thalassemia intermedia and 4% for the major patients. Moreover, the triple alpha arrangement [alpha-alpha-alpha 3, 7] was present in only one Beta thalassemia major Patient. The an1 polymorphism [C-T] was found in 4.8% of the Patients with a frequency of 5.7% for B thalassemia intermedia and 3.7% for the major patients. The mild phenotype of Beta thalassemia intermedia patients could be explained mainly by presence of mild B thalassemia mutations, coinheritance of a globin gene deletion and/or G gamma Xmn1 polymorphism. The search for additional genetic defects in a globin gene or other modifying factors is recommended for unexplained mild Beta thalassemia cases