ABSTRACT
Hepatitis type E virus (HEV) is a significant infectious zoonotic disease that causes hepatitis E. The disease is primarily transmitted via the fecal-oral route through contaminated water or food and is transmissible between species and genera. The causative agent for the disease is the hepatitis type E virus, which is a member of the Hepadnaviridae family and a single-stranded RNA virus. Its 7.2 kb genome mainly contains three open reading frames (ORFs): ORF1 encodes a non-structural polyprotein that mediates viral replication and transcription; ORF2 encodes a capsid protein and free antigen that induce neutralizing antibodies; ORF3 partially overlaps with ORF2 and encodes a small multifunctional protein involved in virion formation and release. HEV has a unique dual life cycle: it is excreted into feces in the form of naked virions but circulates in the blood in the form of "quasi-enveloped" particles. The two kinds of virus particles adsorb and penetrate the host cell in distinct ways, then internalize and decapsulate to replicate the genome, thereby producing more virion and releasing it outside the cell to mediate the virus's spread. This paper reviews the morphological characteristics, genome structure, encoded proteins, and function of HEV virus-like particles in order to provide a theoretical basis for basic research and comprehensive disease prevention and control.
Subject(s)
Humans , Hepatitis E virus/genetics , Hepatitis EABSTRACT
Metabolic memory is a phenomenon that the diabetic complications continue to develop and progress in individuals who exposed a period of high glucose in the early stage and then returned to normal blood glucose after effective control.Diabetic nephropathy (DN) is one of the common diabetic microangiopathy and the main cause of end stage renal disease (ESRD).This review mainly summarizes the relationships between metabolic memory and the development of DN.
ABSTRACT
<p><b>OBJECTIVE</b>To study the relationship of -634G/C gene polymorphism of vascular endothelial growth factor (VEGF) with Henoch-Schonlein purpura nephritis (HSPN) in children.</p><p><b>METHODS</b>One hundred ethnic Han children with HSP, including 50 children with concurrent nephritis (HSPN group) and 50 children without nephritis (HSP without nephritis group), were enrolled. Fifty age-, sex-and ethnics-matched healthy children were used as the control group. VEGF-634G/C genotypes were determined by PCR-RFLP. Plasma VEGF levels were measured using ELISA.</p><p><b>RESULTS</b>CC genotype distribution (32%) and C allele frequency (56%) in the HSPN group were significantly higher than those in the control group (10% and 35% respectively) and the HSP without nephritis group (10% and 33% respectively) (P<0.01). The incidence of nephritis in HSP patients with CC genotype increased significantly when compared with those with GG genotype (76% vs 31%; P<0.01). Plasma VEGF levels in patients with CC genotype (180.5+/- 40.7 pg/mL) were significantly higher than those in patients with CG (145.2+/- 48.3 pg/mL) and GG (101.5+/- 26.5 pg/mL) genotypes (P<0.05).</p><p><b>CONCLUSIONS</b>VEGF-634G/C gene polymorphism may be associated with the development of HSPN. C allele may a susceptible gene of HSPN.</p>
Subject(s)
Child , Child, Preschool , Humans , Gene Frequency , Genotype , Nephritis , Genetics , Polymorphism, Genetic , IgA Vasculitis , Genetics , Vascular Endothelial Growth Factor A , Blood , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship between haplotypes of multilocus markers and ankylosing spondylitis (AS).</p><p><b>METHODS</b>Five families with AS were recruited from Shanghai area. Eleven microsatellite markers around D6S276 were analyzed by Linkage package and by Cyrillic package.</p><p><b>RESULTS</b>Fine linkage analysis showed the significant Lod score values with D6S276 was 3.8821, Lod score values with D6S1691 and D6S1618 near D6S276 were larger than 1.5. The crossover value in 5 pedigrees was 14%. The haplotype analysis showed that the regions between D6S1691 and D6S1618 were associated with AS.</p><p><b>CONCLUSION</b>The regions of D6S1691-D6S276-D6S1618 may harbor a susceptible gene of AS. The specific haplotypes of different pedigrees may play an important role in the presymptomatic diagnosis for AS.</p>
Subject(s)
Female , Humans , Male , Haplotypes , Genetics , Linkage Disequilibrium , Genetics , Pedigree , Spondylitis, Ankylosing , GeneticsABSTRACT
Objective To analyze the clinical characteristics of macrophage activation syndrome (MAS). Methods Clinical data was analyzed in 9 children who had been diagnosed as MAS in our hospital from Jan, 2003 to Aug, 2006. Results Seven children were boys, 2 children were girls, aged 5 months to 12 years. Clinical manifestations included long-term fever, hemophagocytic cell in bone marrow, anemia, arthritis, enlargement of lymph nodes, enlargement of liver and spleen, liver dysfunction, abnormal fat metabolism. Two cases had acute respiratory, distress syndrome(ARDS), 2 cases were complicated with multi- pie organ failure(MOF), two patients died. Glucocorticoid combined with immunosuppressive therapy were effective, HP(Plasma Exchange)was applied in one severe case and was shown to he effective. Conclusion MAS is a serious complication of JIA, especially in systemic-onset juvenile idiopathic arthritis. It is very im- portant to recognize and treat MAS earlier.