Hepatitis C virus infection of human cytotrophoblasts cultured in vitro.

Hepatitis C virus (HCV) infection in the uterus is a significant path of vertical HCV transmission. Some studies consider vertical HCV transmission in the uterus as the result of maternal blood leakage into infant blood, whereas others theorize that HCV is transmitted by the mother to the infant through cells constituting the placenta barrier. Although trophoblasts play an important role in the placenta barrier, no definitive evidence has been presented to prove that cytotrophoblasts can be infected with HCV. The current study investigated whether or not these can be infected with HCV by conducting an experiment, in which cultured human cytotrophoblasts were infected with HCV in vitro. The results were analyzed using reverse transcription polymerase chain reaction (RT-PCR), ultrastructural characteristic changes under an electron microscope, and immunoelectron microscopy. HCV RNA in the supernatant of the cultured medium of the infected group was intermittently detected during the 16-day incubation period using RT-PCR. Under an electron microscope, the ultrastructures of infected human cytotrophoblasts were markedly different from normal cells, demonstrating lysosomal hyperplasia, rough endoplasmic reticulum, decreased lipid droplets, presence of vacuoles, and the appearance of HCV-like particles. Using immunoelectron microscopy, HCV-like particles conjoined with golden granules were also observed. Based on the data, the current study concludes that HCV infects a human cytotrophoblast cultured in vitro; moreover, its ultrastructure changes dramatically upon infection.

Correlation between TIMP-1 expression and liver fibrosis in two rat liver fibrosis models.

AIM: To evaluate serum TIMP-1 level and the correlation between TIMP-1 expression and liver fibrosis in immune-induced and CCL4-induced liver fibrosis models in rats. METHODS: Immune-induced and CCL4-induced liver fibrosis models were established by dexamethasone (0.01 mg) and CCL4 respectively. Serum TIMP-1 level was detected with ELISA, while histopathological grade of liver biopsy was evaluated. Spearman rank-correlation test was used to analyse the difference of the correlation between the TIMP-1 expression and hepatic fibrosis in the two fibrosis models. Furthermore, in situ hybridization was used to determine the expression difference of TIMP-1 mRNA in the two models. RESULTS: Positive correlation existed between serum TIMP-1 level of immune induced group and the histopathological stages of fibrosis liver of corresponding rats (Spearman rank-correlation test, r(s) = 0.812, P < 0.05), and the positive in situ hybridization signal of TIMP-1 mRNA was strong. In CCL4-induced liver fibrosis model, the correlation between the serum TIMP-1 level and the severity of hepatic fibrosis was not statistically significant(Spearman rank-correlation test, r(s) = 0.229, P > 0.05). And compared with immune-induced model, the positive in situ hybridization signal of TIMP-1 mRNA was weaker, while the expression variation was higher in hepatic fibrosis of the same severity. CONCLUSION: The correlations between TIMP-1 expression and liver fibrosis in two rat liver fibrosis models are different. In immune-induced model, serum TIMP-1 level could reflect the severity of liver fibrosis, while in CCL4-induced model, the correlation between the serum TIMP-1 level and the severity of hepatic fibrosis was not statistically significant.

Expression of TIMP-1 and TIMP-2 in rats with hepatic fibrosis.

AIM: To investigate the location and expression of TIMP-1 and TIMP-2 in the liver of normal and experimental hepatic fibrosis in rats. METHODS: The rat models of experimental immunity hepatic fibrosis (n=20) were prepared by the means of immunologic attacking with human serum albumin (HSA), and normal rats (n=10) served as control group. Both immunohistochemistry and in situ hybridization methods were respectively used to detect the TIMP-1 and TIMP-2 mRNA and related antigens in liver. The liver tissue was detected to find out the gene expression of TIMP-1 and TIMP-2 with RT-PCR. RESULTS: The TIMP-1 and TIMP-2 related antigens in livers of experimental group were expressed in myofibroblasts and fibroblasts (TIMP-1: 482+/-65 vs 60+/-20; TIMP-2: 336+/-48 vs 50+/-19, P<0.001). This was the most obvious in portal area and fibrous septum. The positive signals were located in cytoplasm, not in nucleus. Such distribution and location were confirmed by situ hybridization (TIMP-1/beta-actin: 1.86+/-0.47 vs 0.36+/-0.08; TIMP-2/beta-actin: 1.06+/-0.22 vs 0.36+/-0.08, P<0.001). The expression of TIMP-1 and TIMP-2 was seen in the liver of normal rats, but the expression level was very low. However, the expression of TIMP-1 and TIMP-2 in the liver of experimental group was obviously high. CONCLUSION: In the process of hepatic fibrosis, fibroblasts and myofibroblasts are the major cells that express TIMPs. The more serious the hepatic fibrosis is in the injured liver, the higher the level of TIMP-1 and TIMP-2 gene expression.

Current status of severe acute respiratory syndrome in China.

Severe acute respiratory syndrome (SARS), also called infectious atypical pneumonia, is an emerging infectious disease caused by a novel variant of coronavirus (SARS-associated coronavirus, SARS-CoV). It is mainly characterized by pulmonary infection with a high infectivity and fatality. SARS is swept across almost all the continents of the globe, and has currently involved 33 countries and regions, including the mainland China, Hong Kong, Taiwan, North America and Europe. On June 30, 2003, an accumulative total reached 8450 cases with 810 deaths. SARS epidemic was very rampant in March, April and May 2003 in the mainland of China and Hong Kong. Chinese scientists and healthcare workers cooperated closely with other scientists from all over the world to fight the disease. On April 16, 2003, World Health Organization (WHO) formally declared that SARS-CoV was an etiological agent of SARS. Currently, there is no specific and effective therapy and prevention method for SARS. The main treatments include corticosteroid therapy, anti-viral agents, anti-infection, mechanical ventilation and isolation. This disease can be prevented and controlled, and it is also curable. Under the endeavor of the Chinese Government, medical staffs and other related professionals, SARS has been under control in China, and Chinese scientists have also made a great contribution to SARS research. Other studies in developing new detection assays and therapies, and discovering new drugs and vaccines are in progress. In this paper, we briefly review the current status of SARS in China.

Advances in clinical diagnosis and treatment of severe acute respiratory syndrome.

It has been proved that severe acute respiratory syndrome (SARS) is caused by SARS-associated coronavirus, a novel coronavirus. SARS originated in Guangdong Province, the People's Republic of China at the end of 2002. At present, it has spread to more than 33 countries or regions all over the world and affected 8 360 people and killed 764 by May 31,2003. Identification of the SARS causative agent and development of a diagnostic test are important. Detecting disease in its early stage, understanding its pathways of transmission and implementing specific prevention measures for the disease are dependent upon swift progress. Due to the efforts of the WHO-led network of laboratories testing for SARS, tests for the novel coronavirus have been developed with unprecedented speed. The genome sequence reveals that this coronavirus is only moderately related to other known coronaviruses. WHO established the definitions of suspected and confirmed and probable cases. But the laboratory tests and definitions are limited. Until now, the primary measures included isolation, ribavirin and corticosteroid therapy, mechanical ventilation, etc. Other therapies such as convalescent plasma are being explored. It is necessary to find more effective therapy. There still are many problems to be solved in the course of conquering SARS.