The Histopathology Characteristic And The Detection Of Nucleic Acid For The Liver Of HIV Infected Patients

Acquired immunodeficiency syndrome (AIDS) has become a global mischance, though the scientists have given a world of energies, it is not enough to resolve this problem. The end of previous century, highly active antiretroviral therapy (HAART) came out, the patients' immune system has been rebuilt, which make the death from opportunity infection and tumor decreasing and from liver damage or failure increasing comparatively. Follow that, a series of problems is coming, for example, whether human immunodeficiency virus(HIV) can infect liver tissue directly, which cells HIV can invade, whether the liver damage of HIV infectors or AIDS inpatients relate to HIV, how HIV damage the liver, etc.Firstly, we compared the liver biopsy specimens between 13 HIV/HCV co-infected patients and 30 HCV simple infected patients. With the same infect route, no chronic disease history, no antiviral therapy, no co-infected other virus, we compared their clinical data (including sex, age, weigh, infected age, interval of disease, etc.). Next we compared two groups of patients' pathologic change seriatim, including the total grade of the inflammation activity(G) and the total stage of the fibrosis(S), the inflammation state in the portal area and the hepatic lobule, the fibrosis state and the steatosis state, etc. Secondly, we picked up 17 liver specimens(15 biopsy and 2 autopsy) and hybridized by a biotin labeled probe from HIV-1 gag area to detect the HIV-1 RNA in the liver tissue, which primarily discuss whether HIV can infect the liver cells and which cells can be infected.In the first research, we found there are no distinct differences between the two groups in the sex, age, weigh, infected age and internal of diseases, which is comparable. The hepatic function , blood glucose and blood grease yet is matching(p value > 0.05). The compare results of pathology is following: the difference between the two groups in the G and S has not evident statisticalmeaning;For the inflammation of the portal area, there are not distinct differences between the two groups of inpatients in the extent of bile duct injure and monocyte soakage. But in the HCV simple infected group, lymphocyte increased in 16 specimens and lymph follicle can be seen in 9 specimens, in the co-infected group, both no, instead lymphocyte decreased in 7 specimens, which differences is distinct;After analysis for the inflammation in the hepatic lobule, we did not find distinct differences in the extent of monocyte soakage, hydropic or ballooning degeneration, interface hepatitis, spotty or focal necrosis, big/double/vacuole nucleus hepatocyte. But active hyperplasia of the Kupffer cells is 11 in co-infected group and 9 in simple infected group, lymphocyte arranged like a string of beads in 11 of HCV group, but no in HIV/HCV group, which have evident statistical meaning. Otherwise, there are no differences in the fibrosis or not, the extent of fibrosis and fiberboard or not, hepatocyte steatosis or not, the extent and type of steatosis. In the in situ hybridization research, non-parenchymal cells, including mononuclear inflammatory cells in the portal tracts and sinusoidal cells were labeled in all 17 case. Furthermore, in four case the morphology of the HIV-1 positive cells was reproducibly consistent with that of hepatocytes. The specificity of the results was supported by the absence of hybridization from HIV-1 sero-negative subjects and no probe.From our study, following conclusions can be drawn: (1) The HIV co-infection has not evidently changed the course of disease of the HCV infected patients. (2) The inflammation in the portal area and hepatic lobule is comparative for the HIV/HCV co-infection and the HCV simple infection. But the lymphocyte decreased and the lymph follicle and the lymphocyte arranged like a string of beads vanished in the co-infected group. (3) The HIV co-infection has not evidently effected the fibrosis and steatosis .(4) HIV-1 RNA was detected by in situ hybridization in the mononuclear inflammatory cells, sinusoidal cells and the hepatocytes, which demonstrated that HIV can infect parenchymal and non-parenchymal liver cells. Our conclusions need confirm by broadening thesamples.