[You'an Academic] Latest discovery2021-11-30 00:05:25 29 ℃
HiV was quickly penetrated into the central nervous system (CNS), activated glial cells, and triggered infiltration of peripheral monocytes / macrophages. These cells release viral proteins, resulting in inflammatory factors, resulting in significant inflammation, making immunoactive and inhibiting, blood brain barrier damage, all of these factors will lead to neuronal damage, even apoptosis. Combined with anti-reverse transcription viral treatment (CART) systematically inhibits viral replication, and partially restores immune function, but does not eliminate viral proteins in the brain, which is reduced in the number of small propulsion cells shown in the transgenic animal model, and dendritic spin Lost and synaptic protein interrupts are related. In addition, the medical effects of drugs to brain integrity are also worthy of attention. The neurological system system of HIV-related brain injury is still to be elucidated. Brain capacity analysis based on brain MRI helps detect the changes of brain morphology, speculation, myelin formation, neuroprocycular hyperplasia, angiogenesis, dendritic size, quantity, and density may clarify HIV virus caused by The pathogenesis of brain damage.
Studies have shown that non-human probular animals infected monkey immunodeficiency virus (SIV) leads to CD4 + T cell failure and systematic immunodeficiency, the pathogenesis and pathological processes are similar to those in clinical HIV infections, have been widely used to explore nerves Pathogency and treatment strategy. Among them, SIVMAC239 infected with HIV-1 infected with HIV-1 infected human pathogenesis, as a qualified model of nerve HIV infection. In this longitudinal study, the natural processes and CARTs of the brain structure change in the process of the SIV infection are intended to explore the relationship between brain capacity changes and blood, cerebrospinal fluid (CSF) biomarkers. In order to clarify the mechanism of HIV-related brain cognitive damage and the early warning index system for clinical preliminary.
Title: Longitudinal Trajectories of Brain Volume In Combined Antiretroviral Treated and UnTreated Simian Immunodeficiency Virus-Infected RheSUS Macaques
Responsible Newsletter: Capital Medical University Beijing You'an Hospital
DOI: 10.1097 / QAD.0000000000003055
The laboratory data is collected from 1 week, 2, 5, 8, 12, 24, 36, and 48 WPI after infection, before infection. These time points are set in consideration of viruses and physiological conditions that can be detectable in the central nervous system after 1 week of infection. As described above, the SIV RNA level (Trizol extraction) was detected by reverse transcription PCR (RT-PCR), and the viral load in plasma and cerebrospinal fluid was detected. Peripheral blood CD4 + T cells and CD8 + T cell count were analyzed by flow cytometry.
Weight, viral loading, longitudinal change of immunomodes. The difference between the three groups of viral loads, CD4 + T cell count and CD4 + / CD8 + ratio value trajectory and weight were not statistically significant (age, p = 0.594; weight, p = 0.509). Weight of each group (P
The brain capacity of interest is changed over time in all 21 ROIS, and the inter-group interaction has a significant time of volume% (all P
Comparison between different time points indicate that the brain volume of health control group and SIV infected with the galler can be detected, including total gray, total white matter, lateral ventricular volume, right tail core, left shell core, Bilateral hippocampus, bilateral leaves, bilateral temporal leaves, left island leaves, right cerebellings. With the progress of infection and the progression of the course of the disease, SIV + CART-Gangee monkey tail nucleus, hard core, hippocampus, gynecase, top leaf, and temporal lobe gray matter volume becomes small. The Ganji monkey receiving Cart is only the left hippocampus, the right end and the left top leaf. Compared with the health control group, there were differences in the volume of the bilateral temporal brain.
The gray volume is associated with a viral load and a systemic immune condition. Among the SIV + CART-groups, the carma load in plasma is mainly related to the volume of the cortex, including bilateral shell core, bilateral tail nucleus, left secret nest, and right hippocampus. Further, the volume of a few clusters of the cortical cortex (including left teeth / back, the cerebellum V leaf). The front quadrilateral, single-flap, and the upper left extreme brain back and the left corner are also associated with viral load in plasma.
In summary, SIVMAC239 infected with the rhesus monkey as an effective model for studying HIV induced brain changes. It is found that SIV infection may cause global brain atrophy, and Cart can effectively relieve brain damage and even reverse. It is shown that the cerebral cortex is affected by viral loading and immune levels, and the viral load has a great influence on the core (especially the tail core and shell). The system immune function is disclosed is closely related to GMV.
Responsible Author Academic introduction:
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