In persistent viral infections, especially those suffering from congenital infections, there are a large number of viruses in the body, viremia persists for a long time, but the body's response is extremely weak, and the infected animals do not show obvious clinical symptoms. This is the phenomenon of immune tolerance in viral infections. For example, a mouse that is congenitally infected with lymphocytic choriomeningitis virus is always in a healthy state after birth, but at the same time, severe viremia and viremia occur, and almost all lymphocytes of the choroid choriomeningitis virus Infection. When the bovine fetus is infected with bovine viral diarrhea virus in the first half of pregnancy, it also has an insignificant lifetime poisoning state. In addition, mice are inoculated with lactate dehydrogenase-enhancing virus (infected tissue), the virus proliferates in the body macrophages, and high-cost viremia occurs, and often lasts for a lifetime, but the infected mice produce only a small amount of antibodies ( Often combined with the virus as a virus-antibody complex), except for a small number of animals with glomerular nephritis due to deposition of this immune complex on the glomerulus, most of the infected mice do not present clinical symptoms. Leukemia in chickens and mice, as well as subacute and chronic swine fever, often exhibit a similar phenomenon, that is, only cause viremia, but does not present clinical signs. The animal body can tolerate such severe viremia without obvious pathological reaction. What is the reason? The embryonic period receives a large number of viral antigens, which produces immune tolerance, which is of course the main reason. However, in those viral infections in which cellular immunity or humoral immunity causes immunopathology, the immune system is inhibited for some reason, and may also be the cause of the body's ability to tolerate viremia without presenting a pathological response. Zui recently found that different strains of mice have different rates of immune tolerance and tolerance when infected with leukemia virus. It seems that the occurrence of immune tolerance is still affected by genetic factors to some extent. The mechanism by which sputum is immune to tolerance is now known to be the clonal deletion (cell death) and functional clearance (or inactivation) that occurs after mature T, B lymphocytes interact with their specific antigens; Mature antigen-reactive lymphocytes appear, but due to factors such as inhibitory T cells, the growth and differentiation of immunocompetent cells are inhibited, and thus no specific immune response is produced. 
Apoptosis
Apoptosis refers to the spontaneous death process initiated by normal cells of the body after being subjected to physiological or pathological stimulation. Apoptotic cells showed increased intracellular Ca2+ concentration and cAMP, increased RNA and protein synthesis, followed by chromatin condensation, cytoplasmic condensation, resulting in chromosome cleavage and degradation at the nucleosome, forming 185 bp or an integral multiple thereof. DNA fragments of length. After degradation of the cytoplasm and nucleus, zui is finally encapsulated in membranous components, forming apoptotic bodies (ap optosis bodies), which are engulfed by phagocytic cells. Apoptosis, also known as programmed cell death (PCD), is an active, signal-dependent process and is involved in the involvement of multiple genes. Certain factors or factors can specifically induce apoptosis in one or a certain type of cell; certain growth factor-dependent cells also undergo apoptosis when the growth factor is removed. The expression products of many genes have obvious promotion and inhibition effects on apoptosis. Apoptosis of sputum cells belongs to the suicidal behavior of single cells and does not cause local inflammation. Therefore, it is of great significance in preventing the spread of viruses and anti-viral infections. Because of the degradation of the genomic DNA of the cell, the replication or proliferation of the virus is terminated. Apoptosis is one of the important mechanisms of antiviral infection in insects and other primitive organisms that are immune to body fluids. Apoptosis of sputum cells is not conducive to the proliferation and spread of the virus. Some viruses, after infecting target cells, inhibit the apoptosis of host cells, thereby facilitating their survival and replication in host cells. It is known that bcl-2 has an inhibitory effect on apoptosis. Epstein-Barr virus induces the expression of bcl-2 in infected host cells and encodes a similar substance of bcl-2. The E1B 19 kDa protein of adenovirus also has an inhibitory effect on apoptosis. The inhibitory effect of sputum cell apoptosis on viral proliferation has been confirmed by experiments. Cle m et al. (1993) infected the insect cell line SF-21 and larva with a baculovirus with a mutant p35 (which has an effect of inducing apoptosis) and found that p53 mutant baculovirus is present in SF-21 cells. Progeny virus production was significantly lower than its corresponding control wild-type and reversible mutant strains. When infected in larvae, the median lethal dose of p53 mutant baculovirus is 1000 times higher than that of wild-type and reversible mutant strains. After Hz1 baculovirus infection in some SF9 cells, some persistent infected cells undergo apoptosis, but they do not die. After the cells were re-formed into a monolayer, the infection was re-inoculated with the Hz-1 virus, and it was found that the progeny virus production was significantly lower in the cells that had undergone apoptosis than in the parental cells. Apoptotic cells caused by viral infection have been found in cells infected with influenza virus and in animals infected with feline immunodeficiency virus. Is this the active defense response of the host cell to the virus, or the activation of the apoptosis-related genes caused by the virus, which leads to the passive damage of the host cells? It needs further exploration and clarification.
Base and Socket
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Base and Socket
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