Factors that constitute the body's viral infection - animal body

The resistance of the animal body to the animal's body is another important factor in determining viral infection. In animals that have not been infected or have not been artificially immunized, the viral infection process depends on the body's non-specific resistance. The natural resistance called "species immunity" and the acquired immunity of the body will be described in the next chapter "Antiviral immunity". This section only briefly introduces age, nerve activity, hormones, X-ray irradiation, temperature, etc. The effect of factors on viral infection. 
[ZZ (D] Age [ZZ]] is a factor that affects viral infection in animals. In general, young animals are more susceptible to the virus than adult animals. This is particularly evident in certain viral infections. For example, rabies virus and vaccinia virus can proliferate vigorously in chicken embryos, but cannot or not easily proliferate in adult chickens; the amount of Japanese encephalitis virus required to infect 10-week-old mice is higher than that of 10-day-old mice. It is 1 million to 10 million times. Oncogenic adenoviruses and papovaviruses are susceptible to tumors in suckling hamsters and other newborn rodents, but do not cause tumors in adult animals. Neonatal mice are still isolated from the Zui-susceptible experimental animals of the venom toxin virus, and even the only host of certain types of Coxsackie virus. The pseudorabies virus can proliferate in tissue culture cells prepared from chicken embryo heart, muscle, and liver, but cannot be propagated in cultured cells prepared from the same tissues of chicks, and the like. This may be due to the lack of “mature” immune responses (including humoral and cellular immunity) in young animals, inadequate physiological barriers such as blood and brain, and less interferon production in young animal cells. Some people even think that the virus receptors of young animal cells are different from adult animal cells. For example, Kunin pointed out that brain tissue blocks of suckling mice can adsorb Coxsackie B virus more quickly than brain tissue blocks of adult mice. 
[ZZ (D] neural activity [ZZ]] The effect on viral infection is manifested in the incidence and severity of symptoms. Hibernating and drug-sleeping animals often have lower morbidity and mortality than control unsleep animals when infected with a virus. For example, hibernating hedgehogs and bats infected with arboviruses often carry poison over winter, and viremia occurs after hibernation. Sulkin et al applied the Mexican bat as an experimental rabies test: the bats that had been vaccinated with rabies virus were placed at 5-10 °C, the animals showed hibernation, and the virus and the body were inactive; but if they were placed at 29 °C The "cold" virus proliferates and causes the bat to present symptoms of infection. Mice that cause sleep with a small amount of luminal, when infected with Japanese encephalitis virus, often have a longer incubation period than the control mice that do not use the drug, and the mortality rate is also slightly lower. In hibernation or drug sleep, the body temperature, blood pressure and aeration rate decrease, neuromodulation and secretion and motor function decline, and cell phagocytosis is also inhibited, all of which will alter and disrupt the normal nutrition and metabolism of tissues and cells, thereby affecting The adsorption and proliferation of the virus on these tissues and cells may be the cause of less morbidity and mortality. However, it must be pointed out that the above examples of the application of drugs to reduce morbidity and mortality cannot be considered as regular phenomena. Because of the different drugs, different doses, and different viral infections, the results of drug sleep are very inconsistent, and sometimes there is a higher mortality rate than the control group. 
[ZZ (D) hormone [ZZ]] In particular, cortisone preparations often have the effect of inducing viral infection. For example, adrenocorticotropic hormone can significantly increase monkey sensitivity to polio and mice to influenza virus. Adult mice are usually not infected with Coxsackie B virus, but after treatment with cortisone, the susceptibility is almost the same as that of newborn mice. Treatment of chicken embryos with cortisone can increase the production of influenza virus by 2 to 6 times. Hydrocortisone inhibits the production of interferon by chicken embryos, tissue culture cells and animals. It is generally believed that the anti-inflammatory and immunosuppressive effects of cortisone preparations are the main cause of their challenge of viral infection. Other hormones may increase their susceptibility to certain viruses by altering the body's protein metabolism. For example, breast tumor virus can only induce mammary tumors in female rats, but it can also cause tumors if treated with estrogen. 
[ZZ (D] X-ray and other ray [ZZ]] also has the effect of improving the body's sensitivity to viral infection. This is not only because the body's immune mechanism is inhibited, but also because the non-specific defense response changes, which facilitates the proliferation of the virus in the corresponding cells and tissues. Irradiation of 0.155 C/Kg of X-rays or 1.85  104 Bq of radioactive phosphorus can cause lethal infection in adult mice that are not infected with Coxsackie B virus. The cells cultured in vitro stopped after the appropriate amount of X-ray irradiation, but the cellular components could still be synthesized, and as a result, giant cells appeared. Such giant cells are often more susceptible to infection than unirradiated control cells. It has been reported that human embryonic lung passage cells, which are not susceptible to bluetongue virus, can be infected with giant cells after X-ray irradiation. X-ray-irradiated HeLa cells also have a higher susceptibility to Newcastle disease virus than unirradiated control cells, and the virus yield after infection is also relatively high. This increased susceptibility of cells to viruses caused by X-ray irradiation may be a common phenomenon of RNA viruses, and may also be a cause of increased susceptibility of animal organisms to viral infections after X-ray irradiation. However, it must be pointed out that similar phenomena have not been seen in DNA viruses. Primary X-ray irradiated primary rabbit kidney cells were infected with herpes simplex virus and primary chicken embryo cells were infected with vaccinia virus, and the virus yield was lower than that of unirradiated control cells. It has been suggested that this is the result of X-rays disrupting the metabolism of nucleic acids in cells, thereby affecting the synthesis of viral components in the "virus factory" of the nucleus or cytoplasm. 
[ZZ (D] animal body temperature [ZZ]] also has an effect on viral infection. Mice raised at 2 °C were 100 times more sensitive to mousepox (foot disease) virus than mice fed at 20 °C. The former is 2 to 3 ° C lower than the body temperature of the latter. Adult mice were infected with Coxsackie virus and subsequently divided into three groups and housed at different ambient temperatures of 4 ° C, 25 ° C and 36 ° C. The mice fed at 25 °C had a normal body temperature of 37-38 ° C; the mice fed at 4 ° C had a body temperature 2 ° C lower than normal; the mice fed at 36 ° C had a higher body temperature than normal 2 °C. In mice fed at 25 ° C, Coxsackie virus infection was confined to the pancreas, with very few deaths. In mice fed at 36 ° C, the virus did not proliferate and all mice survived. In contrast, in mice fed at 4 ° C, the virus proliferated in a large amount, causing a consistent death infection. A mouse strain adapted to poliovirus was used for intracerebral inoculation. A similar phenomenon occurred: most mice that were bred at room temperature (20 °C) died, while mice fed at 36 °C lost half of their mortality, even Death, the disease period is also longer than the control mice. Increased body temperature may appear to directly or indirectly inhibit viral proliferation by affecting a certain proliferative phase of the virus or stimulating the body's immune response, such as antibody and interferon production. However, it must be pointed out that almost all fevers of 38 to 41 ° C or higher will occur in mammals in the case of severe viral infections. Is this a positive defense response to the body's inhibition of viral proliferation? Or is it a pathological effect stimulated by a virus or a pyrogenic antigen-antibody complex? The situation is complex and is determined by many factors. It is difficult to make a positive or negative answer before it has fully understood its objective laws. Lwoff believes that a highly virulent virus that can proliferate in febrile animals is the result of natural selection.
3. The external environmental conditions indirectly affect the infection process of the virus, including climatic conditions, geographical environment and feeding management methods, in terms of its effects on both viruses and animal organisms.

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