Chetverikova L K, Frolov B A, Kramskaya T A
Research In stitute of Experimental Medicine, U.S.S.R. Academy of Medical Sciences, Leningrad.
Acta Virol. 1987 Sep;31(5):424-33.
The effect of immobilization stress on the course of various forms of influenza infection has been investigated. Influenza was produced in 10-14-week-old inbred mice by intranasal infection with pathogenic influenza virus strain A/PR/8/34 (H1N1) at different doses. Immobilization for 6 hr resulted in the appearance of virus-inhibiting activity in the serum of mice. This activity suppressed the reproduction of test-virus in tissue culture, it was resistant to acid pH 2.0 treatment and to heating at 56 degrees C. However, the high level of virus-inhibiting activity failed to protect the animals from subsequent development of lethal influenza infection. Immobilization stress caused a transient depression of virus induced interferon (IFN) production, as revealed by the use of virus inducer at early intervals after stress. Contemporarily, the stress could aggravate the course of virus infection promoting its transition from non-lethal form into a lethal one and virus penetration into brain.
研究了制动应激对各种形式流感感染病程的影响。通过用不同剂量的致病性甲型流感病毒株A/PR/8/34（H1N1）经鼻内感染10 - 14周龄的近交系小鼠来诱发流感。制动6小时导致小鼠血清中出现病毒抑制活性。这种活性抑制了测试病毒在组织培养中的繁殖，它对pH 2.0的酸性处理和56℃加热具有抗性。然而，高水平的病毒抑制活性未能保护动物免受随后致命性流感感染的发展。如在应激后早期使用病毒诱导剂所显示的，制动应激导致病毒诱导的干扰素（IFN）产生短暂抑制。同时，应激可加重病毒感染的病程，促进其从非致死形式转变为致死形式，并使病毒渗入大脑。
