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猫白血病病毒诱发猫获得性免疫缺陷综合征:下丘脑-垂体-性腺系统中激素反应的改变。

Induction of feline acquired immune deficiency syndrome by feline leukemia virus: alteration in response to hormones in the hypothalamic-pituitary-gonadal system.

作者信息

Wang S W, Teng C S

机构信息

Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh 27606.

出版信息

Proc Soc Exp Biol Med. 1995 Apr;208(4):404-12. doi: 10.3181/00379727-208-43869.

DOI:10.3181/00379727-208-43869
PMID:7700890
Abstract

Male kittens who were infected with the feline leukemia virus (FeLV) were found at various times after exposure to contain a sequence of dysfunction in their hypothalamic-pituitary-gonadal (HPG) system. To understand whether the involved endocrine glands in this system were damaged by FeLV, the hypothalamus, pituitary, and testes were tested for hormonal responsiveness in vivo and in vitro. The infected cats were administered with luteinizing hormone-releasing hormone (LHRH) and human chorionic gonadotropin (hCG). Their response to the treatment was studied, and they were then compared with untreated control cats. Normal response to LHRH for the synthesis of follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone were found in the infected cats prior to 10 weeks of infection. After 10 weeks, the response was reduced by 25%, 38%, and 42%, respectively. Twelve weeks after infection, the response to hCG for testosterone synthesis was drastically reduced. The control cats, however, demonstrated normal prolonged biphasic patterns of response to hCG. The in vivo administration of the tropic hormones had no effect on the titer of FeLV gs antigen in the blood of the infected cats. The medial basal hypothalamus (MBH) from the control cats and cats in their 13th week of infection were cultured in vitro, with the presence of high K+ ion (60 mM). The control MBH responded to K+ ion stimulation for LHRH release. The K(+)-stimulated release of LHRH in the control MBH was 99% higher than that of the infected MBH. In contrast, the amount of unreleased LHRH in the infected MBH was 74% higher than that of the control MBH. In in vitro culture, the control pituitary gland responded markedly higher to LHRH stimulation for the release of gonadotropins (FHS and LH) than that of the infected one (140% compared with 56% for FSH, and 70% compared with 28% for LH, respectively). Whereas, the amount of unreleased FSH and LH in the infected pituitary gland were 59% and 31%, higher than that of the control gland. These results suggest that (i) the progressive development of neuroendocrine glands' dysfunction is related to viral replication time; (ii) the in vivo and in vitro responses to tropic hormones in the infected endocrine glands are drastically reduced; and (iii) this reduction in hormonal response may be caused by defective regulation of peptide hormonal secretion.

摘要

感染猫白血病病毒(FeLV)的雄性小猫在接触病毒后的不同时间被发现其下丘脑 - 垂体 - 性腺(HPG)系统存在一系列功能障碍。为了解该系统中涉及的内分泌腺是否受到FeLV的损害,对下丘脑、垂体和睾丸进行了体内和体外激素反应测试。给感染的猫注射促黄体生成素释放激素(LHRH)和人绒毛膜促性腺激素(hCG)。研究它们对治疗的反应,然后与未治疗的对照猫进行比较。在感染10周之前,感染的猫对LHRH刺激合成促卵泡激素(FSH)、促黄体生成素(LH)和睾酮有正常反应。10周后,反应分别降低了25%、38%和42%。感染12周后,对hCG刺激睾酮合成的反应急剧降低。然而,对照猫对hCG表现出正常的双相延长反应模式。给感染的猫体内注射促性腺激素对其血液中FeLV gs抗原的滴度没有影响。将对照猫和感染13周的猫的内侧基底下丘脑(MBH)进行体外培养,并加入高钾离子(60 mM)。对照MBH对钾离子刺激释放LHRH有反应。对照MBH中钾离子刺激的LHRH释放比感染的MBH高99%。相反,感染的MBH中未释放的LHRH量比对照MBH高74%。在体外培养中,对照垂体对LHRH刺激释放促性腺激素(FHS和LH)的反应明显高于感染的垂体(FSH分别为140%比56%;LH分别为70%比28%)。而感染的垂体中未释放的FSH和LH量分别比对照垂体高59%和31%。这些结果表明:(i)神经内分泌腺功能障碍的渐进发展与病毒复制时间有关;(ii)感染的内分泌腺对促性腺激素的体内和体外反应急剧降低;(iii)激素反应的这种降低可能是由肽类激素分泌的调节缺陷引起的。

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