Hara I, Izui S, McConahey P J, Elder J H, Jensen F C, Dixon F J
Proc Natl Acad Sci U S A. 1981 Jul;78(7):4397-401. doi: 10.1073/pnas.78.7.4397.
In the present study, mice each given a single intraperitoneal injection of Escherichia coli lipopolysaccharide (LPS) responded with increased serum levels of the major envelope glycoprotein, gp70, of endogenous retrovirus. Concentrations of gp70 in their sera began to increase 4 hr after LPS injection, reached maximal 5- to 15-fold increases after 12--24 hr, and returned to the preinjection levels within 3 days. This response occurred only in the strains characterized by high base line levels of serum gp70 (greater than 10 micrograms/ml) such as NZB, NZB X NZW F1, BXSB, MRL, NZW, DBA/2, LG, 129(GIX+), and C57BL/6(GIX+). However, strains such as DBA/1, C3H/St, BALB/c, C57BL/6(GIX-), and 129(GIX-) with lower base line levels of serum gp70 (less than 5 micrograms/ml) made little or no response. This serum gp70 induced by LPS was structurally similar to the gp70 of NZB xenotropic virus that is dominantly expressed in sera from virtually all strains of mice. However, (i) the induced gp70 was virion-free; (ii) xenotropic virus was not isolatable from BXSB, MRL/1, or 129(GIX+) mice injected with LPS; and (iii) amounts of the major structural viral protein, p30, did not increase correspondingly in sera. All of these findings indicate that the increased expression of serum xenotropic viral gp70 in response to LPS did not result from activation of replication-competent xenotropic virus. In addition, the serum gp70 response to LPS was abolished by simultaneous inoculation of an inhibitor of protein synthesis, D-galactosamine. These results strongly suggest that LPS selectively stimulates synthesis of the env gene product, gp70, of NZB xenotropic virus but other viral gene products.
在本研究中,每只经腹腔单次注射大肠杆菌脂多糖(LPS)的小鼠,其血清中内源性逆转录病毒主要包膜糖蛋白gp70的水平均升高。LPS注射后4小时,其血清中gp70的浓度开始升高,12 - 24小时后达到最大升高5至15倍,并在3天内恢复到注射前水平。这种反应仅发生在血清gp70基线水平较高(大于10微克/毫升)的品系中,如NZB、NZB×NZW F1、BXSB、MRL、NZW、DBA/2、LG、129(GIX +)和C57BL/6(GIX +)。然而,血清gp70基线水平较低(小于5微克/毫升)的品系,如DBA/1、C3H/St、BALB/c、C57BL/6(GIX -)和129(GIX -),则几乎没有反应或无反应。LPS诱导产生的这种血清gp70在结构上与NZB嗜异性病毒的gp70相似,而NZB嗜异性病毒在几乎所有小鼠品系的血清中均占主导地位表达。然而,(i)诱导产生的gp70不含病毒颗粒;(ii)从注射LPS的BXSB、MRL/1或129(GIX +)小鼠中无法分离出嗜异性病毒;(iii)血清中主要结构病毒蛋白p30的量并未相应增加。所有这些发现表明,LPS刺激后血清嗜异性病毒gp70表达增加并非由具有复制能力的嗜异性病毒激活所致。此外,同时接种蛋白质合成抑制剂D - 半乳糖胺可消除血清gp70对LPS的反应。这些结果强烈表明,LPS选择性刺激NZB嗜异性病毒env基因产物gp70的合成,但不刺激其他病毒基因产物的合成。