看了一下报告,6个小鼠的试验利用的TNF。我估计任意找6个人,让他感染HBV,1周后给他注射干扰素(INF),也会得到类似的效果。因为本来5个人就会自发痊愈,INF加快了进程而已。剩下的一个,感染没有几天,被感染细胞少,治疗理当很快。
不知道你看的哪里的报告、而且、你的估计、是错误的、
These results were confirmed using mice in which the targets of birinapant, the cIAPs, were ablated in the liver ("knock-out mice"). In C3H mice that do not spontaneously clear HBV, birinapant treatment resulted in loss of HBV-DNA, loss of HBsAg and the appearance of anti-HBsAg antibodies.作者: 战天斗hbv 时间: 2015-4-29 20:33
四十己过 发表于 2015-4-29 20:06
回复 HBVcheck 的帖子
同意7676的意见,如果是成人后期感染,多为急性~
These results were confirmed using mice in which the targets of birinapant, the cIAPs, were ablated in the liver ("knock-out mice"). In C3H mice that do not spontaneously clear HBV, birinapant treatment resulted in loss of HBV-DNA, loss of HBsAg and the appearance of anti-HBsAg antibodies.作者: 战天斗hbv 时间: 2015-4-29 20:40
$GILD: fr Norbert: "Hep B cure is one of our largest research programs right now.....We’re looking at compounds that could inhibit cccDNA.."作者: 战天斗hbv 时间: 2015-5-1 18:29
Chronic HBV Infection Can Be Mimicked in a Mouse Model.
We used a previously described method to induce HBV persistence in immunocompetent mice (6). A plasmid containing a 1.2 over length sequence of HBV genotype A was hydrodynamically injected into mice, but in contrast to the previously published protocol, we did not anesthetize animals. Using this modified technique, we did not observe any injection-associated mortality, and C57BL/6 mice showed persistently high serum HBV DNA levels over 8–12 wk (Fig. 1A). Eventually, HBV DNA levels fell in all animals along with the levels of serum HBV surface antigen (HBsAg) (Fig. S1A). The decline in HBV DNA and HBsAg levels coincided with the appearance of anti-HBV antibodies in the serum (Fig. S1B). The initial control of HBV was followed by relapsing and remitting periods of HBV DNA viremia over many months (Fig. 1A). The plasmid backbone used to deliver HBV could not be detected in hydrodynamically injected animals beyond 5 wk after injection (Fig. S1C). These results suggest that the HBV genome persisted as an integrated or episomal form in hepatocytes after the plasmid that was used to induce infection had been cleared. Viral and subviral particles along with HBV e-antigen were detected in the serum, and HBV pregenomic and subgenomic RNAs were present in the livers of hydrodynamically injected animals (Fig. S1 D–F). Mice in which HBV was introduced by hydrodynamic injection began to control HBV DNA levels over a 12-wk period. The control of HBV DNA was associated with a modest, intermittent increase in levels of serum aspartate aminotransferase and alanine aminotransferase that may indicate hepatocyte dysfunction (Fig. S1 G and H). HBV core antigen (HBcAg) was detected in 4–15% of hepatocytes in infected mice using immunofluorescence staining (Fig. 1B). In contrast to C57BL/6 mice, C3H mice (endotoxin-sensitive strain) could not control serum HBV DNA levels and showed persistent viremia for at least 20 wk after induction of infection (Fig. 1C). The cause of the difference in HBV control between the two strains of mice is not clear and warrants additional investigation. Our C57BL/6 mouse model of HBV recapitulated many aspects of human HBV infection, enabling us using gene-targeted mice to dissect host factors that contributed to the initial control of HBV.
慢性HBV感染可在小鼠模型来模拟。