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[I include some comments from studyforhope from Medhelp that may inform the readers.
Many thanks to studyforhope.]
Studforhope:
The percentage of infected cells does reduce during antiviral reatment but only by about 50 to 90% as numerous cccDNA studies on biopsies have shown.
The key question, in light of the above, is therefore why do antivirals prevent, in most cases, a further progression of liver disease, reduce ALT, inflammation and fibrosis?
While this is now an undisputed fact, most hepatologist will not be able give you an answer to this question because their training in immunology is limited and the detailed mechanisms are only partially clarified.
However, the most likely reason for this very critical and beneficial phenomenon is, that it is the amount/number of virions, secreted and often captured in the liver by macrophages and dendritic cells,
MOSTLY BY THE PRESENCE OF INTACT CORES WITHIN THOSE VIRIONS,
that ACTIVATE immune responses, often of a type with low effectiveness, but a higher grade inflammation cytokine profile, that cause the intensity of inflammation in the liver,
Remember that a virus has to be seen by its products, by immune cells. The core protein, mostly intact or partly assembled cores as well that are displayed to the macrophages upon hepatocyte death is highly immunogenic and has several classII T cell epitopes that will stimulate CD4 helper T cells upon contact with macrophages or dendritic cells . These stimulated cd4 Tcells then produce inflammatory cytokine cocktails and also stimulate Bcells, cd8Tcells and NKcells by direct contact (cd40 ligand mediated).
All this increases the severity of ongoing hepatitis B, is only moderately effective in inhibiting cccDNA expression and HBV replication and leads therefore to the battle with no end that we call chronic hepatitis B.
Antivirals strongly reduce the primary stimulus (the secreted virions) to this vicious cycle, that is how they exert their fundamental benefit. 
Apr 10, 2012
An additional important reason that makes virions so much more immunostimulatory than surface antigen particles ( they actually suppress macrophage activation and dendritic cell activation) is the presence of the single stranded region in the HBV DNA inside the virions. Single stranded DNA is a very strong immunostimulant, it combines with the presence of the core to activate a whole cascade of immune reactions as described above.
It needs to be emphasized that not all cytokines are equally effective to induce antiviral mechanisms inside the infected hepatocytes. Interferon gamma, Interleukin18 and Il-12 are the most effective without having an excessive collateral unspecific proinflammatory effect. Their preferential secretion by cytotoxic cd8 positive Tcells specific for virus specific epitopes is most likely the basis for the sometimes surprising reduction of virimia and cccDNA seen in some patients with very little ALT elevations.
This is the "good" antiviral immunity that is desirable, but we have not yet found the magic switch to turn this on, possibly because it depends both on the presence of high affinity HBV class I epitopes combined with CTLs that are not tolerized and impaired in their response.
We can speculate, that the powerful results that we see currently emerging from the TLR7agonist trials are due to a selective direction of the cytokine response profile in the direction of this "effective, good" immunity, with less collateral damage.
[我从studyforhope从Medhelp一些意见，可告知读者。
非常感谢studyforhope。
studforhope：
感染细胞的比例减少reatment抗病毒药物，但只有约50％至90％，众多活检cccDNA的研究显示。
关键的问题，鉴于上述情况，因此，为什么抗病毒药物预防，在大多数情况下，肝脏疾病的进一步恶化，降低血清ALT，炎症和纤维化？
虽然这是一个不争的事实，大多数肝病将不能够给你这个问题的答案，因为他们的免疫学的培训是有限的，只有部分澄清的详细机制。
然而，这个非常重要和有益的现象最可能的原因是，它是病毒粒子，由巨噬细胞和树突状细胞分泌常常在肝脏中捕获的金额/数量，
大多是由完整的内核在这些病毒颗粒的存在，
激活免疫反应，往往与低效益的类型，但档次较高的炎症细胞因子的个人资料，导致肝脏炎症的强度，
请记住，病毒有免疫细胞，其产品被看到。核心蛋白，大多保存完好或部分组装的核心以及所显示的肝细胞死亡后的巨噬细胞是具有高度免疫原性，并有几个classII T细胞表位，会刺激CD4 +辅助性T细胞与巨噬细胞或树突状细胞接触后。这些刺激的CD4 Tcells然后产生炎性细胞因子鸡尾酒和也刺激Bcells，的cd8Tcells和NKcells的直接接触（CD40配体介导的）。
这一切都增加了正在进行的B型肝炎的严重性，仅仅是适度有效地抑制cccDNA的表达与HBV复制，并因此导致战斗没有结束，我们称之为慢性乙型肝炎
抗病毒药物的强烈减少这种恶性循环的主要刺激（分泌病毒颗粒），这是他们如何发挥他们的根本利益。
2012年04月10日，
另外一个重要原因，使病毒粒子，远远超过表面抗原颗粒（实际上，他们抑制活化巨噬细胞和树突状细胞活化）的免疫刺激的单链区域内的病毒颗粒乙型肝炎病毒DNA的存在。单链DNA是很强的immunostimulant，它结合了激活整个免疫反应级联，如上所述，核心的存在。
需要强调的，并非所有的细胞因子诱导抗病毒感染的肝细胞内的机制同样有效。 Interleukin18和干扰素γ，IL-12是最有效，而无需过多的抵押品的非特异性炎症效果。他们通过CD8细胞毒性的病毒特异性抗原表位的具体积极Tcells优惠分泌是最有可能有时令人惊讶的看到一些患者很少ALT升高的的virimia与cccDNA减少的基础上。
这是“好”的抗病毒免疫，这是可取的，但我们还没有找到打开这个神奇的开关，可能是因为它取决于同时存在，我不tolerized和受损的淋巴细胞表位结合的高亲和力HBV类在他们的反应。
我们可以推测，这是由于强大的结果，我们看到目前新兴从TLR7agonist试验的细胞因子的响应曲线在这个“有效的，良好的”免疫力减少附带损害，方向选择性方向。
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发表于 2012-4-13 23:26
of HBsAg-pulsed DC were evaluated. Circulating unpulsed DC and HBsAg-pulsed DC showed significantly higher levels of T-cell proliferation capacities 1 month after lamivudine therapy compared to proliferation levels before therapy (P < 0.05). HBsAg-pulsed DC also produced significantly higher levels of IL-12 and IFN-
