virus
any member of a unique class of infectious agents, which were originally distinguished by their smallness (hence, they were described as “filtrable” because of their ability to pass through fine ceramic filters that blocked all cells, including bacteria) and their inability to replicate outside of and without assistance of a living host cell. Because these properties are shared by certain bacteria (rickettsiae, chlamydiae), viruses are now characterized by their simple organization and their unique mode of replication. A virus consists of genetic material, which may be either DNA or RNA, and is surrounded by a protein coat and, in some viruses, by a membranous envelope.
Unlike cellular organisms, viruses do not contain all the biochemical mechanisms for their own replication; they replicate by using the biochemical mechanisms of a host cell to synthesize and assemble their separate components. (Some do contain or produce essential enzymes when there is no cellular enzyme that will serve.) When a complete virus particle (virion) comes in contact with a host cell, only the viral nucleic acid and, in some viruses, a few enzymes are injected into the host cell.
Within the host cell the genetic material of a DNA virus is replicated and transcribed into messenger RNA by host cell enzymes, and proteins coded for by viral genes are synthesized by host cell ribosomes. These are the proteins that form the capsid (protein coat); there may also be a few enzymes or regulatory proteins involved in assembling the capsid around newly synthesized viral nucleic acid, in controlling the biochemical mechanisms of the host cell, and in lysing the host cell when new virions have been assembled. Some of these may already have been present within the initial virus, and others may be coded for by the viral genome for production within the host cell.

Because host cells do not have the ability to replicate “viral RNA” but are able to transcribe messenger RNA, RNA viruses must contain enzymes to produce genetic material for new virions. For certain viruses the RNA is replicated by a viral enzyme (transcriptase) contained in the virion, or produced by the host cell using the viral RNA as a messenger. In other viruses a reverse transcriptase contained in the virion transcribes the genetic message on the viral RNA into DNA, which is then replicated by the host cell. Reverse transcriptase is actually a combination of two enzymes: a polymerase that assembles the new DNA copy and an RNase that degrades the source RNA.

In viruses that have membranes, membrane-bound viral proteins are synthesized by the host cell and move, like host cell membrane proteins, to the cell surface. When these proteins assemble to form the capsid, part of the host cell membrane is pinched off to form the envelope of the virion.

Some viruses have only a few genes coding for capsid proteins. Other more complex ones may have a few hundred genes. But no virus has the thousands of genes required by even the simplest cells. Although in general viruses “steal” their lipid envelope from the host cell, virtually all of them produce “envelope proteins” that penetrate the envelope and serve as receptors. Some envelope proteins facilitate viral entry into the cell, and others have directly pathogenic effects.

Some viruses do not produce rapid lysis of host cells, but rather remain latent for long periods in the host before the appearance of clinical symptoms. This carrier state can take any of several different forms. The term latency is used to denote the interval from infection to clinical manifestations. In the lentiviruses, it was formerly mistakenly believed that virus was inactive during this period. The true situation is that lentiviruses are rapidly replicating and spawning dozens of quasi-species until a particularly effective one overruns the ability of the host's immune system to defeat it. Other viruses, however, such as the herpesviruses, actually enter a time known as “viral latency,” when little or no replication is taking place until further replication is initiated by a specific trigger. For many years all forms of latency were thought to be identical, but now it has been discovered that there are different types with basic and important distinctions.

In viral latency, most of the host cells may be protected from infection by immune mechanisms involving antibodies to the viral particles or interferon. Cell-mediated immunity is essential, especially in dealing with infected host cells. Cytotoxic lymphocytes may also act as antigen-presenting cells to better coordinate the immune response. Containment of virus in mucosal tissues is far more complex, involving follicular dendritic cells and Langerhans cells.

Some enveloped RNA viruses can be produced in infected cells that continue growing and dividing without being killed. This probably involves some sort of intracellular regulation of viral growth. It is also possible for the DNA of some viruses to be incorporated into the host cell DNA, producing a carrier state. These are almost always retroviruses, which are called proviruses before and after integration of viral DNA into the host genome.

Few viruses produce toxins, although viral infections of bacteria can cause previously innocuous bacteria to become much more pathogenic and toxic. Other viral proteins, such as some of the human immunodeficiency virus, appear to be actively toxic, but those are the exception, not the rule.

However, viruses are highly antigenic. Mechanisms of pathologic injury to cells include cell lysis; induction of cell proliferation (as in certain warts and molluscum contagiosum); formation of giant cells, syncytia, or intracellular inclusion bodies caused by the virus; and perhaps most importantly, symptoms caused by the host's immune response, such as inflammation or the deposition of antigen-antibody complexes in tissues.

以下为上文的机器翻译
virus 病毒
任何成份的独特种类感染因子，它们的特点是体积小（因此，它们被称为“可过滤的”，因为它们能够通过能够阻止包括细菌在内的所有细胞的精细陶瓷过滤器的能力），并且无法在活的宿主细胞外或没有宿主细胞的帮助下复制。由于某些细菌（立克次氏体，衣原体）具有这些特性，因此病毒的特征在于其简单的组织和独特的复制方式。病毒由遗传物质组成，可以是DNA或RNA，并被蛋白外壳所包围，在某些病毒中被膜外壳包围。
与细胞生物不同，病毒并不包含其自身复制的所有生化机制。它们利用宿主细胞的生化机制进行复制，以合成并组装它们各自的成分。（当没有细胞酶起作用时，某些酶确实会包含或产生必需的酶。）当完整的病毒颗粒（病毒体）与宿主细胞接触时，只有病毒核酸，而在某些病毒中，只有少数几种酶注入宿主细胞。
在宿主细胞内，DNA病毒的遗传物质被宿主细胞酶复制并转录成信使RNA，而病毒基因编码的蛋白质则由宿主细胞核糖体合成。这些是形成衣壳（蛋白质外壳）的蛋白质。在组装新合成的病毒核酸周围的衣壳，控制宿主细胞的生化机制以及在组装新病毒体时裂解宿主细胞时，可能还涉及一些酶或调节蛋白。其中一些可能已存在于初始病毒中，而其他一些可能已被病毒基因组编码以在宿主细胞内产生。

由于宿主细胞不具有复制“病毒RNA”的能力，但能够转录信使RNA，因此RNA病毒必须包含酶以产生新病毒体的遗传物质。对于某些病毒，RNA可通过病毒粒子中包含的病毒酶（转录酶）复制，或由宿主细胞使用病毒RNA作为信使产生。在其他病毒中，病毒粒子中包含的逆转录酶将病毒RNA上的遗传信息转录为DNA，然后由宿主细胞复制。逆转录酶实际上是两种酶的组合：组装新DNA拷贝的聚合酶和降解源RNA的RNase。

在具有膜的病毒中，膜结合的病毒蛋白由宿主细胞合成，并像宿主细胞的膜蛋白一样移动到细胞表面。当这些蛋白质组装形成衣壳时，宿主细胞膜的一部分被夹住以形成病毒体的包膜。

一些病毒只有少数几个编码衣壳蛋白的基因。其他更复杂的基因可能具有数百个基因。但是，没有哪一种病毒具有最简单的细胞所需的数千种基因。尽管在一般情况下，病毒从宿主细胞“窃取”了它们的脂质包膜，但实际上所有病毒都会产生“包膜蛋白”，该蛋白穿透包膜并充当受体。一些包膜蛋白促进病毒进入细胞，而另一些则具有直接的致病作用。

一些病毒不会产生宿主细胞的快速裂解，而是会在临床症状出现之前在宿主中长期保持潜伏状态。该载波状态可以采用几种不同形式中的任何一种。术语潜伏期用于表示从感染到临床表现的间隔。在慢病毒中，以前曾错误地认为病毒在此期间没有活性。真正的情况是，慢病毒正在迅速复制并产生数十个准物种，直到特别有效的慢病毒破坏了宿主免疫系统对其的抵抗能力。但是，其他病毒（例如疱疹病毒）实际上会进入一个称为“病毒潜伏期”的时间，即很少或没有进行任何复制，直到由特定触发器启动进一步复制为止。

在病毒潜伏期中，可通过涉及病毒颗粒或干扰素抗体的免疫机制保护大多数宿主细胞免受感染。细胞介导的免疫力至关重要，尤其是在处理感染的宿主细胞时。细胞毒性淋巴细胞也可以充当抗原呈递细胞，以更好地协调免疫反应。粘膜组织中病毒的遏制要复杂得多，涉及滤泡树突状细胞和朗格汉斯细胞。

可以在受感染的细胞中产生一些包膜的RNA病毒，这些细胞继续生长和分裂而不会被杀死。这可能涉及某种病毒生长的细胞内调节。某些病毒的DNA也可能被整合到宿主细胞的DNA中，从而产生载体状态。这些几乎总是逆转录病毒，在病毒DNA整合入宿主基因组之前和之后称为前病毒。

很少有病毒产生毒素，尽管细菌的病毒感染会导致以前无害的细菌变得更具致病性和毒性。其他病毒蛋白，例如某些人类免疫缺陷病毒，似乎具有积极的毒性，但这些只是例外，并非常规。

但是，病毒具有高度抗原性。细胞病理性损伤的机制包括细胞裂解；诱导细胞增殖（如在某些疣和传染性软体动物中）；由病毒引起的巨细胞，合胞体或细胞内包涵体的形成；可能是最重要的是由宿主的免疫反应引起的症状，例如炎症或组织中抗原抗体复合物的沉积。

由于病毒繁殖几乎完全是通过宿主细胞机制完成的，因此在此过程中很少有一点可以阻止病毒繁殖也不会杀死宿主细胞。因此，对于大多数病毒性疾病没有化学治疗剂。阿昔洛韦是一种抗病毒药物，需要病毒蛋白才能发挥活性。可以通过疫苗接种（主动免疫）预防某些病毒感染，而可以通过免疫球蛋白被动免疫来治疗其他病毒感染，尽管已证明这种病毒感染仅对几十种病毒有效。

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1.专升本可以自主择校吗？

解:

不行，统招制的专升本 不同于 成人本科，对口本科学校是由你的专科学校选择，并且需要与对口本科学院进行协商，一般与对口本科学校签订三年，大概三年一换，如何合作的好，会继续合作。