2016년 4월 25일 월요일

Internal retrovirus

Internal retrovirus

Genealogical tree indicating the internal retroviral classification

With internal retroviral (Endogenous retrovirus, ERV), I point to the thing similar to a retrovirus probably derived from a retrovirus in existing internal viruslike sequence in a genome. Is seen in the genome of the chin statement rope well, and occupy 5–8% (even at least ~1%) of the human genome [1]; [2]. ERV is packaged with genetic kind called the transposon, and it can travel the genome, and is indispensable in gene expression and adjustment (English version); play a role [3]; [4]. According to the researcher, it is suggested that the retrovirus evolved from a flexible gene (English version) called the retrotransposon including ERV. Not only it travels the genome by mutation, but also these genes become the externality and may get infectiousness. From this, all ERV may not be necessarily the results of the genetic insertion by the retrovirus, and there may be the thing which became retroviral former genetic information adversely [5].

Generation

For a retroviral reproduction cycle, it is necessary for the thing which copied the genome of the virus to DNA to be inserted in the nucleus genome of the host (incorporated). Most retroviruses infect a somatic cell, but it is possible to be infected with a generative cell (cell producing an ovum and sperms). A retrovirus may rarely occur in the uncooked food individual which is 存可能. This individual has retroviral genome that is internal retroviral (endogenous retrovirus, ERV) in form incorporated in a genome of the self, and the descendant (English version) will inherit it as the allele that standing is new hereditarily. Much ERV is left in the genome of the host for millions of years. However, in the case of the replication of DNA of the host, I almost receive inactivating mutation and lose the ability to already produce viruses. ERV may be removed surgically partially by the process that the protein coding domain in the virus genome is deleted again by recombination with the same sequence adjacent to a retrovirus incorporated newly called recombinational deletion.

Role in the genome evolution

The internal retrovirus may play an active role in the genome formation. Most studies in this field focus on Homo sapiens and a high primate, but the vertebrates such as a mouse or the sheep are studied deeply [6]; [7] [8] [9]. The sequence often commits LTR (English version) adjacent to ERV genome as a promoter and an enhancer (Long Terminal Repeat), but contributes to transcriptome in form to often produce a tissue-specific variant. In addition, for the function of the host that retroviral origin protein in itself is new particularly breeding and development co; is optimized. The recombination between the homology retroviral origin sequence contributes to gene shuffle and the refinement of the genetic diversity, too. Besides, repressor gene coevolutes it to face harmful retroviral origin sequence potentially.

It is shown that the LTR which bound to Solo-LTR and the complete retroviral origin sequence works as a transcription element in the host gene both. These territories are the insertion to 5' side UTR of the protein coding domain mainly, but a 70-100 kb away gene understands that work [6]; [10] [11] [12]. Most of these elements are inserted in the supporting genetic sense direction, but there is the evidence indicating LTR working as the antisense direction of the adjacent gene and two ways promoter [13]; [14]. In some cases, the LTR functions as a genetic main promoter. For example, there is complete ERV sequence in the promoter domain of human AMY1C. The connected LTR produces amylase of the digestive enzyme only in saliva [15]. In addition, the enzyme which is essential to choler metabolism, bile acid CoA: The main promoter of amino acid N- acyl transferase (English version) (BAAT) is the LTR origin, too [11]; [16].

The insertion of the Solo-ERV-9 LTR might generate the open leading flame (ORF) of the function to cause reproduction of human immune system GTP アーゼ gene (English version) (IRGM) [17]. It is known that there is a new splice part by the ERV insertion. It may be driven like phospholipase A2-like protein by expression of LTR of upper reaches what is incorporated in a gene like a human leptin hormone acceptor directly [18].

However, the LTR functions as one in a large number of promoters in most cases and is often concerned with reproduction and the tissue-specific expression of the gene about outbreak. Actually, 64% of トランスクリプションバリアント where known LTR acts on as a promoter develop in a reproduction organization [19]. Gene CYP19 encoding enzyme aromatase (English version) P450 which is important to estrogen composition as an example develops with brain and the sex organs in most mammals [11]. However, トランスクリプショナルバリアント which assumes LTR about expression in the placenta a promoter controls pregnant estrogen density in the primates [11]. Furthermore, apoptotic inhibition protein (English version) (NAIP) is usually seen broadly, but the LTR of the HERV-P family works as a promoter concerned with the expression with the testicles and the prostate [20]. Other protein such as HSD17B1 which is nitric acid synthetase 3 (NOS3), interleukin-2 receptor B (IL2RB), another intermediate of the estrogen composition is controlled by LTR concerned with the expression in the placenta, but, as for, is detailed, working, it is yet unknown [16]; [21]. It is said that it is a result of the methods of the internalization that there is much expression about generative function, but it may be said that it is the result of there being little DNA methylation with the sex organs [16].

A promoter is not a host gene, and the example of the placenta protein expression checked in greatest detail is absorption of the retroviral origin protein. The retroviral origin membrane fusion-related envelope protein about invasion to the host cell of the virus particle has influence that it is important to mammalian placenta outbreak. 合胞体性栄養膜 forms it of the mammals by envelope protein of the complete form called シンシチン (English version) and functions and functions [8]. These coenocytes act to isolate the maintenance of the trophallaxis and the immune system between a fetus, the mother's body mainly [8]. It is suggested that choice and fixation of these protein to this function took the role that is indispensable for viviparous evolution [22].

In addition, the ERV insertion and the LTR have power to raise chromosome relocation by recombination between the sequence derived from a virus in the heredity stroma which stepped over the chromosome. A gene duplication and deletion are shown to take place by this rearrangement, and genomic plasticity in this way improves, and the dramatic change of the dynamic gene function is angry [23]. In addition, there are many nostalgic elements in mammals special gene about the reaction to stress evolving rapidly and external stimulation [11]. Particularly, a class I (English version) gene of human MHC and the class II (English version) gene have the HERV element density that is higher than other many seats gene families both [18]. It is shown that HERV contributed to the formation of the on a large scale redundant re-kombu lock to duplicate constituting the gene of the HLA class 1 family [24]. HERV is distributed mainly in greater detail between out of this break point blocking or a breakpoint and a breakpoint. From this, for the formation of this block, what a great deal of overlap to cause unequal crossover typically and a deletion event were concerned with is suggested [25]. The generation of this block is inherited as immune ハプロタイプ and works as protection seasonal polymorphism for the widespread antigen. This gives the superiority for other primates to Homo sapiens [24].

Finally the overexpression of insertion to the gene domain of host DNA of ERV and the ERV element or トランスクリプショナルバリアント is more likely to cause the effect that is more harmful than a useful effect. When these appear in a genome, I cause a host, parasitism all of you evolution (English version) and let the overlap of the rep Loesser gene and expansion increase remarkably. These clear most in a mammalian genome in question cause rapid overlap and the rapid increase of the tandem zinc finger gene. There is a high copy number to the thing including zinc finger gene particularly the KRAB domain in the genome of the vertebrate, and the function range is limited to a role of トランスプリション [26]. It is shown that these genes diversified by the multiplex reproduction which got up to control those トランスクプション as a reaction to in the mammals but new retroviral origin sequence or the internal copy and a fixation event [12].

Role in the illness

Ancient, most of ERV seen in a vertebrate genome are inactivated by mutation and come to make fixation (English version) to the straight seed of the host. Therefore, a host does not have the adverse effects except the special situation. Still, as a result of mammalian study except the Homo sapiens such as birds and a mouse, a cat, the koala (English version), it is apparent that ERV which is relatively young (was incorporated recently) causes illness. Therefore, the researcher cites ERV as a factor of some cancers and autoimmune disease of the Homo sapiens, but the conclusive evidence is not found [27]; [28] [29].

It is said that ERV participates in multiple sclerosis (multiple sclerosis, MS) in the Homo sapiens. From the patient who the association between multiple sclerosis and シンシチン gene (ERVWE1 (English version)) which occurred because of the ERV insertion is reported, and contracts a disease by this disease again "multiple sclerosis-related; retroviral", (MSRV) is detected [30]; [31]. That human ERV (HERV) affects ALS [32].

It was reported that a lot of antibodies from the juice of the schizophrenia patient to HERV were detected in 2004. In addition, a sign of schizophrenia was most recent, and the reverse transcriptase which was a retroviral marker was detected in density 4 times as large as symmetric group from the cerebrospinal fluid of seen people [33]. The researcher continues looking for an association between HERV and schizophrenia including possibility to cause infectious schizophrenia [34].

Human internal retroviral

The provirus of human internal retroviral (HERV) constitutes a considerable part of the human genome, and 98,000 ERV elements and fragment occupy 5-8% of the human genome [1]. According to the study announced in 2005, HERV which I can multiply is not found. All seems to have deletion or a meaningless mutant defect. This is because most HERV is only the traces of the original virus incorporated in human genome in old days of millions of years.

But the virus of a certain family is active since the divergence of Homo sapiens and the chimpanzee. This family is called HERV-K (English version) (HML2) and it does not reach 1% among HERV elements, but is one of HERV studied most. The Homo sapiens who usually has more HML2 is found and suggests that this was active until hundreds of thousands of years ago [35]. The age estimate of HERV is carried out traditionally by comparing the LTR (English version) of 3' sides with 5' sides, but this technique is applicable only to HERV of the full length. I can suppose the generation of the HERV insertion only using [36], single LTR by the technique called newer cross-sectional dating. I can suppose age of HERV more exactly and can use this technique for any HERV insertion. Using Cross-sectional dating, it is suggested that thing, HERV-K106 where member HERV-K106 and HERV-K116 of HERV-K(HML2) were active for 800,000 years infected Homo sapiens 150,000 years ago [37]. However, the thing with the infectiousness is not known in HERV-K(HML2) family and is less likely to be active now because I cannot see the thing having ability for complete coding within the announced human genome sequence. In 2006 and 2007, France and a researcher of Eymet Rika composed a version to function of HERV-K(HML2) again independently each [38]; [39].

The evidence of immunoreacting of the T cell for HERV is discovered in the Homo sapiens infected with HIV by an immunologic study [40]. HIV is an infected cell, and, based on a hypothesis that expression of HERV is caused, it is suggested by vaccine targeting HERV antigen when I may remove an HIV infection cell selectively. The potential advantage of this new approach is to be able to evade the difficulty of variation targeting HIV antigens very various fast directly by assuming HERV antigen the substitute marker of the HIV infection cell.

There are some classes where an open leading frame is stored to a human internal retrovirus. For example, family, HERV-K of active HERV develop with the placenta, and they produce protein biologically. In addition, the envelope gene (ERVW-1, ERVFRD-1) of HERV-W (English version) and HERV-FRD (English version) produces シンシチン causing important cell fusion in the cell layer formation of 合胞体性栄養膜 in the placenta outbreak [41]. Notation of HERV is determined by HUGO gene glossology Committee (English version) (HGNC) [42].

Allied item

Source

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