herpes simplex virus type 1

WordNet

1. write by means of a keyboard with types; "type the acceptance letter, please" (同)typewrite
2. a small metal block bearing a raised character on one end; produces a printed character when inked and pressed on paper; "he dropped a case of type, so they made him pick them up"
3. (biology) the taxonomic group whose characteristics are used to define the next higher taxon
4. a subdivision of a particular kind of thing; "what type of sculpture do you prefer?"
5. all of the tokens of the same symbol; "the word `element contains five different types of character"
6. printed characters; "small type is hard to read"
7. identify as belonging to a certain type; "Such people can practically be typed" (同)typecast
8. unornamented; "a simple country schoolhouse"; "her black dress--simple to austerity"
9. any herbaceous plant having medicinal properties
10. (botany) of leaf shapes; of leaves having no divisions or subdivisions (同)unsubdivided
11. having few parts; not complex or complicated or involved; "a simple problem"; "simple mechanisms"; "a simple design"; "a simple substance"
12. a harmful or corrupting agency; "bigotry is a virus that must not be allowed to spread"; "the virus of jealousy is latent in everyone"
13. (virology) ultramicroscopic infectious agent that replicates itself only within cells of living hosts; many are pathogenic; a piece of nucleic acid (DNA or RNA) wrapped in a thin coat of protein
14. a software program capable of reproducing itself and usually capable of causing great harm to files or other programs on the same computer; "a true virus cannot spread to another computer without human assistance" (同)computer virus
15. having only one part or element; "a simplex word has no affixes and is not part of a compound--like `boy compared with `boyish or `house compared with `houseboat"
16. allowing communication in only one direction at a time, or in telegraphy allowing only one message over a line at a time; "simplex system"
17. viral diseases causing eruptions of the skin or mucous membrane
18. any of the animal viruses that cause painful blisters on the skin (同)herpes_virus

PrepTutorEJDIC

1. 〈C〉(…の)『型』,タイプ,類型,種類(kind)《+of+名》 / 〈C〉(その種類の特質を最もよく表している)『典型』,手本,模範《+of+名》 / 〈U〉《集合的に》活字;〈C〉(1個の)活字 / 〈U〉(印刷された)字体,活字 / 〈C〉(貨幣・メダルなどの)模様,図柄 / 〈C〉血液型(blood group) / …‘を'タイプに打つ / (…として)…‘を'分類する《+名+as+名(doing)》 / …‘の'型を決める / タイプライターを打つ
2. 『簡単な』容易な,分かりやすい / (複合に対して)単一の / 『単純な』,込み入っていない / 『純然たる』,全くの / 『飾り気のない』,簡素な,地味な,質素な / 『もったいぶらない』;誠実な,実直な / お人よしの,だまされやすい / 《文》地位のない,普通の,平(ひら)の
3. 薬草,薬用植物
4. ビールス,ろ過性病原体
5. 疱疹(ほうしん)

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/11/23 00:54:53」(JST)

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This article is about the virus. For information about the disease caused by the virus, see Herpes simplex.

Herpes simplex virus
TEM micrograph of a herpes simplex virus.
Virus classification
Group:	Group I (dsDNA)
Order:	Herpesvirales
Family:	Herpesviridae
Subfamily:	Alphaherpesvirinae
Genus:	Simplexvirus
Species
Herpes simplex virus 1 (HSV-1) Herpes simplex virus 2 (HSV-2)

Herpes simplex virus 1 and 2 (HSV-1 and HSV-2), also known as Human herpes virus 1 and 2 (HHV-1 and -2), are two members of the herpes virus family, Herpesviridae, that infect humans. Both HSV-1 (which produces most cold sores) and HSV-2 (which produces most genital herpes) are ubiquitous and contagious. They can be spread when an infected person is producing and shedding the virus. Herpes Simplex can be spread through contact with saliva, such as sharing drinks.

Symptoms of herpes simplex virus infection include watery blisters in the skin or mucous membranes of the mouth, lips or genitals. Lesions heal with a scab characteristic of herpetic disease. Sometimes, the viruses cause very mild or atypical symptoms during outbreaks. However, as neurotropic and neuroinvasive viruses, HSV-1 and -2 persist in the body by becoming latent and hiding from the immune system in the cell bodies of neurons. After the initial or primary infection, some infected people experience sporadic episodes of viral reactivation or outbreaks. In an outbreak, the virus in a nerve cell becomes active and is transported via the neuron's axon to the skin, where virus replication and shedding occur and cause new sores.

Transmission

Main article: Herpes simplex

HSV-1 and -2 are transmitted by contact with an infected area of the skin during re-activations of the virus. Although less likely, the herpes viruses can be transmitted during latency.^{[citation needed]} Transmission is likely to occur during symptomatic re-activation of the virus that causes visible and typical skin sores. Asymptomatic reactivation means that the virus causes atypical, subtle or hard to notice symptoms that are not identified as an active herpes infection. Daily genital swab samples show that HSV-2 is found in a median of 12-28% of days among those who have had an outbreak and 10% of days among those suffering from asymptomatic infection, with many of these episodes occurring without visible outbreak ("subclinical shedding"). For HSV-2, subclinical shedding may account for most of the transmission, and one study found that infection occurred after a median of 40 sex acts. Atypical symptoms are often attributed to other causes such as a yeast infection. HSV-1 is often acquired orally during childhood. It may also be sexually transmitted, including contact with saliva, such as kissing and mouth-to-genital contact (oral sex). HSV-2 is primarily a sexually transmitted infection but rates of HSV-1 genital infections are increasing.

Both viruses may also be transmitted vertically during childbirth, although the real risk is very low. The risk of infection is minimal if the mother has no symptoms or exposed blisters during delivery. The risk is considerable when the mother gets the virus for the first time during late pregnancy.

Herpes simplex viruses can affect areas of skin exposed to contact with an infected person. An example of this is herpetic whitlow which is a herpes infection on the fingers. This was a common affliction of dental surgeons prior to the routine use of gloves when conducting treatment on patients.

Microbiology

Viral structure

Animal herpes viruses all share some common properties. The structure of herpes viruses consists of a relatively large double-stranded, linear DNA genome encased within an icosahedral protein cage called the capsid, which is wrapped in a lipid bilayer called the envelope. The envelope is joined to the capsid by means of a tegument. This complete particle is known as the virion. HSV-1 and HSV-2 each contain at least 74 genes (or open reading frames, ORFs) within their genomes, although speculation over gene crowding allows as many as 84 unique protein coding genes by 94 putative ORFs. These genes encode a variety of proteins involved in forming the capsid, tegument and envelope of the virus, as well as controlling the replication and infectivity of the virus. These genes and their functions are summarized in the table below.

The genomes of HSV1 and HSV2 are complex and contain two unique regions called the long unique region (U_L) and the short unique region (U_S). Of the 74 known ORFs, U_L contains 56 viral genes, whereas U_S contains only 12. Transcription of HSV genes is catalyzed by RNA polymerase II of the infected host. Immediate early genes, which encode proteins that regulate the expression of early and late viral genes, are the first to be expressed following infection. Early gene expression follows, to allow the synthesis of enzymes involved in DNA replication and the production of certain envelope glycoproteins. Expression of late genes occurs last; this group of genes predominantly encode proteins that form the virion particle.

Five proteins from (U_L) form the viral capsid; UL6, UL18, UL35, UL38 and the major capsid protein UL19.

Cellular entry

A simplified diagram of HSV replication

Entry of HSV into the host cell involves interactions of several glycoproteins on the surface of the enveloped virus, with receptors on the surface of the host cell. The envelope covering the virus particle, when bound to specific receptors on the cell surface, will fuse with the host cell membrane and create an opening, or pore, through which the virus enters the host cell.

The sequential stages of HSV entry are analogous to those of other viruses. At first, complementary receptors on the virus and the cell surface bring the viral and cell membranes into proximity. In an intermediate state, the two membranes begin to merge, forming a hemifusion state. Finally, a stable entry pore is formed through which the viral envelope contents are introduced to the host cell. In the case of a herpes virus, initial interactions occur when a viral envelope glycoprotein called glycoprotein C (gC) binds to a cell surface particle called heparan sulfate. A second glycoprotein, glycoprotein D (gD), binds specifically to at least one of three known entry receptors. These include herpesvirus entry mediator(HVEM), nectin-1 and 3-O sulfated heparan sulfate. The receptor provides a strong, fixed attachment to the host cell. These interactions bring the membrane surfaces into mutual proximity and allow for other glycoproteins embedded in the viral envelope to interact with other cell surface molecules. Once bound to the HVEM, gD changes its conformation and interacts with viral glycoproteins H (gH) and L (gL), which form a complex. The interaction of these membrane proteins results in the hemifusion state. Afterward, gB interaction with the gH/gL complex creates an entry pore for the viral capsid. Glycoprotein B interacts with glycosaminoglycans on the surface of the host cell.

Genetic inoculation

After the viral capsid enters the cellular cytoplasm, it is transported to the cell nucleus. Once attached to the nucleus at a nuclear entry pore, the capsid ejects its DNA contents via the capsid portal. The capsid portal is formed by twelve copies of portal protein, UL6, arranged as a ring; the proteins contain a leucine zipper sequence of amino acids which allow them to adhere to each other. Each icosahedral capsid contains a single portal, located in one vertex. The DNA exits the capsid in a single linear segment.

Immune evasion

HSV evades the immune system through interference with MHC class I presentation of antigen on the cell surface. It achieves this through blockade of the transporter associated with antigen processing (TAP) induced by the secretion of ICP-47 by HSV. In the host cell, TAP transports digested viral antigen epitopes from the cytosol to the endoplasmic reticulum, allowing these epitopes to be combined with MHC class I molecules and presented on the surface of the cell. Viral epitope presentation with MHC class I is a requirement for activation of cytotoxic T-lymphocytes (CTLs), the major effectors of the cell-mediated immune response against virally-infected cells. ICP-47 prevents initiation of a CTL-response against HSV, allowing the virus to survive for a protracted period in the host.

Replication

Micrograph showing the viral cytopathic effect of HSV (multi-nucleation, ground glass chromatin).

Following infection of a cell, a cascade of herpes virus proteins, called immediate-early, early, and late, are produced. Research using flow cytometry on another member of the herpes virus family, Kaposi's sarcoma-associated herpesvirus, indicates the possibility of an additional lytic stage, delayed-late. These stages of lytic infection, particularly late lytic, are distinct from the latency stage. In the case of HSV-1, no protein products are detected during latency, whereas they are detected during the lytic cycle.

The early proteins transcribed are used in the regulation of genetic replication of the virus. On entering the cell, an α-TIF protein joins the viral particle and aids in immediate-early transcription. The virion host shutoff protein (VHS or UL41) is very important to viral replication. This enzyme shuts off protein synthesis in the host, degrades host mRNA, helps in viral replication, and regulates gene expression of viral proteins. The viral genome immediately travels to the nucleus but the VHS protein remains in the cytoplasm.

The late proteins are used in to form the capsid and the receptors on the surface of the virus. Packaging of the viral particles — including the genome, core and the capsid - occurs in the nucleus of the cell. Here, concatemers of the viral genome are separated by cleavage and are placed into pre-formed capsids. HSV-1 undergoes a process of primary and secondary envelopment. The primary envelope is acquired by budding into the inner nuclear membrane of the cell. This then fuses with the outer nuclear membrane releasing a naked capsid into the cytoplasm. The virus acquires its final envelope by budding into cytoplasmic vesicles.

Latent infection

HSVs may persist in a quiescent but persistent form known as latent infection, notably in neural ganglia. HSV-1 tends to reside in the trigeminal ganglia, while HSV-2 tends to reside in the sacral ganglia, but note that these are tendencies only, not fixed behavior. During such latent infection of a cell, HSVs express Latency Associated Transcript (LAT) RNA. LAT is known to regulate the host cell genome and interferes with natural cell death mechanisms. By maintaining the host cells, LAT expression preserves a reservoir of the virus, which allows subsequent, usually symptomatic, periodic recurrences or "outbreaks" characteristic of non-latency. Whether or not recurrences are noticeable (symptomatic), viral shedding occurs to produce further infections (usually in a new host, if any). A protein found in neurons may bind to herpes virus DNA and regulate latency. Herpes virus DNA contains a gene for a protein called ICP4, which is an important transactivator of genes associated with lytic infection in HSV-1. Elements surrounding the gene for ICP4 bind a protein known as the human neuronal protein Neuronal Restrictive Silencing Factor (NRSF) or human Repressor Element Silencing Transcription Factor (REST). When bound to the viral DNA elements, histone deacetylation occurs atop the ICP4 gene sequence to prevent initiation of transcription from this gene, thereby preventing transcription of other viral genes involved in the lytic cycle. Another HSV protein reverses the inhibition of ICP4 protein synthesis. ICP0 dissociates NRSF from the ICP4 gene and thus prevents silencing of the viral DNA.

The virus can be reactivated by illnesses such as colds and influenza, eczema, emotional and physical stress, gastric upset, fatigue or injury, by menstruation and possibly exposure to bright sunlight.

Viral genome

The open reading frames (ORFs) of HSV-1
Gene	Protein	Function/description	Gene	Protein	Function/description
UL1	Glycoprotein L [1]	Surface and membrane	UL38	UL38; VP19C [2]	Capsid assembly and DNA maturation
UL2	UL2 [3]	Uracil-DNA glycosylase	UL39	UL39 [4]	Ribonucleotide reductase (Large subunit)
UL3	UL3 [5]	unknown	UL40	UL40 [6]	Ribonucleotide reductase (Small subunit)
UL4	UL4 [7]	unknown	UL41	UL41; VHS [8]	Tegument protein; Virion host shutoff
UL5	UL5 [9]	DNA replication	UL42	UL42 [10]	DNA polymerase processivity factor
UL6	Portal protein UL-6	Twelve of these proteins constitute the capsid portal ring through which DNA enters and exits the capsid.	UL43	UL43 [11]	Membrane protein
UL7	UL7 [12]	Virion maturation	UL44	Glycoprotein C [13]	Surface and membrane
UL8	UL8 [14]	DNA helicase/primase complex-associated protein	UL45	UL45 [15]	Membrane protein; C-type lectin
UL9	UL9 [16]	Replication origin-binding protein	UL46	VP11/12 [17]	Tegument proteins
UL10	Glycoprotein M [18]	Surface and membrane	UL47	UL47; VP13/14 [19]	Tegument protein
UL11	UL11 [20]	virion exit and secondary envelopment	UL48	VP16 (Alpha-TIF) [21]	Virion maturation; activate IE genes by interacting with the cellular transcription factors Oct-1 and HCF. Binds to the sequence 5'TAATGARAT3'.
UL12	UL12 [22]	Alkaline exonuclease	UL49	UL49A [23]	Envelope protein
UL13	UL13 [24]	Serine-threonine protein kinase	UL50	UL50 [25]	dUTP diphosphatase
UL14	UL14 [26]	Tegument protein	UL51	UL51 [27]	Tegument protein
UL15	Terminase [28]	Processing and packaging of DNA	UL52	UL52 [29]	DNA helicase/primase complex protein
UL16	UL16 [30]	Tegument protein	UL53	Glycoprotein K [31]	Surface and membrane
UL17	UL17 [32]	Processing and packaging DNA	UL54	IE63; ICP27 [33]	Transcriptional regulation
UL18	VP23 [34]	Capsid protein	UL55	UL55 [35]	Unknown
UL19	VP5 [36]	Major capsid protein	UL56	UL56 [37]	Unknown
UL20	UL20 [38]	Membrane protein	US1	ICP22; IE68 [39]	Viral replication
UL21	UL21 [40]	Tegument protein	US2	US2 [41]	Unknown
UL22	Glycoprotein H [42]	Surface and membrane	US3	US3 [43]	Serine/threonine-protein kinase
UL23	Thymidine kinase [44]	Peripheral to DNA replication	US4	Glycoprotein G [45]	Surface and membrane
UL24	UL24 [46]	unknown	US5	Glycoprotein J [47]	Surface and membrane
UL25	UL25 [48]	Processing and packaging DNA	US6	Glycoprotein D [49]	Surface and membrane
UL26	P40; VP24; VP22A [50]	Capsid protein	US7	Glycoprotein I [51]	Surface and membrane
UL27	Glycoprotein B [52]	Surface and membrane	US8	Glycoprotein E [53]	Surface and membrane
UL28	ICP18.5 [54]	Processing and packaging DNA	US9	US9 [55]	Tegument protein
UL29	UL29; ICP8 [56]	Major DNA-binding protein	US10	US10 [57]	Capsid/Tegument protein
UL30	DNA polymerase [58]	DNA replication	US11	US11; Vmw21 [59]	Binds DNA and RNA
UL31	UL31 [60]	Nuclear matrix protein	US12	ICP47; IE12 [61]	Inhibits MHC class I pathway by preventing binding of antigen to TAP
UL32	UL32 [62]	Envelope glycoprotein	RS1	ICP4; IE175 [63]	Major transcriptional activator. Essential for progression beyond the immediate-early phase of infection. IEG transcription repressor.
UL33	UL33 [64]	Processing and packaging DNA	ICP0	ICP0; IE110; α0 [65]	E3 ubiquitin ligase that activates viral gene transcription by opposing chromatinization of the viral genome and counteracts intrinsic- and interferon-based antiviral responses.
UL34	UL34 [66]	Inner nuclear membrane protein	LRP1	LRP1 [67]	Latency-related protein
UL35	VP26 [68]	Capsid protein	LRP2	LRP2 [69]	Latency-related protein
UL36	UL36 [70]	Large tegument protein	RL1	RL1; ICP34.5 [71]	Neurovirulence factor. Antagonizes PKR by de-phosphorylating eIF4a. Binds to BECN1 and inactivates autophagy.
UL37	UL37 [72]	Capsid assembly	LAT	none [73]	Latency-associated transcript

Evolution

The Herpes simplex 1 genomes can be classified into six clades. Four of these occur in East Africa with one clade in East Asian and another in Europe/North America. This suggests that this virus may have originated in East Africa. The most recent common ancestor of the Eurasian strains appears to have evolved ~60,000 years ago. The East Asian HSV-1 isolates have an unusual pattern that is currently best explained by the two waves of migration responsible for the peopling of Japan.

The mutation rate has been estimated to be ~1.38×10^-7 subsitutions/site/year.

Treatment and vaccine development

For more details on treatment of herpes simplex virus, see Herpes simplex.

Herpes viruses establish lifelong infections, and the virus cannot yet be eradicated from the body. Treatment usually involves general-purpose antiviral drugs that interfere with viral replication, reduce the physical severity of outbreak-associated lesions, and lower the chance of transmission to others. Studies of vulnerable patient populations have indicated that daily use of antivirals such as acyclovir and valacyclovir can reduce reactivation rates.

Connection between facial sores and Alzheimer's disease

In the presence of a certain gene variation (APOE-epsilon4 allele carriers), a possible link between HSV-1 (i.e., the virus that causes cold sores or oral herpes) and Alzheimer's disease was reported in 1979. HSV-1 appears to be particularly damaging to the nervous system and increases one’s risk of developing Alzheimer’s disease. The virus interacts with the components and receptors of lipoproteins, which may lead to the development of Alzheimer's disease. This research identifies HSVs as the pathogen most clearly linked to the establishment of Alzheimer’s. According to a study done in 1997, without the presence of the gene allele, HSV-1 does not appear to cause any neurological damage or increase the risk of Alzheimer’s. However, a more recent prospective study from 2008 with a cohort of several thousand people showed a high correlation between seropositivity for HSV and Alzheimer's disease, without direct correlation to the APOE-epsilon4 allele. In 2011 Manchester University scientists showed that treating HSV1-infected cells with antiviral agents decreased the accumulation of ß-amyloid and P-tau, and also decreased HSV1 replication as expected.

Multiplicity reactivation

Multiplicity reactivation (MR) is the process by which viral genomes containing inactivating damage interact within an infected cell to form a viable viral genome. MR was originally discovered with the bacterial virus bacteriophage T4, but was subsequently also found with pathogenic viruses including influenza virus, HIV-1, adenovirus simian virus 40, vaccinia virus, reovirus, poliovirus and herpes simplex virus.

When HSV particles are exposed to doses of a DNA damaging agent that would be lethal in single infections, but are then allowed to undergo multiple infection (i.e. two or more viruses per host cell), MR is observed. Enhanced survival of HSV-1 due to MR occurs upon exposure to different DNA damaging agents, including methyl methanesulfonate, trimethylpsoralen (which causes inter-strand DNA cross-links, and UV light. After treatment of genetically marked HIV with trimethylpsoralen, recombination between the marked viruses increases, suggesting that trimethylpsoralen damages stimulate recombination. MR of HSV appears to partially depend on the host cell recombinational repair machinery since skin fibroblast cells defective in a component of this machinery (i.e. cells from Bloom’s syndrome patients) are deficient in MR. These observations suggest that MR in HSV infections involves genetic recombination between damaged viral genomes resulting in production of viable progeny viruses. HSV-1, upon infecting host cells, induces inflammation and oxidative stress. Thus it appears that the HSV genome may be subjected to oxidative DNA damage during infection, and that MR may enhance viral survival and virulence under these conditions.

Use as an anti-cancer agent

Main article: Oncolytic herpes virus

Herpes simplex virus is considered as a potential therapy for cancer and has been extensively clinically tested to assess its oncolytic (cancer killing) ability.

Use in neuronal connection tracing

Main article: Viral neuronal tracing

Herpes simplex virus is also used as a transneuronal tracer defining connections among neurons by virtue of traversing synapses

References

External links

• Genital Herpes - Public Health Agency of Canada
• Herpes simplex: Host viral protein interactions: A database of HSV-1 interacting host proteins
• 3D macromolecular structures of the Herpes simplex virus archived in the EM Data Bank(EMDB)

UpToDate Contents

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• 1. 免疫正常患者における単純ヘルペスウイルス1型感染の治療 treatment of herpes simplex virus type 1 infection in immunocompetent patients
• 2. 単純ヘルペスウイルス1型感染の臨床症状および診断 clinical manifestations and diagnosis of herpes simplex virus type 1 infection
• 3. 単純ヘルペスウイルス1型感染の疫学 epidemiology of herpes simplex virus type 1 infection
• 4. 単純ヘルペスウイルス1型感染の病因 pathogenesis of herpes simplex virus type 1 infection
• 5. 単純ヘルペスウイルス1型脳炎 herpes simplex virus type 1 encephalitis

English Journal

• Estimating seroprevalence of herpes simplex virus type 1 among different Middle East and North African male populations residing in Qatar.

• Nasrallah GK1,2, Dargham SR3, Mohammed LI2, Abu-Raddad LJ3,4.
• Journal of medical virology.J Med Virol.2018 Jan;90(1):184-190. doi: 10.1002/jmv.24916. Epub 2017 Sep 12.
• PMID 28817197

• Application of next-generation sequencing to detect acyclovir-resistant herpes simplex virus type 1 variants at low frequency in thymidine kinase gene of the isolates recovered from patients with hematopoietic stem cell transplantation.

• Fujii H1, Kakiuchi S2, Tsuji M3, Nishimura H4, Yoshikawa T1, Yamada S1, Omura N5, Inagaki T5, Shibamura M6, Harada S1, Taniguchi S3, Saijo M7.
• Journal of virological methods.J Virol Methods.2018 Jan;251:123-128. doi: 10.1016/j.jviromet.2017.10.019. Epub 2017 Oct 23.
• PMID 29074089

• Comparison of different methods for extraction of Cinnamomi ramulus: yield, chemical composition and in vitro antiviral activities.

• Zhou J1,2, Yuan X2, Li L1, Zhang T1,3, Wang B1,3.
• Natural product research.Nat Prod Res.2017 Dec;31(24):2909-2913. doi: 10.1080/14786419.2017.1299724. Epub 2017 Mar 21.
• PMID 28322072

Japanese Journal

• 抑制型免疫受容体PILRαによるヘルペスウイルス1型由来O型糖鎖およびペプチド配列の同時認識と創薬 (AYUMI 構造生物学が推進する医薬基盤とその応用)

• 尾瀬 農之,古川 敦,黒木 喜美子 [他]
• 医学のあゆみ 254(8), 559-565, 2015-08-22
• NAID 40020561224

• Survival of Enveloped and Non-Enveloped Viruses on Inanimate Surfaces

• FIRQUET SWAN,BEAUJARD SOPHIE,LOBERT PIERRE-EMMANUEL [他]
• Microbes and environments 30(2), 140-144, 2015-06
• NAID 40020494141

• CLINICAL INVESTIGATION : Virological and molecular biological evidence supporting herpes simplex virus type 1 corneal latency

• Higaki Shiro,Fukuda Masahiko,Shimomura Yoshikazu
• Japanese journal of ophthalmology : the official international journal of the Japanese Ophthalmological Society 59(2), 131-134, 2015-03
• NAID 40020401170

Related Links

• Herpes simplex virus - Wikipedia, the free encyclopedia

Herpes simplex virus 1 and 2 (HSV-1 and HSV-2), also known as Human herpes virus 1 and 2 (HHV-1 and -2), are two members of ..... "Herpes simplex virus type 1 mediates fusion through a hemifusion intermediate by sequential activity of ...

• 単純ヘルペスウイルス - Wikipedia

HSV-1(Herpes simplex virus type 1)＝学名：HHV-1(human herpesvirus-1); HSV-2 (Herpes simplex virus type 2)＝学名：HHV-2(human herpesvirus-2). 150Kbpの ゲノム全長を持ち、80種類以上の遺伝子をコードしている。宿主の細胞膜を自身の ...

Related Pictures

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★リンクテーブル★

リンク元	「単純ヘルペスウイルス1型」「human herpesvirus 1」
関連記事	「simple」「type」「typed」「typing」「simplex」

「単純ヘルペスウイルス1型」

　　[★]

英

herpes simplex virus type 1, herpes simplex virus 1, HSV-1

同

ヒトヘルペスウイルス1型 HHV-1

• ヘルペスウイルス科シンプレックスウイルス属

-ヒトヘルペスウイルス1型

同

HSV1

「human herpesvirus 1」

　　[★]

• ヒトヘルペスウイルス1型、ヒトヘルペスウイルス1

関

herpes simplex virus 1、herpes simplex virus type 1、HHV-1、HSV-1

「simple」

　　[★]

• adj.

• (比較級simpler-最上級simplest)単純な、簡便な、シンプルな、簡素な、単一の、単一性の、単純性の

関

convenient、mono、parsimonious、plain、simplex、simplicity、simply、single、unity

　 　 　 　 　 　

「type」

　　[★]

• n.

• 型、タイプ、(生物)タイプ標本

(windows)ファイル内容表示(linux -> cat])

ex. type report_20111118.jp.htm | php a.php > report_20111118.jp.jp.jp.html

関

form、mode、pattern、type specimen、typed

　 　 　 　 　 　 　 　

「typed」

　　[★]

• adj.

• 型の

関

form、mode、pattern、type

「typing」

　　[★]

• n.

• タイプで打つこと、タイピング。分類

　

「simplex」

　　[★]

• adj.

• 単一性の、単式

関

simple