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Pussjuka / kyssjuka /Kissing Disease / Epstein-barr virus / EBV

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GiantMicrobes är mjukdjur som ser ut som små, små mikrober - bara det att de är förstorade sådär en miljon gånger. De ger bokstavligen ett ansikte åt förkylningen, fotsvampen, hostan, den dåliga andedräkten eller vägglusen. Varje GIGANTmicrobe är mellan ca 38-50 cm. Med följer ett foto på hur den riktiga mikroben ser ut samt en kort information på engelska.

Ursprungligen skapade i USA att användas i undervisningssyfte, har GIANTmicrobes nu blivit storsäljare i museishoppar, apotek, bokhandlar och designbutiker världen över.

GIANTmicrobes är ett roligt verktyg i undervisningen om hälsa och sjukdomar, men även en uppskattad gåva som passar alla åldrar. Definitivt roligare än ett krya-på-dig kort till en sjuk vän.

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Pussjuka / kyssjuka /Kissing Disease / Epstein-barr virus / EBV

Puss Puss på dig älskling :-)
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A kiss is just a kiss -- unless she's around! 95% of the population has encountered this sweetie pie. Find out who gets her special love.

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Wikipedia:

Körtelfeber

ICD-10ICD-9DiseasesDBMedlinePluseMedicineMeSH
Körtelfeber
Klassifikation och externa resurser
Ett histologiskt prov som visar ett utstryk där man ser blåfärgade atypiska lymfocyter.
B27
075
4387
000591
emerg/319  med/1499
engelsk

Körtelfeberinfektiös mononukleosmononukleos eller kyssjuka, är en infektionssjukdom vars främsta symptom är halsont, hög feber och svullna lymfkörtlar i hals, armhålor och ljumskar. Sjukdomen orsakas av Epstein-Barrvirus (EBV), även kallat humant herpesvirus 4, som sprids mellan människor genom direktkontakt, främst via saliv. Sjukdomen är spridd över hela världen och de flesta människor utsätts för det orsakande viruset någon gång men sjukdomen utvecklas främst hos ungdomar i åldern 10–25 år. Mindre barn som smittas med viruset får ofta inga sjukdomssymtom. Sjukdomen är oftast ofarlig och infektionen brukar läka ut själv. Inkubationstiden är 4–6 veckor. Sjukdomen brukar vara i två till tre veckor, ibland upp mot en månad. Trötthet en längre tid efteråt är vanligt, ibland i flera månader.

Det finns inget vaccin mot sjukdomen. Efter infektion utvecklas en immunitet som gör att man är skyddad mot ytterligare insjuknande. Dock finns information som tyder på att det orsakande viruset som är ett herpesvirus kan finns kvar latent i kroppen och att sjukdomen åter kan bryta ut om personen fått nedsatt immunförsvar.

Symptom

SmittovägarRedigera

Körtelfeber orsakas av Epstein-Barrvirus vilket smittar genom framförallt saliv. På grund av dess tendens att smitta via saliv och att det är känt att kyssar är ett av de sätt som viruset kan spridas på, kallas sjukdomen på engelska bland annatkissing disease. Viruset kan även smitta via kontaktsmitta vid otillräcklig handhygien.

BehandlingRedigera

Körtelfeber orsakas av ett virus och är därför inte möjlig att behandla med antibiotika. Istället brukar symptomen behandlas till exempel med hjälp av febernedsättande medel för att underlätta sjukdomstiden. Receptfria febernedsättande medel finns att tillgå och det rekommenderas att dricka mer än vanligt när man har feber. Antiinflammatoriska läkemedel har också en visad effekt mot halsont med körtelfeber och det finns receptfria och receptbelagda läkemedel av denna typ som kan lindra besvären i halsen och medföra enklare förtäring av både mat och dryck. Sjukvården bör alltid uppsökas för rådgivning och behandling om man mår dåligt och har feber som inte går ner, svårigheter att svälja eller om man fått diagnosen körtelfeber och får ont i magen.

KällorRedigera

Epstein–Barr virus

From Wikipedia, the free encyclopedia
  (Redirected from Epstein Barr)
Jump to: navigation, search

Epstein–BarrVirus classificationSynonyms
Two Epstein–Barr virions
Group:Group I (dsDNA)
Order:Herpesvirales
Family:Herpesviridae
Subfamily:Gammaherpesvirinae
Genus:Lymphocryptovirus
Species:Human herpesvirus 4 (HHV-4)
  • EB virus

The Epstein–Barr virus (EBV), also called human herpesvirus 4 (HHV-4), is a virus of the herpes family, and is one of the most common viruses in humans.

It is best known as the cause of infectious mononucleosis (glandular fever). It is also associated with particular forms of cancer, such as Hodgkin's lymphoma, Burkitt's lymphoma, nasopharyngeal carcinoma, and conditions associated with human immunodeficiency virus (HIV) such as hairy leukoplakia and central nervous system lymphomas.[1][2] There is evidence that infection with the virus is associated with a higher risk of certain autoimmune diseases,[3] especially dermatomyositis, systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome,[4][5] and multiple sclerosis.[6]

Infection with EBV occurs by the oral transfer of saliva[7] and genital secretions.

Most people become infected with EBV and gain adaptive immunity. In the United States, about half of all five-year-old children and 90 to 95 percent of adults have evidence of previous infection.[8] Infants become susceptible to EBV as soon as maternal antibody protection disappears. Many children become infected with EBV, and these infections usually cause no symptoms or are indistinguishable from the other mild, brief illnesses of childhood. In the United States and other developed countries, many people are not infected with EBV in their childhood years. When infection with EBV occurs during adolescence, it causes infectious mononucleosis 35 to 50 percent of the time.[9]

EBV infects B cells of the immune system and epithelial cells. Once the virus's initial lytic infection is brought under control, EBV latently persists in the individual's B cells for the rest of the individual's life.[7]


Virology[edit]

Simplified diagram of the structure of EBV

Structure and genome[edit]

The virus is approximately 120 nm to 180 nm in diameter and is composed of a double helix of DNA wrapped in a protein capsid. The capsid is surrounded by a tegument made of protein, which in turn is surrounded by a envelope made from lipids.[10] The EBV DNA is about 192,000 base pairs long and contains about 85 genes.[7] The viral envelope contains glycoproteins, which are essential to infection of the host cell.[10]

Tropism[edit]

The term viral tropism refers to which cell types EBV infects. EBV can infect a number of different cell types, including B cells and epithelial cells. Under certain cases, it may infect T cells, natural killer cells, and smooth muscle cells.

The viral three-part glycoprotein complexes of gHgLgp42 mediate B cell membrane fusion; while the two-part complexes of gHgL mediate epithelial cell membrane fusion. EBV that are made in the B cells have low numbers of the gHgLgp42 complexes as the three-part complexes interact with HLA class II in the endoplasmic reticulum and are degraded. In contrast, EBV from epithelial cells are rich in the three-part complexes because these cells do not have MHC class II. As a result, EBV made from B cells are more infectious to epithelial cells, and EBV made from epithelial cells are more infectious to B cells.

Replication cycle[edit]

The EBV replication cycle

Entry to the cell[edit]

EBV can infect both B cells and epithelial cells. The mechanisms for entering these two cells are different.

To enter B cells, viral glycoprotein gp350 binds to cellular receptor CD21 (also known as CR2).[11] Then, viral glycoprotein gp42 interacts with cellular MHC class II molecules. This triggers fusion of the viral envelope with the cell membrane, allowing EBV to enter the B cell.[10]

To enter epithelial cells, viral protein BMRF-2 interacts with cellular β1 integrins. Then, viral protein gH/gL interacts with cellular αvβ6/8 integrins. This triggers fusion of the viral envelope with the epithelial cell membrane, allowing EBV to enter the epithelial cell.[10] Unlike B cell entry, epithelial cell entry is actually impeded by viral glycoprotein gp42.[11]

Once EBV enters the cell, the viral capsid dissolves and the viral genome is transported to the cell nucleus.

Lytic replication[edit]

The lytic cycle, or productive infection, results in the production of infectious virions. EBV can undergo lytic replication in both B cells and epithelial cells. In B cells, lytic replication normally only takes place after reactivation from latency. In epithelial cells, lytic replication often directly follows viral entry.[10]

For lytic replication to occur, the viral genome must be linear. The latent EBV genome is circular, so it must linearize in the process of lytic reactivation. During lytic replication, viral DNA polymerase is responsible for copying the viral genome. This contrasts with latency, in which host cell DNA polymerase copies the viral genome.[10]

Lytic gene products are produced in three consecutive stages: immediate-early, early, and late.[10] Immediate-early lytic gene products act as transactivators, enhancing the expression of later lytic genes. Immediate-early lytic gene products include BZLF1 (also known as Zta and ZEBRA) and BRLF1.[10] Early lytic gene products have many more functions, such as replication, metabolism, and blockade of antigen processing. Early lytic gene products include BNLF2.[10] Finally, late lytic gene products tend to be proteins with structural roles, like VCA, which forms the viral capsid. Other late lytic gene products, such as BCRF1, help EBV evade the immune system.[10]

Unlike lytic replication for many other viruses, EBV lytic replication does not inevitably lead to lysis of the host cell because EBV virions are produced by budding from the infected cell. Lytic proteins include gp350 and gp110.[10][12]

Latency[edit]

Unlike lytic replication, latency does not result in production of virions.[10] Instead, the EBV genome circularizes, resides in the cell nucleus as an episome, and is copied by cellular DNA polymerase.[10] In latency, only a portion of EBV's genes are expressed.[7] Latent EBV expresses its genes in one of three patterns, known as latency programs. EBV can latently persist within B cells and epithelial cells, but different latency programs are possible in the two types of cell.

EBV can exhibit one of three latency programs: Latency I, Latency II, or Latency III. Each latency program leads to the production of a limited, distinct set of viral proteins and viral RNAs.[13][14]

Gene ExpressedEBNA-1EBNA-2EBNA-3AEBNA-3BEBNA-3CEBNA-LPLMP-1LMP-2ALMP-2BEBER
ProductProteinProteinProteinProteinProteinProteinProteinProteinProteinncRNAs
Latency I++
Latency II++++++
Latency III++++++++++


Reactivation[edit]

Latent EBV in B cells can be reactivated to switch to lytic replication. This is known to happen in vivo, but what triggers it is not known precisely. In vitro, latent EBV in B cells can be reactivated by stimulating the B cell receptor, so reactivation in vivo probably takes place when latently infected B cells respond to unrelated infections.[10] In vitro, latent EBV in B cells can also be reactivated by treating the cells with sodium butyrate or TPA.[citation needed]

Transformation of B-lymphocytes[edit]

When EBV infects B cells in vitro, lymphoblastoid cell lines eventually emerge that are capable of indefinite growth. The growth transformation of these cell lines is the consequence of viral protein expression.

EBNA-2, EBNA-3C and LMP-1 are essential for transformation, while EBNA-LP and the EBERs are not.[16]

It is postulated that following natural infection with EBV, the virus executes some or all of its repertoire of gene expression programs to establish a persistent infection. Given the initial absence of host immunity, the lytic cycle produces large amounts of virus to infect other (presumably) B-lymphocytes within the host.

The latent programs reprogram and subvert infected B-lymphocytes to proliferate and bring infected cells to the sites at which the virus presumably persists. Eventually, when host immunity develops, the virus persists by turning off most (or possibly all) of its genes, only occasionally reactivating to produce fresh virions. A balance is eventually struck between occasional viral reactivation and host immune surveillance removing cells that activate viral gene expression.

The site of persistence of EBV may be bone marrow. EBV-positive patients who have had their own bone marrow replaced with bone marrow from an EBV-negative donor are found to be EBV-negative after transplantation.[17]

Lewy bodies and multiple system atrophy).[24]

History[edit]

The Epstein–Barr virus is named after Michael Anthony Epstein, a professor emeritus at the University of Bristol, and Yvonne Barr (born 1932 in London), a 1966 Ph.D graduate from the University of London, who together discovered and documented the virus.[25] In 1961, Epstein, a pathologist and expert electron microscopist, attended a lecture on "The Commonest Children's Cancer in Tropical Africa—A Hitherto Unrecognised Syndrome." This lecture, by Denis Parsons Burkitt, a surgeon practicing in Uganda, was the description of the "endemic variant" (pediatric form) of the disease that bears his name. In 1963, a specimen was sent from Uganda to Middlesex Hospital to be cultured. Virus particles were identified in the cultured cells, and the results were published in The Lancet in 1964 by Epstein, Bert Achong, and Barr. Cell lines were sent to Werner and Gertrude Henle at the Children's Hospital of Philadelphia who developed serological markers. In 1967, a technician in their laboratory developed mononucleosis and they were able to compare a stored serum sample, showing that antibodies to the virus developed.[26][27][28] In 1968, they discovered that EBV can directly immortalize B cells after infection, mimicking some forms of EBV-related infections,[29] and confirmed the link between the virus and infectious mononucleosis.[30]

Research[edit]

A relatively complex virus, EBV is not yet fully understood. Laboratories around the world continue to study the virus and develop new ways to treat the diseases it causes. One popular way of studying EBV in vitro is to use bacterial artificial chromosomes.[31] Epstein–Barr virus and its sister virus KSHV can be maintained and manipulated in the laboratory in continual latency. While many viruses are assumed to have this property during infection of their natural host, they do not have an easily managed system for studying this part of the viral lifecycle. Genomic studies of EBV have been able to explore lytic reactivation and regulation of the latent viral episome.[32]

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Epstein–Barr virus infection

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Epstein–Barr virus infectionICD-9OMIMMeSH
Classification and external resources
075
226990
D020031

There are several forms of Epstein–Barr virus infection. Infectious mononucleosis, nasopharyngeal carcinoma, and Burkitt's lymphoma can all be caused by the Epstein–Barr virus.


Pathology[edit]

Infectious mononucleosis[edit]

Epstein–Barr can cause infectious mononucleosis, also known as 'glandular fever', 'Mono' and 'Pfeiffer's disease'. Infectious mononucleosis is caused when a person is first exposed to the virus during or after adolescence. Though once deemed "The Kissing Disease," recent research has shown that transmission of Mono not only occurs from exchanging saliva, but also from contact with the airborne virus.[citation needed] It is predominantly found in the developing world, and most children in the developing world are found to have already been infected by around 18 months of age. Infection of children can occur when adults mouth feed or pre-chew food before giving it to the child.[1] EBV antibody tests turn up almost universally positive. In the United States roughly half of five-year-olds have been infected,.[2]

EBV-associated malignancies[edit]

This photomicrograph depicts leukemia cells that contain Epstein Barr virus using a FA staining technique. Epstein–Barr virus, EBV, is a member of the Herpesvirus family, and is one of the most common human viruses. When infection with EBV occurs during adolescence or young adulthood, it causes infectious mononucleosis 35% to 50% of the time. (CDC)

The strongest evidence linking EBV and cancer formation is found in Burkitt's lymphoma and nasopharyngeal carcinoma. Additionally, it has been postulated to be a trigger for a subset of chronic fatigue syndrome patients[3] as well as multiple sclerosis and other autoimmune diseases.[4]

Burkitt's lymphoma is a type of Non-Hodgkin's lymphoma and is most common in equatorial Africa and is co-existent with the presence of malaria.[5] Malaria infection causes reduced immune surveillance of B cells immortalized by EBV, resulting in an excessive number of B cells and an increased likelihood of an unchecked mutation. Repeated mutations can lead to loss of cell-cycle control, causing excessive proliferation observed as Burkitt's lymphoma. Burkitt's lymphoma commonly affects the jaw bone, forming a huge tumor mass. It responds quickly to chemotherapy treatment, namely cyclophosphamide, but recurrence is common.

Other B cell lymphomas arise in immunocompromised patients such as those with AIDS or who have undergone organ transplantation with associated immunosuppression (Post-Transplant Lymphoproliferative Disorder (PTLPD)). Smooth muscle tumors are also associated with the virus in malignant patients.[6]

Nasopharyngeal carcinoma is a cancer found in the upper respiratory tract, most commonly in the nasopharynx, and is linked to the EBV virus. It is found predominantly in Southern China and Africa, due to both genetic and environmental factors. It is much more common in people of Chinese ancestry (genetic), but is also linked to the Chinese diet of a high amount of smoked fish, which contain nitrosamines, well known carcinogens (environmental).[7]

Clinical symptoms[edit]

Symptoms of infectious mononucleosis are fever, sore throat, and swollen lymph glands. Sometimes, a swollen spleen or liver involvement may develop. Heart problems or involvement of the central nervous system occurs only rarely, and infectious mononucleosis is almost never fatal. There are no known associations between active EBV infection and problems during pregnancy, such as miscarriages or birth defects.[8][9] Although the symptoms of infectious mononucleosis usually resolve in 1 or 2 months, EBV remains dormant or latent in a few cells in the throat and blood for the rest of the person's life. Periodically, the virus can reactivate and is commonly found in the saliva of infected persons. Reactivated and post-latent virus may pass the placental barrier in (also seropositive) pregnant women via macrophages and therefore can infect the fetus. Also re-infection of prior seropositive individuals may occur. In contrast, reactivation in adults usually occurs without symptoms of illness.

EBV also establishes a lifelong dormant infection in some cells of the body's immune system. A late event in a very few carriers of this virus is the emergence of Burkitt's lymphoma and nasopharyngeal carcinoma, two rare cancers. EBV appears to play an important role in these malignancies, but is probably not the sole cause of disease.

Most individuals exposed to people with infectious mononucleosis have previously been infected with EBV and are not at risk for infectious mononucleosis. In addition, transmission of EBV requires intimate contact with the saliva (found in the mouth) of an infected person. Transmission of this virus through the air or blood does not normally occur. The incubation period, or the time from infection to appearance of symptoms, ranges from 4 to 6 weeks. Persons with infectious mononucleosis may be able to spread the infection to others for a period of weeks. However, no special precautions or isolation procedures are recommended, since the virus is also found frequently in the saliva of healthy people. In fact, many healthy people can carry and spread the virus intermittently for life. These people are usually the primary reservoir for person-to-person transmission. For this reason, transmission of the virus is almost impossible to prevent.

The clinical diagnosis of infectious mononucleosis is suggested on the basis of the symptoms of fever, sore throat, swollen lymph glands, and the age of the patient. Usually, laboratory tests are needed for confirmation. Serologic results for persons with infectious mononucleosis include an elevated white blood cell count, an increased percentage of certain atypical white blood cells, and a positive reaction to a "mono spot" test.

Treatment[edit]

There is no specific treatment for infectious mononucleosis, other than treating the symptoms. No antiviral drugs or vaccines are available. Some physicians have prescribed a 5-day course of steroids to control the swelling of the throat and tonsils. The use of steroids has also been reported to decrease the overall length and severity of illness, but these reports have not been published.

It is important to note that symptoms related to infectious mononucleosis caused by EBV infection seldom last for more than 4 months. When such an illness lasts more than 6 months, it is frequently called chronic EBV infection. However, valid laboratory evidence for continued active EBV infection is seldom found in these patients. The illness should be investigated further to determine if it meets the criteria for chronic fatigue syndrome, or CFS. This process includes ruling out other causes of chronic illness or fatigue.