Misplaced Pages

#897102

61-540: KSV or kSv may refer to: Kaposi's sarcoma-associated herpesvirus , a virus Karlsruher SV Rugby , a German club Karyakshama Seva Vibhushanaya (Efficient Service Decoration), a Sri Lanka military medal Kieler Sportvereinigung Holstein, or Holstein Kiel , a football club in Kiel, Schleswig-Holstein, Germany Kilosievert , a unit of radiation Springvale Airport (Queensland) , IATA airport code "KSV" Topics referred to by

122-422: A PI3K inhibitor is added to cells, the cytokine synthesis levels are significantly restored. The fact that cytokine levels are not completely restored indicates there is another pathway activated by cmvIL-10 that is inhibiting cytokine system synthesis. The proposed mechanism is that cmvIL-10 activates PI3K which in turn activates PKB (Akt). PKB may then activate mTOR , which may target Stat3 for phosphorylation on

183-579: A decrease in proliferation of PBMCs. This indicates that cmvIL-10 may lack the stimulatory effects that hIL-10 has on these cells. It was found that cmvIL-10 functions through phosphorylation of the Stat3 protein. It was originally thought that this phosphorylation was a result of the JAK-STAT pathway. However, despite evidence that JAK does indeed phosphorylate Stat3, its inhibition has no significant influence on cytokine synthesis inhibition. Another protein, PI3K ,

244-413: A hallmark of KS. During latency, LANA is the only viral protein that is required for viral replication, which is carried out by the host replication machinery. LANA tethers the viral DNA to cellular chromosomes, inhibits p53 and retinoblastoma protein and suppresses viral genes needed for full virus production and assembly ("lytic replication"). Why only a subset of virus genes expressed during latency

305-604: A latent ("quiet") state. Only a subset of genes that are encoded in the KSHV latency associated region (KLAR) are expressed during latency, including latency-associated nuclear antigen (LANA), vFLIP, vCyclin and 12 microRNAs. Latency is the hallmark of all KSHV-associated etiologies known to date including all KSHV-associated oncogenesis. It has been shown that both protein coding genes such as LANA and noncoding genes (microRNAs) encoded in KLAR are important for KSHV associated tumorigenesis. To study

366-435: A linear manner, countries with high infection rates may see higher seroprevalence in younger age groups. Educational level has shown an inverse correlation with infection rates. Individuals infected with HIV-1 or genital warts are generally more likely to be co-infected with HHV-8. In countries with low seroprevalence, HHV-8 is primarily limited to AIDS and KS patients. In countries with high seroprevalence, infection

427-404: A portal complex that allows entry and exit of DNA into the capsid. All herpesviruses are nuclear-replicating—the viral DNA is transcribed to mRNA within the infected cell's nucleus . Infection is initiated when a viral particle contacts a cell with specific types of receptor molecules on the cell surface . Following binding of viral envelope glycoproteins to cell membrane receptors,

488-504: A significant antitumor effect. Nivolumab is currently an ongoing phase I clinical trial, and Pembrolizumab has shown its function in treatment for HIV and KS patients in phase I and is in a phase II trial for treatment. A thalidomide analog medicine – Pomalidomide was also granted by the FDA in 2011. Pomalidomide was shown to recover the expression of MHC-1 , which help cell display intracellular proteins to cytotoxic T cells, and it also can repress

549-897: Is a known causative agent of four diseases: In the 1970s, the global prevalence rate for HHV-8 was 2 to 10%. The seroprevalence of HHV-8 varies significantly geographically and infection rates in northern European, southeast Asian, and Caribbean countries are between 2-4%, in Mediterranean countries at approximately 10%, and in sub-Saharan African countries at approximately 40%. In South America, infection rates are low in general but are high among Amerindians . Even within individual countries, significant variation can be observed across different regions, with infection rates of about 19.2% in Xinjiang compared to about 9.5% in Hubei , China. Although seroprevalence has been consistently shown to increase with age in

610-470: Is a large family of DNA viruses that cause infections and certain diseases in animals, including humans. The members of this family are also known as herpesviruses . The family name is derived from the Greek word ἕρπειν ( herpein 'to creep'), referring to spreading cutaneous lesions, usually involving blisters, seen in flares of herpes simplex 1, herpes simplex 2 and herpes zoster ( shingles ). In 1971,

671-466: Is approximately 165,000 nucleic acid bases in length. The viral genome consists of a ~145 kilobase -long unique region, encoding all of expressed viral genes, which is flanked by ~20-30 kilobases of terminal repeat sequences. Each terminal repeat unit is 801 bp in length, has 85% G+C content and is oriented in a repetitive head-to-tail fashion. KSHV is a rhadinovirus , a Herpes genus remarkable since it has stolen numerous genes from host cells including, in

SECTION 10

#1732884800898

732-522: Is caused by an unknown sexually transmitted virus that rarely causes tumors unless the host becomes immunosuppressed , as in AIDS. As early as 1984, scientists reported seeing herpesvirus-like structures in KS tumors examined under electron microscopy . Scientists had been searching for the agent causing KS, and over 20 agents were proposed as the possible cause, including cytomegalovirus and HIV itself. The pathogen

793-610: Is chromatinized during latency. It has also been shown that virus encoded microRNA manipulates and interacts not only with host mRNA but also deregulate host long non-coding RNA (lncRNA). More recently, circularRNAs (circRNAs) are recently discovered in both EBV and KSHV Infection with this virus is thought to be lifelong, but a healthy immune system will keep the virus in check. Many people infected with KSHV will never show any symptoms. Kaposi's sarcoma occurs when someone who has been infected with KSHV becomes immunocompromised due to AIDS, medical treatment, or, very rarely, aging. KSHV

854-441: Is different from Wikidata All article disambiguation pages All disambiguation pages Kaposi%27s sarcoma-associated herpesvirus In 1872, Moritz Kaposi described a blood vessel tumor (originally called "idiopathic multiple pigmented sarcoma of the skin") that has since been eponymously named Kaposi's sarcoma (KS). KS was at first thought to be an uncommon tumor of Jewish and Mediterranean populations until it

915-474: Is frequent in childhood, indicating a likely mother-to-child transmission by saliva. In a Zambian survey, all children with KS had mothers who were positive for HHV-8, whereas not all children whose mothers had KS were HHV-8 positive. In another Zambian survey, 13.8% of children were seropositive for HHV-8 by age 4. Seroprevalence has not been shown to vary significantly because of gender or marital status. The most recent common ancestor of this virus in

976-469: Is not fully understood. But it has been shown that the latency associated gene expression can be explained in part by a characteristic epigenetic state that KSHV episome acquires during latency. LANA plays an important role during latency, regulating both host and virus transcripts and binding to multiple active promoters; it also associates with the host protein hSET1 that creates H3K4me3 marks in chromatin. Various signals such as inflammation may provoke

1037-728: Is often accompanied by emergence of nonspecific symptoms , such as low-grade fever, headache, sore throat, malaise , and rash, as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells . In animal models, local trauma and system stress have been found to induce reactivation of latent herpesvirus infection. Cellular stressors like transient interruption of protein synthesis and hypoxia are also sufficient to induce viral reactivation. The three mammalian subfamilies – Alpha -, Beta - and Gamma - herpesviridae – arose approximately 180 to 220 mya . The major sublineages within these subfamilies were probably generated before

1098-542: Is to encode viral proteins that detain the newly formed MHC in the endoplasmic reticulum (ER). The MHC cannot reach the cell surface and therefore cannot activate the T cell response. The MHCs can also be targeted for destruction in the proteasome or lysosome . The ER protein TAP also plays a role in MHC down regulation. Viral proteins inhibit TAP preventing the MHC from picking up a viral antigen peptide. This prevents proper folding of

1159-751: The International Committee on the Taxonomy of Viruses (ICTV) established Herpesvirus as a genus with 23 viruses among four groups. As of 2020, 115 species are recognized, all but one of which are in one of the three subfamilies. Herpesviruses can cause both latent and lytic infections. Nine herpesvirus types are known to primarily infect humans, at least five of which are extremely widespread among most human populations, and which cause common diseases: herpes simplex 1 and 2 (HSV-1 and HSV-2, also known as HHV-1 and HHV-2; both of which can cause orolabial and genital herpes ), varicella zoster (or HHV-3;

1220-459: The capsid , which is itself wrapped in a protein layer called the tegument containing both viral proteins and viral mRNAs and a lipid bilayer membrane called the envelope . This whole particle is known as a virion . The structural components of a typical HSV virion are the Lipid bilayer envelope, Tegument, DNA, Glycoprotein spikes and Nucleocapsid. The four-component Herpes simplex virion encompasses

1281-475: The DNA synthesis enzymes required to replicate the virus genome. During lytic replication, it is believed that the virus genome is replicated as a continuous linear molecule off of an episome (so-called rolling circle model ). As each unit genome is replicated, it is cut within the terminal repeat region, and then packaged into a virus particle (virion). The virus then becomes enveloped with a lipid membrane as it transits

SECTION 20

#1732884800898

1342-674: The ERK/RSK MAPK signaling pathway ORF47 – gL – envelope glycoprotein involved in viral entry ORF49 – may be required for viral gene expression ORF50 – RTA, replication and transcription activator – the major transcription factor driving lytic KSHV reactivation ORF52 – KicGAS – tegument protein required for formation of virions and inhibition of cGAS DNA sensing ORF53 – gN – envelope glycoprotein ORF55 – uncharacterized ORF57 – MTA – regulates RNA stability, export and translation of viral genes Herpesvirus See text Herpesviridae

1403-461: The MHC and therefore the MHC does not reach the cell surface. Below are the nine distinct viruses in this family known to cause disease in humans. In addition to the herpesviruses considered endemic in humans, some viruses associated primarily with animals may infect humans. These are zoonotic infections: In animal virology , the best known herpesviruses belong to the subfamily Alphaherpesvirinae . Research on pseudorabies virus (PrV),

1464-510: The Mediterranean, Iran, and Xinjiang, China, has been estimated to have evolved 29,872 years (95% highest probability density 26,851–32,760 years) ago. the most recent common ancestor for viruses isolated in Xinjiang was 2037 years (95% highest probability density 1843–2229 years) ago. Given the historical links between the Mediterranean and Xinjiang during the Roman period it seems likely that this virus

1525-496: The S727 residue. Another one of the many ways in which herpes viruses evade the immune system is by down regulation of MHC I and MHC II . This is observed in almost every human herpesvirus. Down regulation of MHC I and MHC II can come about by many different mechanisms, most causing the MHC to be absent from the cell surface. As discussed above, one way is by a viral chemokine homolog such as IL-10. Another mechanism to down regulate MHCs

1586-418: The alphaherpesviruses may have been the earliest branch. The time of origin of the genus Iltovirus has been estimated to be 200 mya while those of the mardivirus and simplex genera have been estimated to be between 150 and 100 mya. Herpesviruses are known for their ability to establish lifelong infections. One way this is possible is through immune evasion. Herpesviruses have many different ways of evading

1647-473: The anti-programmed cell death protein 1 ( PD-1 )/programmed death-ligand 1 ( PD-L1 ) has been a great success. Because of KSHV infection, the monocytes increase the expression of PD-1, which is an inhibitory molecule, and cause immune escape in many tumor types. There is high PD-1 expression in NK cells from KS-HIV patients and cause exhausted phenotype. The anti-PD-1 antibody, ( nivolumab or pembrolizumab ), demonstrated

1708-439: The case of KSHV, genes that encode for complement -binding protein, IL-6 , BCL-2 , cyclin -D, a G protein-coupled receptor , interferon regulatory factor and Flice inhibitory protein ( FLIP ), as well as DNA synthesis proteins including dihydrofolate reductase , thymidine kinase , thymidylate synthetase , DNA polymerase and many others. While no other human tumor virus possesses these same genes, other tumor viruses target

1769-414: The causative agent of Aujeszky's disease in pigs, has pioneered animal disease control with genetically modified vaccines. PrV is now extensively studied as a model for basic processes during lytic herpesvirus infection, and for unraveling molecular mechanisms of herpesvirus neurotropism, whereas bovine herpesvirus 1 , the causative agent of bovine infectious rhinotracheitis and pustular vulvovaginitis ,

1830-479: The cause of chickenpox and shingles ), Epstein–Barr (EBV or HHV-4; implicated in several diseases, including mononucleosis and some cancers), and human cytomegalovirus (HCMV or HHV-5). More than 90% of adults have been infected with at least one of these, and a latent form of the virus remains in almost all humans who have been infected. Other human herpesviruses are human herpesvirus 6A and 6B (HHV-6A and HHV-6B) and human herpesvirus 7 (HHV-7), which are

1891-444: The cell (and thus the host) indefinitely. While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free. Chromatin dynamics regulate the transcription competency of entire herpes virus genomes. When the virus enters a cell, the cellular immune response is to protect the cell. The cell does so by wrapping the viral DNA around histones and condensing it into chromatin, causing

KSV - Misplaced Pages Continue

1952-447: The cell-mediated immune response and natural killer cell response, respectively. The similarities between hIL-10 and cmvIL-10 may be explained by the fact that hIL-10 and cmvIL-10 both use the same cell surface receptor, the hIL-10 receptor. One difference in the function of hIL-10 and cmvIL-10 is that hIL-10 causes human peripheral blood mononuclear cells ( PBMC ) to both increase and decrease in proliferation whereas cmvIL-10 only causes

2013-496: The double-stranded DNA genome into an icosahedral nucleocapsid. There is tegument around. Tegument contains filaments, each 7 nm wide. It is an amorphous layer with some structured regions. Finally, it is covered with a lipoprotein envelope. There are spikes made of glycoprotein protruding from each virion. These can expand the diameter of the virus to 225 nm. The diameters of virions without spikes are around 186 nm. There are at least two unglycosylated membrane proteins in

2074-527: The etiological agents for Roseola , and HHV-8 (also known as KSHV) which is responsible for causing Kaposi's sarcoma-associated herpesvirus . HHV here stands for "Human Herpesvirus". In total, more than 130 herpesviruses are known, some of them from mammals, birds, fish, reptiles, amphibians, and molluscs. Among the animal herpesviruses are pseudorabies virus causing Aujeszky's disease in pigs, and bovine herpesvirus 1 causing bovine infectious rhinotracheitis and pustular vulvovaginitis . Additionally,

2135-772: The expression of PD-L1 and increase the CD8+ T cell killing. KSHV encodes for ~90 genes and multiple non-coding RNAs, such as microRNAs. The "ORF" genes are named based on genome position of the homologous genes in the first rhadinovirus described, herpesvirus saimiri. The "K" genes are unique to KSHV, Some KSHV genes have well-characterized functions, while others remain uncharacterized. ORF2 – dihydrofolate reductase ORF8 – gB – envelope glycoprotein involved in viral entry ORF9 – Pol8 – DNA polymerase required for viral DNA replication ORF10 – regulates RNA export and responses to type I IFNs ORF16 – v Bcl2 ORF18, ORF24, ORF30, ORF31, ORF34, ORF66 – viral transcription factors required for

2196-901: The expression of late genes ORF21 – vTK – thymidine kinase ORF22 – gH – envelope glycoprotein involved in viral entry ORF23 – uncharacterized ORF25, ORF26 and ORF65 – capsid proteins ORF33 – involved in viral particle formation ORF34 – unclear function ORF35 – unclear function, mutant does not express early viral genes ORF36 – vPK – viral protein kinase with multiple roles in replication cycle ORF37 – SOX – dual function protein – DNase activity required for genome packaging and RNase activity regulates host gene expression ORF38 – involved in viral particle formation ORF39 – gM – envelope glycoprotein ORF40 and ORF41 – helicase and primase – DNA replication ORF42 – uncharacterized ORF45 – tegument protein, binds and prevents dephosphorylation of p90 ribosomal S6 kinases (RSKs) and ERK for modulate

2257-524: The functions of microRNAs, a detailed protocol of bacmid mutagenesis and a complete set of cell-lines carrying microRNA deletion mutants have been established and are available as a resource to researchers. Additionally, it has been shown that vFLIP and vCyclin interfere with the TGF-β signaling pathway indirectly by inducing the oncogenic host mir17-92 cluster. These observations represents a novel mechanism that may be important for KSHV tumorigenesis and angiogenesis,

2318-424: The host immune system, there is ample chance for clinical intervention to recover this change. One challenge is overexpression inhibitory of target cell repress immune. Under longtime inflammation stimulation, the target cell becomes unable to respond, which leads to an exhausted phenotype. The activation immunotherapies can revive and enhance immune cell function. Comparing to other immunotherapies, therapies targeting

2379-460: The immune system. One such way is by encoding a protein mimicking human interleukin 10 (hIL-10) and another is by downregulation of the major histocompatibility complex II (MHC II) in infected cells. Research conducted on cytomegalovirus (CMV) indicates that the viral human IL-10 homolog, cmvIL-10, is important in inhibiting pro-inflammatory cytokine synthesis. The cmvIL-10 protein has 27% identity with hIL-10 and only one conserved residue out of

2440-413: The mammalian radiation of 80 to 60 mya. Speciations within sublineages took place in the last 80 million years probably with a major component of cospeciation with host lineages. All the currently known bird and reptile species are alphaherpesviruses. Although the branching order of the herpes viruses has not yet been resolved, because herpes viruses and their hosts tend to coevolve this is suggestive that

2501-486: The nine amino acids that make up the functional site for cytokine synthesis inhibition on hIL-10. There is, however, much similarity in the functions of hIL-10 and cmvIL-10. Both have been shown to down regulate IFN-γ , IL-1α , GM-CSF , IL-6 and TNF-α , which are all pro-inflammatory cytokines. They have also been shown to play a role in downregulating MHC I and MHC II and up regulating HLA-G (non-classical MHC I). These two events allow for immune evasion by suppressing

KSV - Misplaced Pages Continue

2562-474: The nucleus and the cytoplasm to exit the cell. Thus, whereas KSHV genome is circular in the nucleus of latently infected cells, it is packaged into infectious viruses as a linear molecule. When the virus enters into lytic replication, thousands of virus particles can be made from a single cell, which usually results in death of the infected cell. It was discovered in 2020 that infection with the SARS-CoV-2 virus,

2623-478: The outer envelope of the virion. There are also 11 glycoproteins. These are gB, gC, gD, gE, gG, gH, gI, gJ, gK, gL and gM. Tegument contains 26 proteins. They have duties such as capsid transport to the nucleus and other organelles, activation of early gene transcription, and mRNA degradation. The icosahedral nucleocapsid is similar to that of tailed bacteriophage in the order Caudovirales . This capsid has 161 capsomers consisting of 150 hexons and 11 pentons, as well as

2684-498: The replication of herpesviruses such as KSHV have been used to successfully prevent development of Kaposi's sarcoma, although once the tumor develops these drugs are of little or no use. For patients with AIDS-KS, the most effective therapy is highly active antiretroviral therapy to reduce HIV infection. AIDS patients receiving adequate anti-HIV treatment may have up to a 90% reduction in Kaposi's sarcoma occurrence. Although KSHV affects

2745-448: The same cellular pathways illustrating that at a basic level, all tumor viruses appear to attack the same cellular control pathways, so-called tumor suppressor pathways. Crucial for the entry of KSHV into cells are the EPH receptor A2 , Hrs, TSG101 , and a few integrins (whose identity has yet to be confirmed). After infection, the virus enters into lymphocytes via macropinosomes . Once

2806-403: The same term [REDACTED] This disambiguation page lists articles associated with the title KSV . If an internal link led you here, you may wish to change the link to point directly to the intended article. Retrieved from " https://en.wikipedia.org/w/index.php?title=KSV&oldid=1250822468 " Category : Disambiguation pages Hidden categories: Short description

2867-498: The species Iguanid herpesvirus 2 is currently unassigned to a genus and subfamily. See Herpesvirales#Taxonomy for information on taxonomic history, phylogenetic research, and the nomenclatural system. All members of the Herpesviridae share a common structure; a relatively large, monopartite, double-stranded, linear DNA genome encoding 100–200 genes encased within an icosahedral protein cage (with T=16 symmetry) called

2928-419: The virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus. Within the nucleus, replication of viral DNA and transcription of viral genes occurs. During symptomatic infection, infected cells transcribe lytic viral genes. In some host cells, a small number of viral genes termed latency-associated transcript (LAT) accumulate, instead. In this fashion, the virus can persist in

2989-472: The virus is contracted are not well understood. Healthy individuals can be infected with the virus and show no signs or symptoms, due to the immune system's ability to keep the infection in check. Infection is of particular concern to the immunocompromised . Cancer patients receiving chemotherapy, AIDS patients, and organ transplant patients are all at a high risk of showing signs of infection. . Recent advances in sequencing technologies have uncovered that virus

3050-407: The virus is transmitted through non-sexual routes in developing countries. KSHV is a herpesvirus , and is a large double-stranded DNA virus with a protein covering that packages its nucleic acids, called the capsid , which is then surrounded by an amorphous protein layer called the tegument , and finally enclosed in a lipid envelope derived in part from the cell membrane. KSHV has a genome which

3111-400: The virus newly infects a cell, the lipid membrane is shed and the virion travels to the nucleus. The viral genome is released where it circularizes into an episome through a poorly understood process that appears to involve homologous recombination of the terminal repeats. The viral episome is chromatinized upon entry into the host cell nucleus. After entry, the virus typically remains in

SECTION 50

#1732884800898

3172-612: The virus to become dormant, or latent. If cells are unsuccessful and the chromatin is loosely bundled, the viral DNA is still accessible. The viral particles can turn on their genes and replicate using cellular machinery to reactivate, starting a lytic infection. Reactivation of latent viruses has been implicated in a number of diseases (e.g. shingles , pityriasis rosea ). Following activation, transcription of viral genes transitions from LAT to multiple lytic genes; these lead to enhanced replication and virus production. Often, lytic activation leads to cell death . Clinically, lytic activation

3233-507: The virus to enter into lytic replication. The primary viral protein responsible for the switch between latent and lytic replication is known as the ORF50 Replication Transactivation Activator (RTA). When cell signaling conditions activate the generation of RTA, it in turn activates synthesis of a stereotypic cascade of secondary and tertiary viral proteins that ultimately make components of the virus capsid and also

3294-448: The virus which causes COVID-19 , may induce the lytic reactivation of KSHV in the human body, causing the herpes virus to cease latency and begin the formation of cancerous cells. Further, it was discovered that some medications used to treat the infection with SARS-CoV-2, namely Nafamostat and Azithromycin , ended up promoting the production of mature virions, "... potentially inducing KSHV lytic reactivation." The mechanisms by which

3355-555: The virus, caution should be used by sex partners in having unprotected sex and activities where saliva might be shared during sexual activity. Prudent advice is to use condoms when needed and avoid deep kissing with partners who may have KSHV infections. Kaposi's sarcoma is usually a localized tumor that can be treated either surgically or through local irradiation. Chemotherapy with drugs such as liposomal anthracyclines or paclitaxel may be used, particularly for invasive disease. Antiviral drugs, such as ganciclovir , that target

3416-563: Was also found to phosphorylate Stat3. PI3K inhibition, unlike JAK inhibition, did have a significant impact on cytokine synthesis. The difference between PI3K and JAK in Stat3 phosphorylation is that PI3K phosphorylates Stat3 on the S727 residue whereas JAK phosphorylates Stat3 on the Y705 residue. This difference in phosphorylation positions seems to be the key factor in Stat3 activation leading to inhibition of pro-inflammatory cytokine synthesis. In fact, when

3477-532: Was introduced to Xinjiang along the Silk Road . The mutation rate was estimated to be 3.44 × 10 substitutions per site per year (95% highest probability density 2.2 × 10 to 4.71 × 10 ). However, the global distribution of different genotypes of KSHV and the potential transmission path need further studies. Typing of isolates is based on the variable K1 membrane protein. Six types are recognised (A–F). Since persons infected with KSHV will asymptomatically give

3538-590: Was later determined to be extremely common throughout sub-Saharan African populations. This led to the first suggestions in the 1950s that this tumor might be caused by a virus. With the onset of the AIDS epidemic in the early 1980s, there was a sudden resurgence of KS affecting AIDS patients, with up to 50% of reported AIDS patients having this tumor—an extraordinary rate of cancer predisposition. Careful analysis of epidemiologic data by Valerie Beral, Thomas Peterman and Harold Jaffe , led these investigators to propose that KS

3599-440: Was that if a virus causes KS, the genomic DNA in the two samples should be precisely identical except for DNA belonging to the virus. In their initial RDA experiment, they isolated two small DNA fragments that represented less than 1% of the actual viral genome. These fragments were similar (but still distinct from) the known herpevirus sequences, indicating the presence of a new virus. Starting from these fragments, this research team

3660-718: Was then able to sequence the entire genome of the virus less than two years later. The discovery of this herpesvirus sparked considerable controversy and scientific in-fighting until sufficient data had been collected to show that indeed KSHV was the causative agent of Kaposi's sarcoma. The virus is now known to be a widespread infection of people living in sub-Saharan Africa; intermediate levels of infection occur in Mediterranean populations (including Lebanon, Saudi Arabia, Italy, and Greece) and low levels of infection occur in most Northern European and North American populations. Gay and bisexual men are more susceptible to infection (through still unknown routes of sexual transmission) whereas

3721-420: Was ultimately identified in 1994 by Yuan Chang and Patrick S. Moore , a wife and husband team at Columbia University , through the isolation of DNA fragments from a herpesvirus found in a KS tumor in an AIDS patient. Chang and Moore used representational difference analysis , or RDA, to find KSHV by comparing KS tumor tissue from an AIDS patient to his own unaffected tissue. The idea behind this experiment

SECTION 60

#1732884800898
#897102