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Kaposi's sarcoma-associated herpesvirus (KSHV) is the eighth human herpesvirus; its formal name according to the International Committee on Taxonomy of Viruses (ICTV) is HHV-8. In 1872, Moritz Kaposi described a blood vessel tumor[3] (originally called "idiopathic multiple pigmented sarcoma of the skin") that has since been eponymously named Kaposi's sarcoma (KS).
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.
After infection, the virus enters into lymphocytes via macropinosomes where it remains in a latent ("quiet") state expressing the viral latency-associated nuclear antigen, LANA. The viral genome consists of a ~145 kbase long unique region, encoding all of expressed viral genes, which is flanked by ~20-30 kbases of terminal repeat sequences.[9] Each terminal repeat unit is 801 bp in length, has 85% G+C content and is oriented in a repetitive head-to-tail fashion. The primary viral protein responsible for the switch between latent and lytic replication is the ORF50 Replication Transactivation Activator (RTA).
Infection with this virus is thought to be lifelong, but a healthy immune system will keep the virus in check. Since persons infected with KSHV will asymptomatically give the virus, caution should be used by sex partners in having unprotected sex and activities where saliva might be shared during sexual activity. Kaposi's sarcoma is usually a localized tumor that can be treated either surgically or through local irradiation. Vironome of Kaposi sarcoma associated herpesvirus-inflammatory cytokine syndrome in an AIDS patient reveals co-infection of human herpesvirus 8 and human herpesvirus 6A.
KSHV inflammatory cytokine syndrome (KICS) is a newly described condition characterized by systemic illness as a result of systemic, lytic KSHV infection. Oral human papillomavirus and human herpesvirus-8 infections among human immunodeficiency virus type 1-infected men and women in Italy. BACKGROUND: Oral human papillomavirus (HPV) and human herpesvirus-8 (HHV8) infections are sexually transmitted and respectively associated with the development of oropharyngeal carcinoma and Kaposi sarcoma. Human herpesvirus 6, HHV-6 o herpesvirus humano 6, tambien conocido antiguamente como human B-lymphotropic virus (HBLV) o virus linfotropico B humano es un virus de la familia Herpesviridae, uno de los 8 (HHV-1 a HHV-8) que infecta a los humanos.[1] Existen dos subtipos de HHV-6, denominados HHV-6A (el virus linfotropico B humano) y HHV-6B (relacionado con la roseola infantil). HHV-6B es responsable de hasta un 93% de las infecciones primarias en Europa y America del Norte.
La reactivacion del HHV-6 puede causar enfermedades graves en las personas trasplantadas y puede dar lugar a episodios de rechazo, a menudo en conjuncion con otros betaherpesviridae. El HHV-6 tambien ha sido encontrado en pacientes de esclerosis multiple[5] e implicado como cofactor en varias otras enfermedades, incluyendo el sindrome de fatiga cronica,[6] fibromialgia, sida,[7] y epilepsia del lobulo temporal[8] pero todavia no se ha establacido el vinculo definitivo.
Human herpesvirus 7 — Closely related to HHV 6, human herpesvirus 7 has also been linked to roseola. Like other herpesviruses, its informal name (KSHV) is used interchangeably with its ICTV name. KS was thought to be an uncommon tumor of Jewish and Mediterranean populations until it was realized that it is actually quite common throughout sub-Saharan Africa.

Moore, a wife and husband team at Columbia University in 1994,[5][6][7] by isolating DNA fragments of a herpesvirus from a Kaposi's sarcoma (KS) tumor in an AIDS patient. The virus exists as a naked circular piece of DNA called an episome and uses the cellular replication machinery to replicate itself. During latency, the virus genome depends on the host replication machinery and replicates as closed circular episome ("plasmid") using sequences within the terminal repeats as a replication origin. 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. Prudent advice is to use condoms when needed and avoid deep kissing with partners with KSHV and HIV infections or whose status is unknown. Chemotherapy with drugs such as liposomal anthracyclines or paclitaxel may be used, particularly for invasive disease.
Tales infecciones usualmente causan fiebre, con en el 10% de los casos exantema subita (roseola, erupcion).[3] Las infecciones primarias por HHV-6 cuentan hasta el 20% de las hospitalizaciones infantiles en los Estados Unidos[4] y se asocian con varias complicaciones mas graves, como encefalitis, linfadenopatia, miocarditis y mielosupresion. Researchers believe it may also cause seizures and other central nervous system symptoms in children. This virus causes Kaposi's sarcoma, a cancer commonly occurring in AIDS patients,[1] as well as primary effusion lymphoma[2] and some types of multicentric Castleman's disease.
As early as 1984, scientists had reported seeing herpesvirus-like structures in KS tumors by electron microscopy. It is a rhadinovirus, and is remarkable since it has stolen numerous genes from host cells including 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.
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"). When the virus reactivates into lytic replication, it is believed that the virus genome is replicated as a continuous linear molecule off from an episome (so called rolling circle model).
Kaposi's sarcoma occurs when someone who has been infected with KSHV becomes immunocompromised due to AIDS, medical treatment or very rarely aging. Antiviral drugs, such as ganciclovir, that target the replication of herpesviruses such as KSHV have been used to successfully prevent development of Kaposi's sarcoma,[24] although once the tumor develops these drugs are of little or no use.
Despues de la infeccion primaria, el virus se establece en el mieloide y en la medula osea y permanece latente por el tiempo de vida del huesped. Aunque hasta el 100% de la poblacion ha estado expuesta (seropositivo) al HHV-6, hay muy pocos casos de infecciones primarias en los adultos.
With the onset of the AIDS epidemic in the early 1980s, there was a sudden epidemic resurgence of KS affecting primarily gay and bisexual AIDS patients with up to 50% of reported AIDS patients having this tumor—an extraordinary rate of cancer predisposition. Scientists by then had been searching for the agent causing Kaposi's sarcoma and over 20 agents had been described as the possible cause of KS, including cytomegalovirus and HIV itself. Various signals such as inflammation may provoke the virus to enter into lytic replication.

As each unit genome is replicated, it is cut within the terminal repeat region, and then packaged into a virus particle (virion).
Cancer patients receiving chemotherapy, AIDS patients and organ transplant patients are all at a high risk of showing signs of infection. For patients with AIDS-KS, the most effective therapy is highly active antiretroviral therapy to reduce HIV infection.[25] AIDS patients receiving adequate anti-HIV treatment may have up to a 90% reduction in Kaposi's sarcoma occurrence. El virus periodicamente se reactiva desde el estado latente, con ADN de HHV-6 siendo detectable en un 20-25% de los adultos sanos en los Estados Unidos.
En los Estados Unidos, estos casos se han relacionado mas con el HHV-6A, que se supone mas patogeno y mas neurotropico y se ha vinculado a varios trastornos relacionado con el sistema nervioso central. Careful analysis of epidemiologic data by Valerie Beral, Thomas Peterman and Harold Jaffe,[4] led these investigators to propose that KS is caused by an unknown sexually transmitted virus that rarely causes tumors unless the host becomes immunosuppressed, as in AIDS. 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.
When this occurs, the viral episome starts replicating itself in the form of linear DNA molecules that are packaged into virus particles which are expelled from the cell, to infect new cells or to be transmitted to a new host. The virus then becomes enveloped with a lipid membrane as it transits the nucleus and the cytoplasm to exit the cell. En la mayoria de los casos, estas re-activaciones a menudo son asintomaticas, pero en individuos inmunodeprimidos puede haber complicaciones graves.
The idea behind this experiment 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. 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. Thus, whereas KSHV genome is circular in the nucleus of latently infected cells, it is packaged into infectious viruses as a linear molecule. In their initial RDA experiment, they isolated two small DNA fragments that represented less than 1% of the actual viral genome.
Once the virus newly infects a cell, the lipid membrane is shed and the virion travels to the nucleus.
These fragments were similar to but distinct from known herpevirus sequences indicating the presence of a new virus. The viral genome is released where it recircularizes through a poorly understood process that appears to involve homologous recombination.
Starting from these fragments, this research team was then able to sequence the entire genome of the virus less than two years later.

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