Abstract:The pathobiology of Kaposi's sarcoma: advances since the onset of the AIDS epidemicSince the perplexing early Kaposi's sarcoma (KS) observations at the dawn of the acquired immunodeficiency syndrome epidemic, KS has been extensively studied, revealing a complex disease. The identification and complete elucidation of the genome of its causal agent, the KS-associated herpesvirus/human herpesvirus 8, have shed important insights into the pathobiology of this disease. The purpose of this review is to describe the … Show more
“…In latency, the expression of viral genes is kept to the minimum to maintain the episome and to enable it to persist through cell replication cycles. In the lytic state, the virus reactivates the production of entire virions and lyses the newly infected host cells (Jenner et al, 2001;Dourmishev et al, 2003;zur Hausen, 2006;Horenstein et al, 2008).…”
Section: Viral Epigenomes In Human Tumorigenesis Af Fernandez and M Ementioning
Viruses are associated with 15-20% of human cancers worldwide. In the last century, many studies were directed towards elucidating the molecular mechanisms and genetic alterations by which viruses cause cancer. The importance of epigenetics in the regulation of gene expression has prompted the investigation of virus and host interactions not only at the genetic level but also at the epigenetic level. In this study, we summarize the published epigenetic information relating to the genomes of viruses directly or indirectly associated with the establishment of tumorigenic processes. We also review aspects such as viral replication and latency associated with epigenetic changes and summarize what is known about epigenetic alterations in host genomes and the implications of these for the tumoral process. The advances made in characterizing epigenetic features in cancer-causing viruses have improved our understanding of their functional mechanisms. Knowledge of the epigenetic changes that occur in the genome of these viruses should provide us with markers for following cancer progression, as well as new tools for cancer therapy.
“…In latency, the expression of viral genes is kept to the minimum to maintain the episome and to enable it to persist through cell replication cycles. In the lytic state, the virus reactivates the production of entire virions and lyses the newly infected host cells (Jenner et al, 2001;Dourmishev et al, 2003;zur Hausen, 2006;Horenstein et al, 2008).…”
Section: Viral Epigenomes In Human Tumorigenesis Af Fernandez and M Ementioning
Viruses are associated with 15-20% of human cancers worldwide. In the last century, many studies were directed towards elucidating the molecular mechanisms and genetic alterations by which viruses cause cancer. The importance of epigenetics in the regulation of gene expression has prompted the investigation of virus and host interactions not only at the genetic level but also at the epigenetic level. In this study, we summarize the published epigenetic information relating to the genomes of viruses directly or indirectly associated with the establishment of tumorigenic processes. We also review aspects such as viral replication and latency associated with epigenetic changes and summarize what is known about epigenetic alterations in host genomes and the implications of these for the tumoral process. The advances made in characterizing epigenetic features in cancer-causing viruses have improved our understanding of their functional mechanisms. Knowledge of the epigenetic changes that occur in the genome of these viruses should provide us with markers for following cancer progression, as well as new tools for cancer therapy.
“…Some analyses (6,30,48) have favored classifying it as a lytic gene, while others (47) suggest that it can be expressed in some PEL cells that do not stain for lytic markers, though these cells represented only 5% of all LANA ϩ cells. Most recent reviews, however, have not included v-IL-6 on the list of known latent genes (19,25,29,31).…”
“…19 This virus, a member of the herpesvirus family, was named KS-associated herpesvirus (KSHV) and later classified as human herpesvirus 8 (HHV-8). 20 In subequatorial Africa, over 30% of the general population carries HHV-8 antibodies. Seropositivity for the virus ranges from 10 to 25% in the Mediterranean area.…”
Section: Kaposi Sarcomamentioning
confidence: 99%
“…Where KS is not endemic, the seroprevalence of HHV-8 is around 2-5%. 20 Evidence exists for saliva as a route of transmission. Transmission to children within families in endemic regions such as the Mediterranean and subequatorial Africa is not likely to be sexual, further supporting a salivary and close contact mode of transmission.…”
Section: Kaposi Sarcomamentioning
confidence: 99%
“…The role of a sexual route of transmission in the male homosexual population remains under debate. 20 When KS is seen in the GIT, the spindled component is often prominent, but it can be subtle in the stomach (Figures 3a and b). These cells form slit-like spaces that frequently contain red blood cells.…”
Interpretation of gastrointestinal tract mesenchymal lesions is simplified merely by knowing in which anatomic layer they are usually found. For example, Kaposi sarcoma is detected on mucosal biopsies, whereas inflammatory fibroid polyp is nearly always in the submucosa. Gastrointestinal stromal tumors (GISTs) are generally centered in the muscularis propria. Schwannomas are essentially always in the muscularis propria. Mesenteric lesions are usually found in the small bowel mesentery. Knowledge of the favored layer is even most important in interpreting colon biopsies, as many mesenschymal polyps are encountered in the colon. Although GISTs are among the most common mesenchymal lesions, we will concentrate our discussion on other mesenchymal lesions, some of which are in the differential diagnosis of GIST, and point out some diagnostic pitfalls, particularly in immunolabeling.
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