Abstract
Kaposi sarcoma herpesvirus (KSHV), taxonomical name human gammaherpesvirus 8, is a phylogenetically old human virus that co-evolved with human populations, but is now only common (seroprevalence greater than 10%) in sub-Saharan Africa, around the Mediterranean Sea, parts of South America and in a few ethnic communities. KSHV causes three human malignancies, Kaposi sarcoma, primary effusion lymphoma, and many cases of the plasmablastic form of multicentric Castleman's disease (MCD) as well as occasional cases of plasmablastic lymphoma arising from MCD; it has also been linked to rare cases of bone marrow failure and hepatitis. As it has colonized humans physiologically for many thousand years, cofactors are needed to allow it to unfold its pathogenic potential. In most cases, these include immune defects of genetic, iatrogenic or infectious origin, and inflammation appears to play an important role in disease development. Our much improved understanding of its life cycle and its role in pathogenesis should now allow us to develop new therapeutic strategies directed against key viral proteins or intracellular pathways that are crucial for virus replication or persistence. Likewise, its limited (for a herpesvirus) distribution and transmission should offer an opportunity for the development and use of a vaccine to prevent transmission.This article is part of the themed issue ‘Human oncogenic viruses’.
Highlights
Kaposi sarcoma herpesvirus (KSHV), taxonomical name human gammaherpesvirus 8, is a phylogenetically old human virus that co-evolved with human populations, but is only common in sub-Saharan Africa, around the Mediterranean Sea, parts of South America and in a few ethnic communities
KSHV causes three human malignancies, Kaposi sarcoma, primary effusion lymphoma, and many cases of the plasmablastic form of multicentric Castleman’s disease (MCD) as well as occasional cases of plasmablastic lymphoma arising from MCD; it has been linked to rare cases of bone marrow failure and hepatitis
Of particular interest could be the early phase of the lytic replication cycle, which appears to be adopted by the virus in lymphatic endothelial cells and in many KS biopsies, as well as in MCD and some primary effusion lymphoma (PEL) tumours, and during which key viral proteins with pathogenic properties are expressed
Summary
First described by Moritz Kaposi in 1872 as ‘idiopathic multiple pigmented sarcoma of the skin’ occurring mainly in elderly males of Mediterranean origin [1], Kaposi sarcoma (KS) has long been considered an unusual neoplasm. KS was rare in those who had contracted HIV through blood donations and among HIV-infected women [4] These observations, together with a further detailed epidemiological analysis of the behavioural risk factors among people with HIV/AIDS, led to the conclusion that KS was most likely caused by a new sexually transmissible infectious agent that appeared to be transmitted independently of HIV. These predictions led to attempts in several laboratories to identify the putative transmissible cause of KS and eventually to the discovery, by Yuan Chang, Patrick Moore and colleagues, of sequence fragments belonging to a new human herpesvirus in biopsies of AIDS-associated KS [5]. KSHV was classified as a class I carcinogen by IARC/WHO in 2009 [20,21]
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