Kaposi's sarcoma: Presence of herpes-type virus particles in a tumor specimen

doi:10.1016/S0046-8177(84)80309-3

Human Pathology

Volume 15, Issue 12, December 1984, Pages 1145-1146

https://doi.org/10.1016/S0046-8177(84)80309-3 Get rights and content

Three Kaposi's sarcoma biopsy specimens obtained from three African patients with typical nodular cutaneous tumors were investigated morphologically for cellular modifications suggestive of a viral origin. In one case a Kaposi's sarcoma cell of the endothelial type contained a few intranuclear herpes-type viral inclusions. The present findings complement previous reports of herpes-type viral particles in Kaposi's sarcoma cultured cell lines and suggest that, at least under certain conditions, Kaposi's sarcoma cells enter a virus-producing phase.

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Gammaherpesvirus entry and fusion: A tale how two human pathogenic viruses enter their host cells
2019, Advances in Virus Research
Citation Excerpt :
The first report of AIDS described that approximately 37% of the patients had KS (Centers For Disease Control, 1982b), HIV was only identified shortly afterward (Barre-Sinoussi et al., 1983; Gallo et al., 1984). In 1984, herpes-like structures were found in KS lesions using electron microscopy (Walter et al., 1984), but at that time several other viruses were discussed to be causative. It was another decade and more than a century after the first report of KS that Chang and Moore identified that a herpesvirus was present in tumor cells using representational difference analysis using DNA from a KS lesion from an AIDS patient (Chang et al., 1994).
The prototypical human γ-herpesviruses Epstein-Barr virus (EBV) and Kaposi Sarcoma-associated herpesvirus (KSHV) are involved in the development of malignancies. Like all herpesviruses, they share the establishment of latency, the typical architecture, and the conserved fusion machinery to initiate infection. The fusion machinery reflects virus-specific adaptations due to the requirements of the respective herpesvirus. For example, EBV evolved a tropism switch involving either the B- or epithelial cell-tropism complexes to activate fusion driven by gB. Most of the EBV entry proteins and their cellular receptors have been crystallized providing molecular details of the initial steps of infection. For KSHV, a variety of entry and binding receptors has also been reported but the mechanism how receptor binding activates gB-driven fusion is not as well understood as that for EBV. However, the downstream signaling pathways that promote the early steps of KSHV entry are well described. This review summarizes the current knowledge of the key players involved in EBV and KSHV entry and the cell-type specific mechanisms that allow infection of a wide variety of cell types.
The conundrum of causality in tumor virology: The cases of KSHV and MCV
2014, Seminars in Cancer Biology
Citation Excerpt :
In the 1970s, the herpesvirus cytomegalovirus (CMV) was first proposed as the likely cause for KS, based mainly on antibody reactivity studies [36]. Careful electron microscopy soon revealed scattered herpes-like capsids in an African KS tumor [37]. KS had first been described by Moriz Kaposi in 1872 as an aggressive tumor in five patients that quickly led to death [38].
Controversy has plagued tumor virology since the first tumor viruses were described over 100 years ago. Methods to establish cancer causation, such as Koch's postulates, work poorly or not at all for these viruses. Kaposi's sarcoma herpesvirus (KSHV/HHV8) and Merkel cell polyomavirus (MCV) were both found using nucleic acid identification methods but they represent opposite poles in the patterns for tumor virus epidemiology. KSHV is uncommon and has specific risk factors that contribute to infection and subsequent cancers. MCV and Merkel cell carcinoma (MCC), in contrast, is an example in which mutations to our normal viral flora contribute to cancer. Given the near-ubiquity of human MCV infection, establishing cancer causality relies on molecular evidence that does not fit comfortably within traditional infectious disease epidemiological models. These two viruses reveal some of the challenges and opportunities for inferring viral cancer causation in the age of molecular biology.
Human herpesvirus 8 infections in patients with immunodeficiencies
2008, Human Pathology
Citation Excerpt :
They called the virus KS herpesvirus, now recognized as human herpesvirus 8 (HHV-8). Retrospectively, one can extrapolate that the results published by Giraldo et al [5] in 1972 and by Walter et al [6] in Human Pathology in 1984, describing the presence of herpes-type virus particles in KS, were the first identification of HHV-8. Different tools were developed that allowed molecular and seroepidemiologic studies.
In 1994, Chang et al described a novel herpesvirus in tissues from patients with Kaposi sarcoma, referred to as Kaposi sarcoma herpesvirus or human herpesvirus 8. They used a very sophisticated technique of molecular biology to isolate unknown DNA sequences from Kaposi sarcoma lesions, which were not present in normal tissues. It turned out that these sequences corresponded to a previously unrecognized gamma herpesvirus highly homologous to human herpesvirus 4 (Epstein-Barr virus) and to herpesvirus saimiri. Contrary to Epstein-Barr virus, human herpesvirus 8 is not ubiquitous. The seroprevalence of human herpesvirus 8 varies greatly worldwide, with 1% to 10% of people being infected in developed countries and up to 80% of infected individuals in some areas of sub-Saharan and equatorial Africa. Human herpesvirus 8 is associated with a limited spectrum of tumors, mostly observed in immunodeficient individuals with HIV infection. Beside Kaposi sarcoma and multicentric Castleman disease, human herpesvirus 8 is associated with primary effusion lymphoma, but unlike Epstein-Barr virus, human herpesvirus 8 is not involved in epithelial tumors. Different proteins of the virus can be detected in infected cells. Antibodies against the latent nuclear antigen 1 are available in routine pathology and represent a powerful tool to detect the virus in human tissues. Although Epstein-Barr virus is the most frequent causative agent of lymphomas in immunocompromised individuals, a systematic screening of such tumors with specific antibodies reveals that the implication of human herpesvirus 8 infection is probably underestimated. Recent descriptions of non-Hodgkin lymphoma in endemic areas, solid localizations of primary effusion lymphoma, and posttransplantation lymphoproliferations have expanded the spectrum of human herpesvirus 8–related lymphoproliferative disorders. In this review, we will be presenting an overview of the recent concepts regarding human herpesvirus 8 and related disorders.
Kaposi's sarcoma-associated herpesvirus (KSHV or HHV8) in primary effusion lymphoma: Ultrastructural demonstration of herpesvirus in lymphoma cells
1996, Blood
Recent molecular evidence suggests an association with a new herpesvirus, Kaposi’s sarcoma-associated herpesvirus (KSHV/HHV - 8), and primary effusion lymphomas (PELs). PELs have a characteristic morphology, phenotype, and clinical presentation, with malignant effusions in the absence of a contiguous solid tumor mass. We have established a cell line (KS - 1) from a KSHV-positive human immunodeficiency virus (HlV)-negative patient with pleural cavity-based lymphoma that was passaged into triple-immunodeficient BNX mice. In contrast to cell lines from body cavity-based lymphomas derived from HIV-positive individuals that contain both KSHV and Epstein Barr viral genome, these cells contain only KSHV, allowing for uncontaminated virologic studies. Ultrastructural examination identified malignant cells with features of late differentiating B cells (immunoblasts). Cells with viral cytopathic effect contained typical 110-nm intranuclear herpesvirus nucleocapsids and complete cytoplasmic virions, confirming the association of PEL with KSHV.
Kaposi's sarcoma and KSHV
1995, The Lancet
Detection of cytomegalovirus DNA in classic and epidemic Kaposi's sarcoma by in situ hybridization
1988, Human Pathology
Several lines of evidence have suggested an etiologic association of cytomegalovirus (CMV) with Kaposi's sarcoma. This contention is supported by a pathoepidemiologic survey of 54 cases of acquired immunodeficiency syndrome (AIDS) at our own institution. Of the 27 patients with documented Kaposi's sarcoma, 24 (89%) showed histologic evidence of CMV infection (cytomegalic cells with viral inclusions), whereas only 9 (33%) of the patients with AIDS without Kaposi's sarcoma showed hallmarks of CMV infection. In an attempt to address this question further, we have searched for the presence of CMV nucleic acid sequences in a series of 25 patients with AIDS and Kaposi's sarcoma, using the technique of in situ DNA hybridization. The reliability of the in situ technique is demonstrated, and the technique is shown to be more sensitive than the detection of viral inclusions within Kaposi's sarcoma lesions by routine light microscopy. However, only 20% of our cases showed evidence of CMV involvement, and the CMV-positive cells within the affected Kaposi's sarcoma lesions were few and sparsely distributed. In addition, a companion series of 6 elderly patients with “classic” Kaposi's sarcoma showed no evidence of CMV infection by either conventional microscopy or in situ hybridization. These results do not support the notion of a strong association between Kaposi's sarcoma and CMV, unless the CMV sequences are present at a copy number too low for detection by these methods. The implications of these findings in light of current theories of CMV oncogenesis are discussed.

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¹: Received from the Institut d’Anatomie Pathologique, Faculté de Médecine, Strasbourg, France, the Hôpital Universitaire de Libreville, Gabon, and the Département d’Anatomie Pathologique, Hôpital de la Timone, Marseille, France.

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Kaposi's sarcoma: Presence of herpes-type virus particles in a tumor specimen

Hum Pathol

Special report: epidemiologic aspects of the current outbreak of Kaposi's sarcoma and opportunistic infections

N Engl J Med

Remarks on sex, age and racial distribution of Kaposi's sarcoma and on possible pathogenic factors

Acta Union Int Contre Cancer

Herpes-type virus particles in tissue culture of Kaposi's sarcoma from different geographic regions

J Natl Cancer Inst