Chapter 3 : Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8)

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As epidemiologic evidence accumulates, it is becoming increasingly clear that Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) (or human herpesvirus 8 [HHV-8]) is the likely infectious cause of KS and related neoplastic disorders. Immunosuppression is an important cofactor in KS pathogenesis, as shown by the occurrence of KS in post-transplant patients and its occasional regression after the reduction of iatrogenic immunosuppression. Whether KS is a hyperplastic process driven by cytokine dysregulation or represents the oligo-or monoclonal-expansion of virus-transformed endothelial cells remains controversial. Near-universal detection of KSKSHV DNA in all of the histologically indistinguishable forms of KS suggests that they share a common etiology. In addition to studies suggesting persistence of KSHV in prostate tissues from KS patients, one study has found that dorsal root ganglia may harbor viral DNA in patients with AIDS-KS. Cultivation of the virus in cells uninfected with Epstein-Barr virus (EBV) has led to the development of serologic tests and studies of KSHV gene expression during latency and lytic replication. The close correspondence between signal pathways activated by EBV infection and those activated by virus-encoded homologs during KSHV infection is seen for interleukin-6 (IL-6) signal transduction. DNA tumor viruses have been essential tools in dissecting out transformation pathways, and KSHV promises to provide a unique model for investigating virus-induced transformation. The unique epidemiology of KSHV and its public health importance, especially to parts of sub-Saharan Africa, suggest that this virus be accorded an important priority in the development of techniques for its control and treatment.

Citation: Schulz T, Chang Y, Moore P. 1998. Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8), p 87-134. In McCance D (ed), Human Tumor Viruses. ASM Press, Washington, DC. doi: 10.1128/9781555818289.ch3
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Image of Figure 1
Figure 1

Photomicrograph of a KS lesion showing characteristic spindle cells interwoven into the dermis and forming intersecting bands of tumor cells with irregular capillary channels underneath an intact epidermis. A prominent inflammatory infiltrate of plasma cells, lymphocytes, and macrophages is frequently present, suggesting an immunologic response to tumor-specific antigens (magnification, ×23; hematoxylin and eosin stain).

Citation: Schulz T, Chang Y, Moore P. 1998. Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8), p 87-134. In McCance D (ed), Human Tumor Viruses. ASM Press, Washington, DC. doi: 10.1128/9781555818289.ch3
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Image of Figure 2
Figure 2

Characteristic immunofluorescence staining of the KSHV-infected BCP-1 cell line with serum at 1:160 dilution from a patient with KS. The KSHV LANA encoded by ORF73 forms a speckled nuclear pattern, suggesting sub-nuclear localization, which is distinguishable from the diffuse, nonspecific cytoplasmic seroreactivity that is commonly seen with BCBL/PEL cell lines ( ).

Citation: Schulz T, Chang Y, Moore P. 1998. Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8), p 87-134. In McCance D (ed), Human Tumor Viruses. ASM Press, Washington, DC. doi: 10.1128/9781555818289.ch3
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Figure 3

(A) Immunoglobulin G (IgG) antibody kinetics of seroconversion with the LANA IFA for six homosexual, HIV-positive men followed by the MACS study who developed KS. All six patients seroconverted from a LANA IFA endpoint titer of 1:40 or less to greater than 1:160 at time 0 and were subsequently followed for 43 to 96 months until they developed KS (marked by X). Antibody titers did not significantly vary after seroconversion, suggesting that seroconversion is caused by initial KSHV infection rather than reactivation associated with immunosuppression. (B) Cumulative LANA seropositivity rate by IFA (solid line) and WB (dashed line) for 40 homosexual, HIV-positive men from entry into the MACS study until development of KS at time 0. Seroconversion rates were linear over time for both assays, with the median seropositivity rate being 32 months by WB and 46 months by IFA. Estimated sensitivities of these latent antigen assays at KS onset (0 timepoint) are 80 to 90%. Reprinted with permission from reference .

Citation: Schulz T, Chang Y, Moore P. 1998. Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8), p 87-134. In McCance D (ed), Human Tumor Viruses. ASM Press, Washington, DC. doi: 10.1128/9781555818289.ch3
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Figure 4

Extracellular, mature KSHV particles, found among cellular debris of lysed KS-1 cells which were derived from a body cavity-based lymphoma chronically infected with KSHV. These virus particles are seen exhibiting two different planes of sectioning through the center of the virus particles. Both of these mature herpesvirus particles exhibit an electron-dense viral DNA core region, surrounded by spherical capsid structure. The capsids of the virions are enclosed by an electron-lucent layer surrounded by the viral envelopes, which are seen with attached protein spikes. (Courtesy D. Ablashi.)

Citation: Schulz T, Chang Y, Moore P. 1998. Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8), p 87-134. In McCance D (ed), Human Tumor Viruses. ASM Press, Washington, DC. doi: 10.1128/9781555818289.ch3
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Figure 5

The KSHV -140.5-kb LUR encodes at least 81 ORFs and is flanked by the TR region composed of multiple TR units. Additional genes are likely to be delineated through experimental studies. Genes with homology to other herpesviruses (solid black) fall into regions which are well characterized gene blocks (1 through 7; open segments) conserved among herpesviruses. Genes unique to KSHV and related rhadinoviruses, some of which are homologs to cell signaling and regulatory genes, are designated with a K prefix (open segments) and lie in intervening nonconserved gene blocks. Terminal repeat sequences are composed of reiterated arrays of 801-bp units having high G:C content. Reprinted with permission from reference .

Citation: Schulz T, Chang Y, Moore P. 1998. Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8), p 87-134. In McCance D (ed), Human Tumor Viruses. ASM Press, Washington, DC. doi: 10.1128/9781555818289.ch3
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Figure 6

vIL-6 expression (Vector Red chromagen) in KSHV-infected plasmacytoid infiltrate found in the spleen of a patient with posttransplantation KS and generalized lymphadenopathy ( ). Cells show typical cytoplasmic immunostaining for vIL-6 expression (red) with nuclear exclusion (magnification, × 230; Mayer's hematoxylin counterstain).

Citation: Schulz T, Chang Y, Moore P. 1998. Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8), p 87-134. In McCance D (ed), Human Tumor Viruses. ASM Press, Washington, DC. doi: 10.1128/9781555818289.ch3
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