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The FEBS Journal Dec 2022Epstein-Barr virus (EBV; human herpesvirus 4; HHV-4) and Kaposi sarcoma-associated herpesvirus (KSHV; human herpesvirus 8; HHV-8) are human gammaherpesviruses that have... (Review)
Review
Epstein-Barr virus (EBV; human herpesvirus 4; HHV-4) and Kaposi sarcoma-associated herpesvirus (KSHV; human herpesvirus 8; HHV-8) are human gammaherpesviruses that have oncogenic properties. EBV is a lymphocryptovirus, whereas HHV-8/KSHV is a rhadinovirus. As lymphotropic viruses, EBV and KSHV are associated with several lymphoproliferative diseases or plasmacytic/plasmablastic neoplasms. Interestingly, these viruses can also infect epithelial cells causing carcinomas and, in the case of KSHV, endothelial cells, causing sarcoma. EBV is associated with Burkitt lymphoma, classic Hodgkin lymphoma, nasopharyngeal carcinoma, plasmablastic lymphoma, lymphomatoid granulomatosis, leiomyosarcoma, and subsets of diffuse large B-cell lymphoma, post-transplant lymphoproliferative disorder, and gastric carcinoma. KSHV is implicated in Kaposi sarcoma, primary effusion lymphoma, multicentric Castleman disease, and KSHV-positive diffuse large B-cell lymphoma. Pathogenesis by these two herpesviruses is intrinsically linked to viral proteins expressed during the lytic and latent lifecycles. This comprehensive review intends to provide an overview of the EBV and KSHV viral cycles, viral proteins that contribute to oncogenesis, and the current understanding of the pathogenesis and clinicopathology of their related neoplastic entities.
Topics: Humans; Epstein-Barr Virus Infections; Endothelial Cells; Herpesvirus 4, Human; Sarcoma, Kaposi; Herpesvirus 8, Human; Lymphoma, Large B-Cell, Diffuse; Viral Proteins
PubMed: 34536980
DOI: 10.1111/febs.16206 -
Scientific Reports Aug 2021Human herpesvirus 8 (HHV8) is endemic in Africa, although studies of this infection are rare in Congo. We evaluated seroprevalence and HHV-8 diversity among people...
Human herpesvirus 8 (HHV8) is endemic in Africa, although studies of this infection are rare in Congo. We evaluated seroprevalence and HHV-8 diversity among people living with HIV. We included 353 patients receiving highly active antiretroviral therapy. Antibodies against HHV-8 latency-associated nuclear antigen were detected by indirect immunofluorescence. In HHV-8 positive patients, we performed HHV-8 quantification in blood and saliva by real-time PCR and typing by Sanger sequencing of K1 open reading frame. HHV-8 seroprevalence was 19%, being male (odd ratio [OR] = 1.741, [95% Confidence interval {CI}, 0.97-3.07]; p = 0.0581) and having multiple sex partners before HIV diagnosis (OR = 1.682, [CI 95%, 0.97-2.92]; p = 0.0629) tended to be associated with HHV-8 seropositivity. Of the 64 HHV-8 seropositive patients, HHV-8 DNA was detected in 10 (16%) in saliva, 6 (9%) in whole-blood and in 2 (3%) in both whole-blood and saliva. Three out of 6 HHV-8 strains were subtypes A5, 2 subtype B1 and 1 subtype C. HHV-8 seroprevalence was relatively low with more frequent carriage in men, associated with asymptomatic oral excretion and a predominance of subtype A5. These data tend to support the hypothesis of horizontal transmission in people living with HIV in Brazzaville.
Topics: Adult; Africa; Antibodies, Viral; Cross-Sectional Studies; Female; Follow-Up Studies; HIV; HIV Infections; Herpesviridae Infections; Herpesvirus 8, Human; Humans; Male; Middle Aged; Phylogeny; Prognosis; Prospective Studies; Saliva; Seroepidemiologic Studies
PubMed: 34465868
DOI: 10.1038/s41598-021-97070-4 -
Viruses Sep 2020Kaposi's sarcoma-associated herpesvirus (KSHV) also known as human herpesvirus 8 (HHV-8), is linked to several human malignancies including Kaposi sarcoma (KS), primary... (Review)
Review
Kaposi's sarcoma-associated herpesvirus (KSHV) also known as human herpesvirus 8 (HHV-8), is linked to several human malignancies including Kaposi sarcoma (KS), primary effusion lymphoma (PEL), multicentric Castleman's disease (MCD) and recently KSHV inflammatory cytokine syndrome (KICS). As with other diseases that have a significant inflammatory component, current therapy for KSHV-associated disease is associated with significant off-target effects. However, recent advances in our understanding of the pathogenesis of KSHV have produced new insight into the use of cytokines as potential therapeutic targets. Better understanding of the role of cytokines during KSHV infection and tumorigenesis may lead to new preventive or therapeutic strategies to limit KSHV spread and improve clinical outcomes. The cytokines that appear to be promising candidates as KSHV antiviral therapies include interleukins 6, 10, and 12 as well as interferons and tumor necrosis factor-family cytokines. This review explores our current understanding of the roles that cytokines play in promoting KSHV infection and tumorigenesis, and summarizes the current use of cytokines as therapeutic targets in KSHV-associated diseases.
Topics: Animals; Castleman Disease; Chemokines; Cytokines; Herpesviridae Infections; Herpesvirus 8, Human; Host-Pathogen Interactions; Humans; Immunomodulation; Lymphoma, Primary Effusion; Sarcoma, Kaposi; Signal Transduction
PubMed: 32998419
DOI: 10.3390/v12101097 -
Recent Results in Cancer Research.... 2014Human herpesvirus 8 (HHV-8), also known as Kaposi's sarcoma-associated herpesvirus (KSHV), is the second identified human gammaherpesvirus. Like its relative... (Review)
Review
Human herpesvirus 8 (HHV-8), also known as Kaposi's sarcoma-associated herpesvirus (KSHV), is the second identified human gammaherpesvirus. Like its relative Epstein-Barr virus, HHV-8 is linked to B-cell tumors, specifically primary effusion lymphoma and multicentric Castleman's disease, in addition to endothelial-derived KS. HHV-8 is unusual in its possession of a plethora of "accessory" genes and encoded proteins in addition to the core, conserved herpesvirus and gammaherpesvirus genes that are necessary for basic biological functions of these viruses. The HHV-8 accessory proteins specify not only activities deducible from their cellular protein homologies but also novel, unsuspected activities that have revealed new mechanisms of virus-host interaction that serve virus replication or latency and may contribute to the development and progression of virus-associated neoplasia. These proteins include viral interleukin-6 (vIL-6), viral chemokines (vCCLs), viral G protein-coupled receptor (vGPCR), viral interferon regulatory factors (vIRFs), and viral antiapoptotic proteins homologous to FLICE (FADD-like IL-1β converting enzyme)-inhibitory protein (FLIP) and survivin. Other HHV-8 proteins, such as signaling membrane receptors encoded by open reading frames K1 and K15, also interact with host mechanisms in unique ways and have been implicated in viral pathogenesis. Additionally, a set of micro-RNAs encoded by HHV-8 appear to modulate expression of multiple host proteins to provide conditions conducive to virus persistence within the host and could also contribute to HHV-8-induced neoplasia. Here, we review the molecular biology underlying these novel virus-host interactions and their potential roles in both virus biology and virus-associated disease.
Topics: Herpesviridae Infections; Herpesvirus 8, Human; Host-Pathogen Interactions; Humans; Molecular Biology; Virus Replication
PubMed: 24008302
DOI: 10.1007/978-3-642-38965-8_13 -
Virology Journal Sep 2005In 1994, Chang and Moore reported on the latest of the gammaherpesviruses to infect humans, human herpesvirus 8 (HHV-8). This novel herpesvirus has and continues to... (Review)
Review
In 1994, Chang and Moore reported on the latest of the gammaherpesviruses to infect humans, human herpesvirus 8 (HHV-8). This novel herpesvirus has and continues to present challenges to define its scope of involvement in human disease. In this review, aspects of HHV-8 infection are discussed, such as, the human immune response, viral pathogenesis and transmission, viral disease entities, and the virus's epidemiology with an emphasis on HHV-8 diagnostics.
Topics: Antibody Formation; Genes, Viral; Genome, Viral; Herpesviridae Infections; Herpesvirus 8, Human; Humans; Immunity, Cellular; Immunity, Innate; Sarcoma, Kaposi
PubMed: 16138925
DOI: 10.1186/1743-422X-2-78 -
Microbes and Infection Mar 2004The discovery of human herpesvirus 8 (HHV-8) has opened a new field in the biology and in the clinical definition of HHV-8-associated diseases. Various aspects of... (Review)
Review
The discovery of human herpesvirus 8 (HHV-8) has opened a new field in the biology and in the clinical definition of HHV-8-associated diseases. Various aspects of epidemiology, laboratory diagnosis and treatment of HHV-8 infection are still controversial. This review will summarise the most recent findings on the modalities of viral transmission in geographic areas where the virus is endemic as compared with those where the infection is sporadic. The studies on the interactions between HHV-8 and Epstein-Barr virus in the promotion of tumorigenesis will be then emphasised. This review will finally address the problems still open in the laboratory diagnosis and in the definition of antiviral drug susceptibility of HHV-8. Solving satisfactorily these issues will be necessary to better understand the epidemiology of HHV-8 infection, to reduce the risk of viral transmission, the progression of infected hosts to HHV-8-related malignancies and to achieve more active treatment options for these clinical conditions.
Topics: Antiviral Agents; Herpesviridae Infections; Herpesvirus 4, Human; Herpesvirus 8, Human; Humans; Organ Transplantation
PubMed: 15065569
DOI: 10.1016/j.micinf.2003.11.013 -
Transfusion Oct 2013Human herpesvirus 8 (HHV-8) is likely transmitted through blood transfusion in high-prevalence areas. The efficacy of leukoreduction filtration for reducing HHV-8 in...
BACKGROUND
Human herpesvirus 8 (HHV-8) is likely transmitted through blood transfusion in high-prevalence areas. The efficacy of leukoreduction filtration for reducing HHV-8 in blood has not been reported.
STUDY DESIGN AND METHODS
Blood was drawn from 45 human immunodeficiency virus-positive men either with Kaposi's sarcoma (KS; n=21) or without KS (n=24) and subject to leukoreduction filtration. HHV-8 viral load was measured in plasma and in blood before and after filtration.
RESULTS
Twelve subjects, all with KS, had detectable HHV-8 viremia before filtration with viral loads of 10(2) to 10(5) copies/mL (mean, 3 × 10(4) copies/mL). After filtration, seven of 12 subjects no longer had detectable HHV-8 in their blood, and five of 12 subjects had detectable HHV-8 that was 90% reduced on average from prefiltration levels. The presence of HHV-8 in the blood after filtration was strongly associated with prefiltration viral loads greater than 1000 copies/mL and the presence of cell-free virus in plasma. None of the subjects without KS had detectable levels of HHV-8 virus in blood before or after filtration.
CONCLUSION
Cell-associated HHV-8 appeared to be effectively removed by leukoreduction filtration. Cell-free HHV-8 was present in 42% of subjects as 1% to 20% of the total virus which was not removed by filtration.
Topics: DNA, Viral; Herpesvirus 8, Human; Humans; Leukocyte Reduction Procedures; Male; Viral Load; Viremia
PubMed: 23362994
DOI: 10.1111/trf.12108 -
The Israel Medical Association Journal... Jul 2006Today, more than 10 years and 2000 articles since human herpesvirus 8 was first described by Chang et al., novel insights into the transmission and molecular biology of... (Review)
Review
Today, more than 10 years and 2000 articles since human herpesvirus 8 was first described by Chang et al., novel insights into the transmission and molecular biology of HHV-8 have unveiled a new spectrum of diseases attributed to the virus. The association of HHV-8 with proliferative disorders--including Kaposi's sarcoma, multicentric Castleman disease and primary effusion lymphoma--is well established. Other aspects of HHV-8 infection are currently the subject of accelerated research. Primary HHV-8 infection may manifest as a mononucleosis-like syndrome in the immunocompetent host, or in various forms in the immunocompromised host. The association of HHV-8 with primary pulmonary hypertension was observed by Cool et al. in 2003, but six clinical trials evaluating the role of HHV-8 in pulmonary hypertension have not been able to replicate this intriguing observation. It has been speculated that HHV-8 may secondarily infect proliferating endothelium in patients with pulmonary hypertension. HHV-8 epidemiology, modes of transmission, new spectrum of disease and treatment are presented and discussed.
Topics: Adult; Antiviral Agents; Bone Marrow; Child; Herpesvirus 8, Human; Humans; Hypertension, Pulmonary; Immunocompromised Host; Lymphohistiocytosis, Hemophagocytic; Male; Molecular Biology; Sarcoma, Kaposi
PubMed: 16889165
DOI: No ID Found -
Archives of Pathology & Laboratory... Aug 2002Human herpesvirus 8 (HHV-8) is the presumed etiologic agent of Kaposi sarcoma (KS), the most common neoplasm in patients with acquired immunodeficiency syndrome. Current...
CONTEXT
Human herpesvirus 8 (HHV-8) is the presumed etiologic agent of Kaposi sarcoma (KS), the most common neoplasm in patients with acquired immunodeficiency syndrome. Current evidence indicates HHV-8 is necessary, but not sufficient, for KS development without the involvement of other cofactors. One potentially important cofactor is human immunodeficiency virus type 1 (HIV-1). Although HIV-1 is not essential for development of KS, studies have shown factors released from HIV-1-infected cells, including HIV-1 proteins and cytokines, promote the growth of KS cells in vitro. Recently, studies have shown that coculture of HIV-1-infected T cells with HHV-8-infected primary effusion lymphoma cell lines results in HHV-8 reactivation. This response was due, in part, to cytokines. However, only a portion of induced HHV-8 replication could be accounted for by cytokine stimulation, indicating that other factors, including HIV-1-associated proteins, may also be involved.
OBJECTIVE
To investigate a possible role for HIV-1 gp120 in HHV-8 reactivation.
DESIGN
Using an in vitro model system, we examined the effect of recombinant HIV-1 gp120 protein on HHV-8 replication in latently infected primary effusion lymphoma cell lines.
MAIN OUTCOME MEASURES
Reactivation of HHV-8 was analyzed using Northern blot analysis and quantitative polymerase chain reaction for ORF26 messenger RNA expression, a gene encoding for the HHV-8 minor capsid protein produced only during reactivation. The results were extended and confirmed using a luciferase reporter construct driven by the HHV-8 ORF50 promoter, the first promoter activated during HHV-8 replication.
RESULTS
No evidence of enhanced HHV-8 replication was found following treatment with HIV-1 gp120. In addition, HIV-1 gp120 was unable to act synergistically with interferon-gamma or hepatocyte growth factor/scatter factor to enhance reactivation of the virus in infected primary effusion lymphoma cell lines.
CONCLUSIONS
HIV-1 gp120 does not appear to be responsible for the reactivation of HHV-8 demonstrated in our previous studies. Further studies are necessary to determine if other HIV-associated proteins, particularly Tat, gp160, and/or gp41, which are also released from infected cells, may be important in inducing HHV-8 reactivation.
Topics: HIV Envelope Protein gp120; Herpesvirus 8, Human; Humans; Open Reading Frames; Promoter Regions, Genetic; Virus Activation; Virus Replication
PubMed: 12171492
DOI: 10.5858/2002-126-0941-HHRAHI -
PloS One 2008Herpesvirus infection of placenta may be harmful in pregnancy leading to disorders in fetal growth, premature delivery, miscarriage, or major congenital abnormalities....
Herpesvirus infection of placenta may be harmful in pregnancy leading to disorders in fetal growth, premature delivery, miscarriage, or major congenital abnormalities. Although a correlation between human herpesvirus 8 (HHV-8) infection and abortion or low birth weight in children has been suggested, and rare cases of in utero or perinatal HHV-8 transmission have been documented, no direct evidence of HHV-8 infection of placenta has yet been reported. The aim of this study was to evaluate the in vitro and in vivo susceptibility of placental cells to HHV-8 infection. Short-term infection assays were performed on placental chorionic villi isolated from term placentae. Qualitative and quantitative HHV-8 detection were performed by PCR and real-time PCR, and HHV-8 proteins were analyzed by immunohistochemistry. Term placenta samples from HHV-8-seropositive women were analyzed for the presence of HHV-8 DNA and antigens. In vitro infected histocultures showed increasing amounts of HHV-8 DNA in tissues and supernatants; cyto- and syncitiotrophoblasts, as well as endothelial cells, expressed latent and lytic viral antigens. Increased apoptotic phenomena were visualized by the terminal deoxynucleotidyl transferase-mediated deoxyuridine nick end-labeling method in infected histocultures. Ex vivo, HHV-8 DNA and a latent viral antigen were detected in placenta samples from HHV-8-seropositive women. These findings demonstrate that HHV-8, like other human herpesviruses, may infect placental cells in vitro and in vivo, thus providing evidence that this phenomenon might influence vertical transmission and pregnancy outcome in HHV-8-infected women.
Topics: Apoptosis; DNA, Viral; Endothelial Cells; Female; Herpesviridae Infections; Herpesvirus 8, Human; Humans; Immunohistochemistry; Placenta; Placenta Diseases; Pregnancy; Trophoblasts
PubMed: 19115001
DOI: 10.1371/journal.pone.0004073