Molecular characterization of Kaposi’s sarcoma-associated herpesvirus/human herpesvirus-8 strains from Russia

Lacoste, Vincent; Kadyrova, E. L.; Chistiakova, Irina; Gurtsevitch, Vladimir; Judde, Jean-Gabriel; Gessain, Antoine

doi:10.1099/0022-1317-81-5-1217

Cited by 37 publications

(37 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A comparison of PEL specimens and anatomically distinct KS lesions taken over time from nine individuals harbored identical viruses (551,552), suggesting that K1 variation does not occur over the lifetime of a single infected host. However, K1 genes isolated from biopsy specimens obtained 4 months apart in Russian patients had acquired up to 5 nucleotide and amino acid changes in four of the seven patients (276). Although these current PCR-based genotyping methods have suggested that infection by a single KSHV variant predominates, and may be exclusive, in many individuals, isolation of recombinant genomes argues strongly that coincident infection of a single host by different KSHV subtypes must occur.…”

Section: Kshv Subtypes and Geographic Variabilitymentioning

confidence: 98%

“…The M K15 allele was identified in 14 of 49 West and Central, but not East, African samples by Lacoste et al (275); however, it was not detected among 21 African KSHV specimens by Zong et al (with the exception of three U.S. AIDS patients with West African heritage) (551). In a small Russian cohort, four of seven samples harbored virus with M alleles (276). It has been postulated that the M K15 alleles are derived from a novel, possibly nonhuman, rhadinovirus by ancient recombination events and that the M allele may be evolving toward a higher prevalence in the population (551).…”

Section: Kshv Subtypes and Geographic Variabilitymentioning

confidence: 99%

See 1 more Smart Citation

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Dourmishev

Palmeri

et al. 2003

Microbiol Mol Biol Rev

309

367

View full text Add to dashboard Cite

Kaposi's sarcoma had been recognized as unique human cancer for a century before it manifested as an AIDS-defining illness with a suspected infectious etiology. The discovery of Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus-8, in 1994 by using representational difference analysis, a subtractive method previously employed for cloning differences in human genomic DNA, was a fitting harbinger for the powerful bioinformatic approaches since employed to understand its pathogenesis in KS. Indeed, the discovery of KSHV was rapidly followed by publication of its complete sequence, which revealed that the virus had coopted a wide armamentarium of human genes; in the short time since then, the functions of many of these viral gene variants in cell growth control, signaling apoptosis, angiogenesis, and immunomodulation have been characterized. This critical literature review explores the pathogenic potential of these genes within the framework of current knowledge of the basic herpesvirology of KSHV, including the relationships between viral genotypic variation and the four clinicoepidemiologic forms of Kaposi's sarcoma, current viral detection methods and their utility, primary infection by KSHV, tissue culture and animal models of latent- and lytic-cycle gene expression and pathogenesis, and viral reactivation from latency. Recent advances in models of de novo endothelial infection, microarray analyses of the host response to infection, receptor identification, and cloning of full-length, infectious KSHV genomic DNA promise to reveal key molecular mechanisms of the candidate pathogeneic genes when expressed in the context of viral infection

show abstract

Section: Kshv Subtypes and Geographic Variabilitymentioning

confidence: 98%

Section: Kshv Subtypes and Geographic Variabilitymentioning

confidence: 99%

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Dourmishev

Palmeri

et al. 2003

Microbiol Mol Biol Rev

309

367

View full text Add to dashboard Cite

show abstract

“…In Europe and North America, groups A and C predominate (264). Geographic strain variation in gene sequences has been identified in viruses isolated from Japan, Kuwait, Europe, Russia, Australia, South America, and the United States (94,153,195,196,297). Although specific variants have not been associated with different pathologies, the high level of strain variability in HHV-8 may have important functional implications, although no serological differences have been noted using the currently available serological assays.…”

Section: Structure and Morphologymentioning

confidence: 99%

Spectrum of Kaposi's Sarcoma-Associated Herpesvirus, or Human Herpesvirus 8, Diseases

Ablashi¹,

Chatlynne²,

Whitman³

et al. 2002

Clin Microbiol Rev

275

182

View full text Add to dashboard Cite

Human herpesvirus 8 (HHV-8), also known as Kaposi's sarcoma-associated herpesvirus (KSHV), discovered in 1994, is a human rhadinovirus (gamma-2 herpesvirus). Unlike other human herpesviruses (herpes simplex virus, Epstein-Barr virus, varicella-zoster virus, cytomegalovirus, HHV-6, and HHV-7), it is not widespread in the general population and has many unique proteins. HHV-8 is strongly associated with all subtypes of Kaposi's sarcoma (KS), multicentric Castleman's disease, and a rare form of B-cell lymphoma, primary effusion lymphoma. In addition, HHV-8 DNA sequences have been found in association with other diseases, but the role of the virus in these diseases is largely unconfirmed and remains controversial. The seroprevalence of HHV-8, based on detection of latent and lytic proteins, is 2 to 5% in healthy donors except in certain geographic areas where the virus is endemic, 80 to 95% in classic KS patients, and 40 to 50% in HIV-1 patients without KS. This virus can be transmitted both sexually and through body fluids (e.g., saliva and blood). HHV-8 is a transforming virus, as evidenced by its presence in human malignancies, by the in vitro transforming properties of several of its viral genes, and by its ability to transform some primary cells in culture. It is not, however, sufficient for transformation, and other cofactors such as immunosuppressive cytokines are involved in the development of HHV-8-associated malignancies. In this article, we review the biology, molecular virology, epidemiology, transmission, detection methods, pathogenesis, and antiviral therapy of this newly discovered human herpesvirus

show abstract

“…One hundred forty-five unique nucleotide sequences encoding all of ORF-K1 were collected from the National Center for Biotechnology Information (GenBank) (3,10,11,19). Sequences that contained in-frame insertions (including the putative K1-D strain sequences thus far reported) were excluded from the present analysis, and sequences that clustered weakly within K1-A, -B, and -C strains were also excluded.…”

mentioning

confidence: 99%

Kaposi's Sarcoma-Associated Herpesvirus Cytotoxic T Lymphocytes Recognize and Target Darwinian Positively Selected Autologous K1 Epitopes

Stebbing

Bourboulia

Johnson³

et al. 2003

J Virol

View full text Add to dashboard Cite

Kaposi's sarcoma-associated herpesvirus (KSHV) is the infectious cause of Kaposi's sarcoma (KS) and certain lymphoproliferations particularly in the context of human immunodeficiency virus (HIV) type 1-induced immunosuppression. The introduction of effective therapies to treat HIV has led to a decline in the incidence of KS, suggesting that immune responses may play a role in controlling KSHV infection and pathogenesis. Cytotoxic-T-lymphocyte (CTL) activity against KSHV proteins has been demonstrated; however, the identification of KSHV CTL epitopes remains elusive and problematic. Although the herpesvirus genomic layout is generally conserved, KSHV encodes a unique hypervariable protein, K1, with intense biological selection pressure at specific amino acid sites. To investigate whether this variability is partly driven by cellular immunity, we designed K1 peptides that match only the unique viral sequence for every individual studied here (autologous peptides). We identified functional CTL epitopes within K1's most variable areas, and we show that a given individual responds only to autologous peptides and not to peptides from other individuals. Furthermore, these epitopes are highly conserved sequences within KSHV isolates from a specific strain but are not conserved between different strains. We conclude that CTL recognition contributes to K1, and therefore to KSHV, evolution.Cytotoxic-T-lymphocyte (CTL) responses against viral infections are often limited to reactivity against a few immunodominant epitopes, the identity of these being strongly influenced by the major histocompatibility complex (MHC) class I alleles of the host (17,35). The majority of these epitopes have been identified in conserved sites, and this may be due in part to our inability to detect non-cross-reactive epitopes in variable domains (30). The importance of CTLs in controlling viral replication is supported by models of CD8-depleted animals with AIDS in which decreased numbers of CTLs result in high viral loads (28) and by the frequent selection of human immunodeficiency virus (HIV) or simian immunodeficiency virus mutants in vivo that are no longer recognized by CTLs and therefore escape immune surveillance (5, 24). Kaposi's sarcoma-associated herpesvirus (KSHV) can establish chronic infections, as can other herpesviruses, such as Epstein-Barr virus (EBV), varicella-zoster virus, and cytomegalovirus (26). CTLs against KSHV proteins in HIV-1-positive (22) and HIV-1-negative (32) individuals have been demonstrated; however, there are only four MHC class I-restricted epitopes in KSHV that have been identified thus far (1,20,31,33).The KSHV K1 open reading frame (ORF-K1) encodes a 46-kDa transmembrane glycoprotein that has been shown to induce foci of transformation in rat fibroblasts (14), enhance KSHV lytic replication (12), cooperate in NF-B signaling in vitro (27) and in vivo (25), and potentially maintain latent infection by blocking B-cell activation and therefore the induction of lytic replication (13). ORF-K1, located at the extr...

show abstract

Molecular characterization of Kaposi’s sarcoma-associated herpesvirus/human herpesvirus-8 strains from Russia

Cited by 37 publications

References 10 publications

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Spectrum of Kaposi's Sarcoma-Associated Herpesvirus, or Human Herpesvirus 8, Diseases

Kaposi's Sarcoma-Associated Herpesvirus Cytotoxic T Lymphocytes Recognize and Target Darwinian Positively Selected Autologous K1 Epitopes

Contact Info

Product

Resources

About