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Pagina 1 a partire dal 575 risultati
Antagonism of host antiviral responses by Kaposi's sarcoma-associated herpesvirus tegument protein ORF45.
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Virus infection of a cell generally evokes an immune response by the host to defeat the intruder in its effort. Many viruses have developed an array of strategies to evade or antagonize host antiviral responses. Kaposi's sarcoma-associated herpesvirus (KSHV) is demonstrated in this report to be able
The use of antiviral drugs in the prevention and treatment of Kaposi sarcoma, multicentric Castleman disease and primary effusion lymphoma.
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Kaposi sarcoma-associated herpesvirus [KSHV, also known as human herpesvirus 8 (HHV-8)] is the most recently identified member of the human herpesvirus family. Kaposi sarcoma (KS), primary effusion lymphoma, and multicentric Castleman disease are all associated with KSHV infection. Although the
Discovery of Novel Latency-Associated Nuclear Antigen Inhibitors as Antiviral Agents Against Kaposi´s Sarcoma-Associated Herpesvirus.
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With the aim to develop novel antiviral agents against Kaposi's Sarcoma Herpesvirus (KSHV) we are targeting the latency-associated nuclear antigen (LANA). This protein plays an important role for the viral genome maintenance during latent infection. LANA has the ability to tether the viral genome to
Identification of new antiviral agents against Kaposi's sarcoma-associated herpesvirus (KSHV) by high-throughput drug screening reveals the role of histamine-related signaling in promoting viral lytic reactivation.
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Kaposi's sarcoma-associated herpesvirus (KSHV) causes several human cancers, such as Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL). Current treatment options for KSHV infection and virus associated diseases are sometimes ineffective, therefore, more effectively antiviral agents are
Beta-interferon therapy in patients with poor-prognosis Kaposi sarcoma related to the acquired immunodeficiency syndrome (AIDS). A phase II trial with preliminary evidence of antiviral activity and low incidence of opportunistic infections.
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OBJECTIVE
To study the efficacy of high doses of beta-ser-interferon (recombinant human 17-serine beta-interferon) in patients with human immunodeficiency virus (HIV) infection and Kaposi sarcoma.
METHODS
A nonrandomized, controlled trial of two high-dose regimens of beta-ser-interferon administered
Binding of Kaposi's sarcoma-associated herpesvirus K-bZIP to interferon-responsive factor 3 elements modulates antiviral gene expression.
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Kaposi's sarcoma-associated herpesvirus encodes numerous regulatory proteins capable of modulating viral and cellular gene expression and affecting host cell functions. K-bZIP, a leucine zipper-containing transcription factor encoded by ORFK8, is one such protein. During infection, transcription of
Kaposi's sarcoma of the pancreas mimicking pancreatic cancer in an HIV-infected patient. Clinical diagnosis by detection of HHV 8 in bile and complete remission following antiviral and cytostatic therapy with paclitaxel.
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BACKGROUND
Diagnosis of pancreatic cancer is usually made by endoscopic retrograde cholangiopancreatography (ERCP) and corresponding findings in computed tomography (CT) or magnetic resonance imaging. Kaposi's sarcoma, a frequent tumor in individuals with a late-stage HIV infection, can be located
Immunotherapy of a murine leukemia virus-infected, chemically induced murine sarcoma with antiviral antibodies.
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Many murine tumor models associated with murine leukemia virus(es) (MuLV) have been successfully treated by passive administration of antiviral antibodies. There is a large body of virus-negative tumors, however, which are lowly antigenic and thus refractory to such approaches. Therefore, an
Evasion and subversion of interferon-mediated antiviral immunity by Kaposi's sarcoma-associated herpesvirus: an overview.
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Viral invasion of a host cell triggers immune responses with both innate and adaptive components. The innate immune response involving the induction of type I interferons (alpha and beta interferons [IFN-α and -β]) constitutes the first line of antiviral defenses. The type I IFNs signal the
In vitro antiviral drug sensitivity of the Kaposi's sarcoma-associated herpesvirus.
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OBJECTIVE
Kaposi's sarcoma-associated herpesvirus (KSHV), or human herpesvirus 8, has been implicated as the causative agent of Kaposi's sarcoma. Retrospective studies show that the risk of development of Kaposi's sarcoma is significantly lower in AIDS patients who received ganciclovir or
Effect of antiviral drugs used to treat cytomegalovirus end-organ disease on subsequent course of previously diagnosed Kaposi's sarcoma in patients with AIDS.
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OBJECTIVE
To evaluate the association of ganciclovir (GCV) and foscarnet (PFA) therapy with the outcome of previously diagnosed Kaposi's sarcoma (KS) after initiating antiviral therapy for cytomegalovirus (CMV) end-organ disease.
METHODS
Retrospective study.
METHODS
KS progression was defined as a
Sensitivity of Kaposi's sarcoma-associated herpesvirus replication to antiviral drugs. Implications for potential therapy.
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Using a cell line (termed BCBL-1) derived from a peripheral effusion (body cavity-based) lymphoma latently infected with Kaposi's sarcoma-associated herpesvirus (KSHV), we recently reported the successful induction of KSHV replication in culture (Renne, R., W. Zhong, B. Herndier, M. McGrath, N.
The interferon-inducible antiviral protein Daxx is not essential for interferon-mediated protection against avian sarcoma virus.
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BACKGROUND
The antiviral protein Daxx acts as a restriction factor of avian sarcoma virus (ASV; Retroviridae) in mammalian cells by promoting epigenetic silencing of integrated proviral DNA. Although Daxx is encoded by a type I (α/β) interferon-stimulated gene, the requirement for Daxx in the
Antiviral activity of (+)-rutamarin against Kaposi's sarcoma-associated herpesvirus by inhibition of the catalytic activity of human topoisomerase II.
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Kaposi's sarcoma-associated herpesvirus (KSHV) is an etiological agent of several AIDS-associated malignancies, including Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman's disease (MCD). Its lytic replication cycle has been proven to be critical for the
Discovery of Kaposi's sarcoma herpesvirus-encoded circular RNAs and a human antiviral circular RNA.
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Noncoding RNAs have substantial effects in host-virus interactions. Circular RNAs (circRNAs) are novel single-stranded noncoding RNAs which can decoy other RNAs or RNA-binding proteins to inhibit their functions. The role of circRNAs is largely unknown in the context of Kaposi's sarcoma herpesvirus
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