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2008年23卷6期

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Review

The Importance of Heparan Sulfate in Herpesvirus Infection

Christopher D, Deepak Shukla

2008, 23(6): 383 doi: 10.1007/s12250-008-2992-1

Herpes simplex virus type-1 (HSV-1) is one of many pathogens that use the cell surface glycosaminoglycan heparan sulfate as a receptor. Heparan sulfate is highly expressed on the surface and extracellular matrix of virtually all cell types making it an ideal receptor. Heparan sulfate interacts with HSV-1 envelope glycoproteins gB and gC during the initial attachment step during HSV-1 entry. In addition, a modified form of heparan sulfate, known as 3-O-sulfated heparan sulfate, interacts with HSV-1 gD to induce fusion between the viral envelope and host cell membrane. The 3-O-sulfation of heparan sulfate is a rare modification which occurs during the biosynthesis of heparan sulfate that is carried out by a family of enzymes known as 3-O-sulfotransferases. Due to its involvement in multiple steps of the infection process, heparan sulfate has been a prime target for the development of agents to inhibit HSV entry. Understanding how heparan sulfate functions during HSV-1 infection may not only be critical for inhibiting infection by this virus, but it may also be crucial in the fight against many other pathogens as well.

Molecular Modification of a HSV- 1 Protein and Its Associated Gene Transcriptional Regulation

Yan-chun CHE, Li JIANG, Qi-han LI

2008, 23(6): 394 doi: 10.1007/s12250-008-2994-z

The molecular modifications of Herpes Simplex Virus Type I (HSV-1) proteins represented by acetylation and phosphorylation are essential to its biological functions. The cellular chromatin-remodeling/ assembly is involved in HSV-1 associated gene transcriptional regulation in human cells harboring HSV-1 lytic or latent infections. Further investigation on these biological events would provide a better understanding of the mechanisms of HSV-1 viral gene transcriptional regulation

The Herpes Simplex Virus Type 1 Multiple Function Protein ICP27*

Lei ZHAO#, Wen-bo ZHU#, Qiong DING, Gui-qing PENG, Chun-fu ZHENG*

2008, 23(6): 399 doi: 10.1007/s12250-008-2993-0

The herpes simplex virus type 1 (HSV-1) infected-cell protein 27 (ICP27) is an essential, highly conserved protein involved in various steps of HSV-1 gene regulation as well as in the shut-off of host gene expression during infection. It functions primarily at the post-transcriptional level in inhibiting precursor mRNA splicing and in promoting nuclear export of viral transcripts. Recently, many novel functions performed by the HSV-1 ICP27 protein were shown, including leptomycin B resistance, inhibition of the typeⅠinterferon signaling, regulation of the viral mRNA translation and determining the composition of HSV-1 virions.

Nuclear Egress of Herpesviruses*

Richard J. Roller*

2008, 23(6): 406 doi: 10.1007/s12250-008-3004-1

Herpesviruses assemble and fill their capsids in the infected cell nucleus, and must then move this enormous macromolecular assembly across the nuclear membrane and into the cytoplasm. Doing so is a complex, multi-step process that involves envelopment of the capsid at the inner nuclear membrane and de-envelopment by fusion with the outer nuclear membrane. This process is orchestrated by viral proteins, but requires the modification of cellular structures and mechanisms including the nuclear lamina. In this review I summarize recent research on the mechanism of nuclear envelopment and the viral and cellular systems involved in its execution.

Herpes Simplex Viruses and Induction of Interferon Responses

Yijie Ma, Dustin Verpooten, Bin He*

2008, 23(6): 416 doi: 10.1007/s12250-008-2999-7

Herpes simplex viruses (HSV) are human pathogens responsible for a variety of diseases, including localized mucocutaneous lesions, encephalitis, and disseminated diseases. HSV infection leads to rapid induction of innate immune responses. A critical part of this host response is the type I IFN system including the induction of type I IFNs, IFN-mediated signaling and amplification of IFN response. This provides the host with immediate countermeasure during acute infection to limit initial viral replication and to facilitate an appropriate adaptive immune response. However, HSV has devised multiple strategies to evade and interfere with innate immunity. This review will focus on the induction of type I IFN response by HSV during acute infection and current knowledge of mechanisms by which HSV interferes with this induction process.

T Cell Receptor Signaling Pathways: New Targets for Herpes Simplex Virus

jia CAO, peng LI, chi ZHANG, zhu ZHANG

2008, 23(6): 429 doi: 10.1007/s12250-008-3000-5

Herpes simplex viruses (HSV-1 and HSV-2) cause global morbidity and synergistically correlate with HIV infection. HSV exists life-long in a latent form in sensory neurons with intermittent reactivation, in despite of host immune surveillance. While abundant evidence for HSV interfering with innate immune responses so as to favor the replication and propagation of the virus, several lines of evidence declare that HSV attenuates adaptive immunity by various mechanisms, including but not limited to the ablation of antigen presentation, induction of apoptosis, and interruption of cellular signaling. In this review, we will focus on the perturbative role of HSV in T cells signaling.

Pathogenetic Consequences of Cytomegalovirus-Host Co-evolution*

Gerardo Abenes, Fenyong Liu*

2008, 23(6): 438 doi: 10.1007/s12250-008-3003-2

Co-evolution has been shown to result in an adaptive reciprocal modification in the respective behaviors of interacting populations over time. In the case of host-parasite co-evolution, the adaptive behavior is most evident from the reciprocal change in fitness of host and parasite-manifested in terms of pathogen survival versus host resistance. Cytomegaloviruses and their hosts represent a pairing of populations that has co-evolved over hundreds of years. This review explores the pathogenetic consequences emerging from the behavioral changes caused by co-evolutionary forces on the virus and its host.

Angiogenesis, Kaposi’s Sarcoma and Kaposi’s Sarcoma- associated Herpesvirus*

Tao KANG, chun Ye, jiang gao, ding WANG

2008, 23(6): 449 doi: 10.1007/s12250-008-2998-8

Tumor angiogenesis is the uncontrolled growth of blood vessels in tumors, serving to supply nutrients and oxygen, and remove metabolic wastes. Kaposi’s sarcoma (KS), a multifocal angioproliferative disorder characterized by spindle cell proliferation, neo-angiogenesis, inflammation, and edema, is associated with infection by Kaposi’s sarcoma-associated herpesvirus (KSHV). Recent studies indicate that KSHV infection directly promotes angiogenesis and inflammation through an autocrine and paracrine mechanism by inducing pro-angiogenic and pro-inflammatory cytokines. Many of these cytokines are also expressed in KS lesions, implicating a direct role of KSHV in the pathogenesis of this malignancy. Several KSHV genes are involved in KSHV-induced angiogenesis. These studies have provided insights into the pathogenesis of KS, and identified potential therapeutic targets for this malignancy.

Identification and Function of MicroRNAs Encoded by Herpesviruses

qiang Bai, fen Lei, ding Wang, jiang Gao

2008, 23(6): 459 doi: 10.1007/s12250-008-2997-9

MicroRNAs (miRNAs) play important roles in eukaryotes, plants and some viruses. It is increasingly clear that miRNAs-encoded by viruses can affect the viral life cycle and host physiology. Viral miRNAs could repress the innate and adaptive host immunity, modulate cellular signaling pathways, and regulate the expression of cellular and viral genes. These functions facilitate viral acute and persistent infections, and have profound effects on the host cell survival and disease progression. Here, we discuss the miRNAs encoded by herpesviruses, and their regulatory roles involved in virus-host interactions.

The Biology of Kaposi’s Sarcoma-Associated Herpesvirus and the Infection of Human Immunodeficiency Virus*

Di QIN, Chun LU

2008, 23(6): 473 doi: 10.1007/s12250-008-2996-x

Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV-8), is discovered in 1994 from Kaposi’s sarcoma (KS) lesion of an acquired immunodeficiency syndrome (AIDS) patient. In addition to its association with KS, KSHV has also been implicated as the causative agent of two other AIDS-associated malignancies: primary effusion lymphoma (PEL) and multicentric Castleman’s disease (MCD). KSHV is a complex DNA virus that not only has the ability to promote cellular growth and survival for tumor development, but also can provoke deregulated angiogenesis, inflammation, and modulate the patient’s immune system in favor of tumor growth. As KSHV is a necessary but not sufficient etiological factor for KS, human immunodeficiency virus (HIV) is a very important cofactor. Here we review the basic information about the biology of KSHV, development of pathogenesis and interaction between KSHV and HIV.

Prevention and Treatment of KSHV-associated Diseases with Antiviral Drugs*

Ren-rong TIAN, Qing-jiao LIAO, Xulin CHEN*

2008, 23(6): 486 doi: 10.1007/s12250-008-2995-y

Kaposi’s sarcoma-associated herpesvirus (KSHV) was first identified as the etiologic agent of Kaposi’s sarcoma (KS) in 1994. KSHV infection is necessary, but not sufficient for the development of Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman disease (MCD). Advances in the prevention and treatment of KSHV-associated Diseases have been achieved, even though current treatment options are ineffective, or toxic to many affected persons. The identification of new targets for potential future therapies and the randomized trial to evaluate the efficacy of new antivirals are required.