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		<title>Viruses: Transmission of Retroviruses across Virological Synapses</title>
		<link>http://www.mdpi.com/journal/viruses/special_issues/transmission-virological-synapse/</link>
		<description>Dear Colleagues,
Virological synapses are multimolecular structures induced by retroviruses in immune cells to mediate high-speed cell-to-cell viral dissemination. In only a few years the idea of synaptic retroviral spread has emerged and grown into an exciting new field of research. The similarities between immunological and virological synapses are helping us to understand both the pathogenesis of retroviral infection and the normal cell biology of immune cell communication. The review articles presented in this special edition of Viruses bring together diverse facets of the molecular virology, cell biology and immunology of virological synapses, updating the reader and highlighting controversies and gaps in our knowledge along the way.
Prof. Dr. Quentin J. Sattentau Guest Editor
Submission
All manuscripts should be submitted to viruses@mdpi.com with a copy to the Guest Editor. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.   Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed Open Access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. For the first couple of issues, to be published in 2009 and 2010, the Article Processing Charges (APC) in this Open Access journal will be waived for well-prepared manuscripts. English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.</description>
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							<rdf:li rdf:resource="http://www.mdpi.com/1999-4915/2/8/1704/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1999-4915/2/8/1666/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1999-4915/2/8/1603/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1999-4915/2/7/1427/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1999-4915/2/6/1306/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1999-4915/2/6/1261/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1999-4915/2/5/1239/" />
            				<rdf:li rdf:resource="http://www.mdpi.com/1999-4915/2/4/1008/" />
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	<item rdf:about="http://www.mdpi.com/1999-4915/2/8/1704/">
	<title>Viruses, Vol. 2, Pages 1704-1717: Dendritic Cells and HIV-1 Trans-Infection</title>
	<link>http://www.mdpi.com/1999-4915/2/8/1704/</link>
	<description>Dendritic cells initiate and sustain immune responses by migrating to sites of pathogenic insult, transporting antigens to lymphoid tissues and signaling immune specific activation of T cells through the formation of the immunological synapse. Dendritic cells can also transfer intact, infectious HIV-1 to CD4 T cells through an analogous structure, the infectious synapse. This replication independent mode of HIV-1 transmission, known as trans-infection, greatly increases T cell infection in vitro and is thought to contribute to viral dissemination in vivo. This review outlines the recent data defining the mechanisms of trans-infection and provides a context for the potential contribution of trans-infection in HIV-1 disease.</description>
	
	<guid>http://www.mdpi.com/1999-4915/2/8/1704/</guid>
	<pubDate>Tue, 17 Aug 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>Viruses</prism:publicationName>
	<prism:publicationDate>2010-08-17</prism:publicationDate>
	<prism:volume>2</prism:volume>
	<prism:number>8</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>1704</prism:startingPage>
		<prism:endingPage>1717</prism:endingPage>
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	<dc:title>Dendritic Cells and HIV-1 Trans-Infection</dc:title>
	<dc:date>2010-08-17</dc:date>
	<dc:identifier>doi: 10.3390/v2081704</dc:identifier>
		<dc:creator>David McDonald</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1999-4915/2/8/1666/">
	<title>Viruses, Vol. 2, Pages 1666-1680: HIV-1 Virological Synapse: Live Imaging of Transmission</title>
	<link>http://www.mdpi.com/1999-4915/2/8/1666/</link>
	<description>A relatively new aspect of HIV-1 biology is the ability of the virus to infect cells by direct cellular contacts across a specialized structure, the virological synapse. This process was recently described through live cell imaging. Together with the accumulated knowledge on cellular and molecular structures involved in cell-to-cell transmission of HIV-1, the visualization of the virological synapse in video-microscopy has brought exciting new hypotheses on its underlying mechanisms. This review will recapitulate current knowledge with a particular emphasis on the questions live microscopy has raised.</description>
	
	<guid>http://www.mdpi.com/1999-4915/2/8/1666/</guid>
	<pubDate>Thu, 12 Aug 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>Viruses</prism:publicationName>
	<prism:publicationDate>2010-08-12</prism:publicationDate>
	<prism:volume>2</prism:volume>
	<prism:number>8</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>1666</prism:startingPage>
		<prism:endingPage>1680</prism:endingPage>
		<prism:issn>1999-4915</prism:issn>
	
	<dc:title>HIV-1 Virological Synapse: Live Imaging of Transmission</dc:title>
	<dc:date>2010-08-12</dc:date>
	<dc:identifier>doi: 10.3390/v2081666</dc:identifier>
		<dc:creator>Jerome Feldmann</dc:creator>
		<dc:creator>Olivier Schwartz</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1999-4915/2/8/1603/">
	<title>Viruses, Vol. 2, Pages 1603-1620: Macrophages and Cell-Cell Spread of HIV-1</title>
	<link>http://www.mdpi.com/1999-4915/2/8/1603/</link>
	<description>Macrophages have been postulated to play an important role in the pathogenesis of HIV-1 infection. Their ability to cross the blood-brain barrier and their resistance to virus-induced cytopathic effects allows them to serve as reservoirs for long-term infection. Thus, exploring the mechanisms of virus transmission from macrophages to target cells such as other macrophages or T lymphocytes is central to our understanding of HIV-1 pathogenesis and progression to AIDS, and is vital to the development of vaccines and novel antiretroviral therapies. This review provides an overview of the current understanding of cell-cell transmission in macrophages.</description>
	
	<guid>http://www.mdpi.com/1999-4915/2/8/1603/</guid>
	<pubDate>Thu, 05 Aug 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>Viruses</prism:publicationName>
	<prism:publicationDate>2010-08-05</prism:publicationDate>
	<prism:volume>2</prism:volume>
	<prism:number>8</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>1603</prism:startingPage>
		<prism:endingPage>1620</prism:endingPage>
		<prism:issn>1999-4915</prism:issn>
	
	<dc:title>Macrophages and Cell-Cell Spread of HIV-1</dc:title>
	<dc:date>2010-08-05</dc:date>
	<dc:identifier>doi: 10.3390/v2081603</dc:identifier>
		<dc:creator>Kayoko Waki</dc:creator>
		<dc:creator>Eric O. Freed</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1999-4915/2/7/1427/">
	<title>Viruses, Vol. 2, Pages 1427-1447: The HTLV-1 Virological Synapse</title>
	<link>http://www.mdpi.com/1999-4915/2/7/1427/</link>
	<description>Human T-lymphotropic virus-1 (HTLV-1) spreads efficiently between T-cells via a tight and highly organized cell-cell contact known as the virological synapse. It is now thought that many retroviruses and other viruses spread via a virological synapse, which may be defined as a virus-induced, specialized area of cell-to-cell contact that promotes the directed transmission of the virus between cells. We summarize here the mechanisms leading to the formation of the HTLV-1 virological synapse and the role played by HTLV-1 Tax protein. We propose a model of HTLV-1 transmission between T-cells based on the three-dimensional ultrastructure of the virological synapse. Finally, in the light of recent advances, we discuss the possible routes of HTLV-1 spread across the virological synapse.</description>
	
	<guid>http://www.mdpi.com/1999-4915/2/7/1427/</guid>
	<pubDate>Wed, 07 Jul 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>Viruses</prism:publicationName>
	<prism:publicationDate>2010-07-07</prism:publicationDate>
	<prism:volume>2</prism:volume>
	<prism:number>7</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>1427</prism:startingPage>
		<prism:endingPage>1447</prism:endingPage>
		<prism:issn>1999-4915</prism:issn>
	
	<dc:title>The HTLV-1 Virological Synapse</dc:title>
	<dc:date>2010-07-07</dc:date>
	<dc:identifier>doi: 10.3390/v2071427</dc:identifier>
		<dc:creator>Mohamed Nejmeddine</dc:creator>
		<dc:creator>Charles R.M. Bangham</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1999-4915/2/6/1306/">
	<title>Viruses, Vol. 2, Pages 1306-1321: Cell-to-Cell Spread of Retroviruses</title>
	<link>http://www.mdpi.com/1999-4915/2/6/1306/</link>
	<description>Viruses from several families use direct cell-to-cell infection to disseminate between cells. Retroviruses are a relatively recent addition to this list, and appear to spread cell-to-cell by induction of multimolecular complexes termed virological synapses that assemble at the interface between infected and receptor-expressing target cells. Over the past five years, detailed insight into the cellular and molecular basis of virological synapse-mediated retroviral cell-to-cell spread has been obtained, but important questions and controversies have been raised that remain to be resolved. This review will focus on recent advances in the field with emphasis on areas in which work still needs to be done.</description>
	
	<guid>http://www.mdpi.com/1999-4915/2/6/1306/</guid>
	<pubDate>Thu, 10 Jun 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>Viruses</prism:publicationName>
	<prism:publicationDate>2010-06-10</prism:publicationDate>
	<prism:volume>2</prism:volume>
	<prism:number>6</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>1306</prism:startingPage>
		<prism:endingPage>1321</prism:endingPage>
		<prism:issn>1999-4915</prism:issn>
	
	<dc:title>Cell-to-Cell Spread of Retroviruses</dc:title>
	<dc:date>2010-06-10</dc:date>
	<dc:identifier>doi: 10.3390/v2061306</dc:identifier>
		<dc:creator> Sattentau</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1999-4915/2/6/1261/">
	<title>Viruses, Vol. 2, Pages 1261-1278: T Cell Polarization at the Virological Synapse</title>
	<link>http://www.mdpi.com/1999-4915/2/6/1261/</link>
	<description>Cell-to-cell spread of HIV-1 between CD4+ T cells takes place at multimolecular structures called virological synapses. A defining feature of the virological synapse is polarization of viral assembly and budding at sites of T cell-T cell contact. Recent work is beginning to address how viral proteins are targeted to the virological synapse and the molecular mechanisms that regulate HIV-1 egress by cell-to-cell spread. This review discusses our current understanding of these processes and considers how T cell polarization during other forms of intercellular communication may provide insight into HIV-1 assembly and dissemination.</description>
	
	<guid>http://www.mdpi.com/1999-4915/2/6/1261/</guid>
	<pubDate>Mon, 31 May 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>Viruses</prism:publicationName>
	<prism:publicationDate>2010-05-31</prism:publicationDate>
	<prism:volume>2</prism:volume>
	<prism:number>6</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>1261</prism:startingPage>
		<prism:endingPage>1278</prism:endingPage>
		<prism:issn>1999-4915</prism:issn>
	
	<dc:title>T Cell Polarization at the Virological Synapse</dc:title>
	<dc:date>2010-05-31</dc:date>
	<dc:identifier>doi: 10.3390/v2061261</dc:identifier>
		<dc:creator> Jolly</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1999-4915/2/5/1239/">
	<title>Viruses, Vol. 2, Pages 1239-1260: HIV-1 Virological Synapse is not Simply a Copycat of the Immunological Synapse</title>
	<link>http://www.mdpi.com/1999-4915/2/5/1239/</link>
	<description>The virological synapse (VS) is a tight adhesive junction between an HIV-infected cell and an uninfected target cell, across which virus can be efficiently transferred from cell to cell in the absence of cell-cell fusion. The VS has been postulated to resemble, in its morphology, the well-studied immunological synapse (IS). This review article discusses the structural similarities between IS and VS and the shared T cell receptor (TCR) signaling components that are found in the VS. However, the IS and the VS display distinct kinetics in disassembly and intracellular signaling events, possibly leading to different biological outcomes. Hence, HIV-1 exploits molecular components of IS and TCR signaling machinery to trigger unique changes in cellular morphology, migration, and activation that facilitate its transmission and cell-to-cell spread.</description>
	
	<guid>http://www.mdpi.com/1999-4915/2/5/1239/</guid>
	<pubDate>Fri, 21 May 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>Viruses</prism:publicationName>
	<prism:publicationDate>2010-05-21</prism:publicationDate>
	<prism:volume>2</prism:volume>
	<prism:number>5</prism:number>
	<prism:section>Review</prism:section>
	<prism:startingPage>1239</prism:startingPage>
		<prism:endingPage>1260</prism:endingPage>
		<prism:issn>1999-4915</prism:issn>
	
	<dc:title>HIV-1 Virological Synapse is not Simply a Copycat of the Immunological Synapse</dc:title>
	<dc:date>2010-05-21</dc:date>
	<dc:identifier>doi: 10.3390/v2051239</dc:identifier>
		<dc:creator> Vasiliver-Shamis</dc:creator>
		<dc:creator> Dustin</dc:creator>
		<dc:creator> Hioe</dc:creator>
	
	<cc:license rdf:resource="http://creativecommons.org/licenses/by/3.0/" />
</item>
	<item rdf:about="http://www.mdpi.com/1999-4915/2/4/1008/">
	<title>Viruses, Vol. 2, Pages 1008-1010: Retroviruses and the Third Synapse</title>
	<link>http://www.mdpi.com/1999-4915/2/4/1008/</link>
	<description>The direct movement of viruses between contacting cells as a mode of dissemination distinct from the release of cell-free virions was hinted at in pioneering experiments first reported almost eighty years ago [1], and confirmed and extended 30 years later [2,3]. This early work was carried out using the tools of the time in the absence of the modern cell biological, immunological and virological techniques available today. As such, although many of the basic concepts were established for cell-to-cell spread prior to the discovery of retroviruses, descriptions of the molecular and cellular mechanisms underlying this phenomenon were lacking. Papers from two decades ago revealed that HIV-1 could spread between cultured lymphocytes by cell-to-cell spread [4], proposed that this mechanism of dissemination was substantially more efficient than diffusion-limited spread of cell-free virions [5,6], and suggested that this might be a mechanism of evasion from antibody neutralization [4]. [...]</description>
	
	<guid>http://www.mdpi.com/1999-4915/2/4/1008/</guid>
	<pubDate>Thu, 15 Apr 2010 00:00:00 CEST</pubDate>
	
	<prism:publicationName>Viruses</prism:publicationName>
	<prism:publicationDate>2010-04-15</prism:publicationDate>
	<prism:volume>2</prism:volume>
	<prism:number>4</prism:number>
	<prism:section>Editorial</prism:section>
	<prism:startingPage>1008</prism:startingPage>
		<prism:endingPage>1010</prism:endingPage>
		<prism:issn>1999-4915</prism:issn>
	
	<dc:title>Retroviruses and the Third Synapse</dc:title>
	<dc:date>2010-04-15</dc:date>
	<dc:identifier>doi: 10.3390/v2041008</dc:identifier>
		<dc:creator> Sattentau</dc:creator>
	
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