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<pubDate>Thu, 21 Aug 2008 07:47:08 BST</pubDate>


	<title>CiteULike: wsjames' Dong</title>
	<description>CiteULike: wsjames' Dong</description>


	<link>http://www.citeulike.org/user/wsjames/author/Dong</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/wsjames/article/2805568"/>
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<item rdf:about="http://www.citeulike.org/user/wsjames/article/2805568">
    <title>Productive infection of human immunodeficiency virus type 1 in dendritic cells requires fusion-mediated viral entry</title>
    <link>http://www.citeulike.org/user/wsjames/article/2805568</link>
    <description>&lt;i&gt;Virology, Vol. 375, No. 2. (5 June 2008), pp. 442-451.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Human immunodeficiency virus type 1 (HIV-1) enters dendritic cells (DCs) through endocytosis and viral receptor-mediated fusion. Although endocytosis-mediated HIV-1 entry can generate productive infection in certain cell types, including human monocyte-derived macrophages, productive HIV-1 infection in DCs appears to be dependent on fusion-mediated viral entry. It remains to be defined whether endocytosed HIV-1 in DCs can initiate productive infection. Using HIV-1 infection and cellular fractionation assays to measure productive viral infection and entry, here we show that HIV-1 enters monocyte-derived DCs predominately through endocytosis; however, endocytosed HIV-1 cannot initiate productive HIV-1 infection in DCs. In contrast, productive HIV-1 infection in DCs requires fusion-mediated viral entry. Together, these results provide functional evidence in understanding HIV-1 cis-infection of DCs, suggesting that different pathways of HIV-1 entry into DCs determine the outcome of viral infection.</description>
    <dc:title>Productive infection of human immunodeficiency virus type 1 in dendritic cells requires fusion-mediated viral entry</dc:title>

    <dc:creator>Alicia Janas</dc:creator>
    <dc:creator>Chunsheng Dong</dc:creator>
    <dc:creator>Jian-Hua Wang</dc:creator>
    <dc:creator>Li Wu</dc:creator>
    <dc:identifier>doi:10.1016/j.virol.2008.01.044</dc:identifier>
    <dc:source>Virology, Vol. 375, No. 2. (5 June 2008), pp. 442-451.</dc:source>
    <dc:date>2008-05-16T16:51:45-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Virology</prism:publicationName>
    <prism:volume>375</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>442</prism:startingPage>
    <prism:endingPage>451</prism:endingPage>
    <prism:category>entry</prism:category>
    <prism:category>fusion</prism:category>
    <prism:category>hiv</prism:category>
    <prism:category>macrophage</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/wsjames/article/2545580">
    <title>West Nile virus genome cyclization and RNA replication require two pairs of long-distance RNA interactions</title>
    <link>http://www.citeulike.org/user/wsjames/article/2545580</link>
    <description>&lt;i&gt;Virology, Vol. 373, No. 1. (30 March 2008), pp. 1-13.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;West Nile virus (WNV) genome cyclization and replication require two pairs of long-distance RNA interactions. Besides the previously reported 5'CS/3'CSI (conserved sequence) interaction, a 5'UAR/3'UAR (upstream AUG region) interaction also contributes to genome cyclization and replication. WNVs containing mutant 5'UARs capable of forming the 5'/3' viral RNA interaction were replicative. In contrast, WNV containing a 5'UAR mutation that abolished the 5'/3' viral RNA interaction was non-replicative; however, the replication defect could be rescued by a single-nucleotide adaptation that restored the 5'/3' RNA interaction. The 5'UAR/3'UAR interaction is critical for RNA synthesis, but not for viral translation. Antisense oligomers targeting the 5'UAR/3'UAR interaction effectively inhibited WNV replication. Phylogenic analysis showed that the 3'UAR could alternate between pairing with the 5'UAR or with the 3' end of the flaviviral genome. Therefore, the 5'UAR/3'UAR pairing may release the 3' end of viral genome (as a template) during the initiation of minus-strand RNA synthesis.</description>
    <dc:title>West Nile virus genome cyclization and RNA replication require two pairs of long-distance RNA interactions</dc:title>

    <dc:creator>Bo Zhang</dc:creator>
    <dc:creator>Hongping Dong</dc:creator>
    <dc:creator>David Stein</dc:creator>
    <dc:creator>Patrick Iversen</dc:creator>
    <dc:creator>Pei-Yong Shi</dc:creator>
    <dc:identifier>doi:10.1016/j.virol.2008.01.016</dc:identifier>
    <dc:source>Virology, Vol. 373, No. 1. (30 March 2008), pp. 1-13.</dc:source>
    <dc:date>2008-03-17T11:32:47-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Virology</prism:publicationName>
    <prism:volume>373</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>1</prism:startingPage>
    <prism:endingPage>13</prism:endingPage>
    <prism:category>flavivirus</prism:category>
    <prism:category>replication</prism:category>
    <prism:category>structure</prism:category>
</item>



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