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	<title>Comments on: Assembly of influenza virus</title>
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	<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/</link>
	<description>About viruses and viral disease</description>
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		<title>By: me</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-30918</link>
		<dc:creator>me</dc:creator>
		<pubDate>Sat, 04 Feb 2012 22:30:00 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-30918</guid>
		<description>Ammonia? So thats why those McDonalds burgers were able to kill the viral infections I got from vaccinations! </description>
		<content:encoded><![CDATA[<p>Ammonia? So thats why those McDonalds burgers were able to kill the viral infections I got from vaccinations!</p>
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		<title>By: Ottar Stensvold</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-29944</link>
		<dc:creator>Ottar Stensvold</dc:creator>
		<pubDate>Fri, 18 Nov 2011 16:51:00 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-29944</guid>
		<description>It is known that ammonia (NH3) can inactivate single-stranded RNA viruses, but the mechanism is not unraveled. I suggest ammonia can twist the RNPs shown down to the right in the picture.

Ottar Stensvold</description>
		<content:encoded><![CDATA[<p>It is known that ammonia (NH3) can inactivate single-stranded RNA viruses, but the mechanism is not unraveled. I suggest ammonia can twist the RNPs shown down to the right in the picture.</p>
<p>Ottar Stensvold</p>
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	<item>
		<title>By: Raphael</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-21702</link>
		<dc:creator>Raphael</dc:creator>
		<pubDate>Thu, 28 Jan 2010 06:58:29 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-21702</guid>
		<description>I´m wondering about the function of Neuraminidases, which is only described for the budding process. In the first step of an infectious cycle HA binds to the sialic acid cell receptor. The situation is the same as in the budding process...HA binds to sialic acid. My question is why NA does not cleave sialic acid in the initial step? Or on the other hand are some newly assembled virions again cooperated into the infected cell cause HA should be already active in the newly assembled virions?</description>
		<content:encoded><![CDATA[<p>I´m wondering about the function of Neuraminidases, which is only described for the budding process. In the first step of an infectious cycle HA binds to the sialic acid cell receptor. The situation is the same as in the budding process&#8230;HA binds to sialic acid. My question is why NA does not cleave sialic acid in the initial step? Or on the other hand are some newly assembled virions again cooperated into the infected cell cause HA should be already active in the newly assembled virions?</p>
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		<title>By: Raphael</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-20000</link>
		<dc:creator>Raphael</dc:creator>
		<pubDate>Wed, 27 Jan 2010 22:58:29 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-20000</guid>
		<description>I´m wondering about the function of Neuraminidases, which is only described for the budding process. In the first step of an infectious cycle HA binds to the sialic acid cell receptor. The situation is the same as in the budding process...HA binds to sialic acid. My question is why NA does not cleave sialic acid in the initial step? Or on the other hand are some newly assembled virions again cooperated into the infected cell cause HA should be already active in the newly assembled virions?</description>
		<content:encoded><![CDATA[<p>I´m wondering about the function of Neuraminidases, which is only described for the budding process. In the first step of an infectious cycle HA binds to the sialic acid cell receptor. The situation is the same as in the budding process&#8230;HA binds to sialic acid. My question is why NA does not cleave sialic acid in the initial step? Or on the other hand are some newly assembled virions again cooperated into the infected cell cause HA should be already active in the newly assembled virions?</p>
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	<item>
		<title>By: caileyculbetson</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-19263</link>
		<dc:creator>caileyculbetson</dc:creator>
		<pubDate>Sat, 12 Dec 2009 18:07:25 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-19263</guid>
		<description>Hey, I really need help with this project! I am 16 and single guys get at me!</description>
		<content:encoded><![CDATA[<p>Hey, I really need help with this project! I am 16 and single guys get at me!</p>
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		<title>By: Manish Rijal</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-17044</link>
		<dc:creator>Manish Rijal</dc:creator>
		<pubDate>Wed, 19 Aug 2009 00:41:03 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-17044</guid>
		<description>the mode of action of tamiflu and relenza is clearly illustrated but it woild have been better if tha mode of action other two vaccine were given.similarly the assembly of virus is slightly unclear so please make it clear.</description>
		<content:encoded><![CDATA[<p>the mode of action of tamiflu and relenza is clearly illustrated but it woild have been better if tha mode of action other two vaccine were given.similarly the assembly of virus is slightly unclear so please make it clear.</p>
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		<title>By: Influenza neuraminidase and H5N1 pathogenicity</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-13500</link>
		<dc:creator>Influenza neuraminidase and H5N1 pathogenicity</dc:creator>
		<pubDate>Tue, 28 Jul 2009 13:02:07 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-13500</guid>
		<description>[...] (HA) and neuraminidase (NA). The NA, shown in yellow in the illustration, is an enzyme that removes sialic acids from the surface of the cell, so that newly formed virions can be released. The NA protein is [...]</description>
		<content:encoded><![CDATA[<p>[...] (HA) and neuraminidase (NA). The NA, shown in yellow in the illustration, is an enzyme that removes sialic acids from the surface of the cell, so that newly formed virions can be released. The NA protein is [...]</p>
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		<title>By: Packaging of the segmented influenza RNA genome</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-2307</link>
		<dc:creator>Packaging of the segmented influenza RNA genome</dc:creator>
		<pubDate>Fri, 26 Jun 2009 14:02:33 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-2307</guid>
		<description>[...] influenza virus assembly, viral RNAs and viral proteins – called a ribonucleoprotein complex or RNP -  travels to the [...]</description>
		<content:encoded><![CDATA[<p>[...] influenza virus assembly, viral RNAs and viral proteins – called a ribonucleoprotein complex or RNP -  travels to the [...]</p>
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		<title>By: Isis</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-1232</link>
		<dc:creator>Isis</dc:creator>
		<pubDate>Sat, 23 May 2009 01:24:41 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-1232</guid>
		<description>Very informative, interesting on how this virus works. Great article!</description>
		<content:encoded><![CDATA[<p>Very informative, interesting on how this virus works. Great article!</p>
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		<title>By: profvrr</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-1192</link>
		<dc:creator>profvrr</dc:creator>
		<pubDate>Thu, 21 May 2009 02:09:30 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-1192</guid>
		<description>How the parts know where to go isn&#039;t fully understood. There are&lt;br&gt;clearly &#039;signals&#039; on various components that allow them to interact&lt;br&gt;(protein-protein, or RNA-protein interactions). Proteins destined for&lt;br&gt;the plasma membrane have specific signals that sort them there. The&lt;br&gt;cytoplasm is a crowded place, so such signals are very important.&lt;br&gt;However, viruses often reprogram the cellular biosynthetic activities&lt;br&gt;so that mainly their proteins/nucleic acids are made. For example,&lt;br&gt;cell translation is often inhibited so that most of the new proteins&lt;br&gt;made are those of the virus.&lt;br&gt;&lt;br&gt;As for NA removing sialic acid - this occurs when the newly&lt;br&gt;synthesized NA is inserted into the plasma membrane, just before viral&lt;br&gt;budding occurs. By the time the virion forms, the sialic acid has been&lt;br&gt;removed. When the virion attaches, it is rapidly taken into the cell&lt;br&gt;before the NA can work. In cells where the virus is not taken up -&lt;br&gt;such as red blood cells - the virus will attach, and in time, as the&lt;br&gt;NA removes the sialic acid, the virus falls off of the cells.</description>
		<content:encoded><![CDATA[<p>How the parts know where to go isn&#39;t fully understood. There are<br />clearly &#39;signals&#39; on various components that allow them to interact<br />(protein-protein, or RNA-protein interactions). Proteins destined for<br />the plasma membrane have specific signals that sort them there. The<br />cytoplasm is a crowded place, so such signals are very important.<br />However, viruses often reprogram the cellular biosynthetic activities<br />so that mainly their proteins/nucleic acids are made. For example,<br />cell translation is often inhibited so that most of the new proteins<br />made are those of the virus.</p>
<p>As for NA removing sialic acid &#8211; this occurs when the newly<br />synthesized NA is inserted into the plasma membrane, just before viral<br />budding occurs. By the time the virion forms, the sialic acid has been<br />removed. When the virion attaches, it is rapidly taken into the cell<br />before the NA can work. In cells where the virus is not taken up -<br />such as red blood cells &#8211; the virus will attach, and in time, as the<br />NA removes the sialic acid, the virus falls off of the cells.</p>
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		<title>By: Mauricio Carrillo-Tripp</title>
		<link>http://www.virology.ws/2009/05/19/assembly-of-influenza-virus/comment-page-1/#comment-1180</link>
		<dc:creator>Mauricio Carrillo-Tripp</dc:creator>
		<pubDate>Wed, 20 May 2009 13:48:07 +0000</pubDate>
		<guid isPermaLink="false">http://www.virology.ws/?p=1449#comment-1180</guid>
		<description>This is fascinating. How do all individual parts &quot;know&quot; when and where to go? How do they find their way in space and time to be at the right location at the precise time?&lt;br&gt;One way I can explain this is that they are everywhere all the time (well, most of the time). So this means there have to be lots and lots of copies of each individual component everywhere in the cell at a specific time. Is there a mechanism by which the virus &quot;forces&quot; the cell to make its parts instead of the cell&#039;s owns (or at least in greater quantities)? &lt;br&gt;My other question relates to the HA and NA proteins, both found in the virus membrane surface. So, HA binds to the sialic acid, while NA removes it from the cell surface. I&#039;m confused about when the later happens. I&#039;m not sure if it is true, but from the diagrams it appears that HA is &#039;longer&#039; than NA. So when the virus first attach to the cell through the HA binding to the sialic acid, NA can&#039;t reach it, therefore the sialic acid stays. However, during the budding process, NA now is closer to the sialic acid than HA, and now that it&#039;s in reach, it can remove it.</description>
		<content:encoded><![CDATA[<p>This is fascinating. How do all individual parts &#8220;know&#8221; when and where to go? How do they find their way in space and time to be at the right location at the precise time?<br />One way I can explain this is that they are everywhere all the time (well, most of the time). So this means there have to be lots and lots of copies of each individual component everywhere in the cell at a specific time. Is there a mechanism by which the virus &#8220;forces&#8221; the cell to make its parts instead of the cell&#39;s owns (or at least in greater quantities)? <br />My other question relates to the HA and NA proteins, both found in the virus membrane surface. So, HA binds to the sialic acid, while NA removes it from the cell surface. I&#39;m confused about when the later happens. I&#39;m not sure if it is true, but from the diagrams it appears that HA is &#39;longer&#39; than NA. So when the virus first attach to the cell through the HA binding to the sialic acid, NA can&#39;t reach it, therefore the sialic acid stays. However, during the budding process, NA now is closer to the sialic acid than HA, and now that it&#39;s in reach, it can remove it.</p>
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