text: user7054: Is it possible that the fusion with cell propriety of Human Herpes virus, I see X14112.1 in GenBank is due to protein UL36 (tegument of virus) starting in linear position 2685 ???
  H R R A R S L A
  
  there are similarities with SarsCov2 virus protein S in name MN908947.3 in GenBank position 681.
  P R R A R S V A
  
  It is strange but the now (21-12-2020) the new Sars2 Great Britain strain is more near to that UL36 piece, it seems already:
  H R R A R S V A
  
  Herpes virus protein UL36 and SarsCov2 virus protein S[1200 position], have  too
  L Q E L G K
  
  i find in internet they call it "Glutaminase kidney isoform, mitochondrial"
  
  user3848: I can answer that ... I'm afraid no. What you are asking is whether there is any similarity in their cellular receptor binding or "fusion loops" because the motifs look a bit similar.
  These are very different viruses and you need to appreciate just how different they are,
  Human herpes is a double stranded DNA virus resulting in a chronic infection. It has a vast genome of >150kb, which includes cytokine mimics and proteins that we have no idea what they do. The protein you are referring to is likely a surface antigen in a virus covered in different surface antigens. However, this protein is involved in blocking the beta inferon response is considered a protease - not fusion loop and appears to have some sort of complex replication function involving the capsid. Finally, there is also the question of which human herpes 1 to 8. Here you are referring to HHV1 but for example HHV3 is chickenpox (okay its an acute not chronic infection) and HHV5 is cytomegliovirus (congenitcal infection).
  COVID-19 is a simple virus of a 30Kb genome of a single stranded positive sense RNA, causing an acute infection. I agree the Spike protein is much bigger than most RNA viruses, but the receptor-binding is tightly defined with ACE-2. It forms a classic RNA icosahedral virus, singly covered in Spike protein. I have no doubt it will go through conformational change like other RNA viruses in receptor binding but the protein involved is singularly involved in cell entry - thats its job.
  Summary
  There are large differences between HHV1 and COVID-19 for,
  
  Viruses; DNA double stranded vs RNA single stranded
  Infections; chronic vs. acute
  Transmission; vertical/integration? direct contact vs. respiratory
  Ultimately very different proteins
  Finally very different functions
  
  At best this would be heavily  scrutinised as a virological assumption.
  Bioformatics If you really wanted to follow this up you could compare the structures around these motifs, because COVID-19 is close to SARS and assess this possibility ... but you would need to be careful about the conformational changes Spike goes through in receptor-binding.
  Advice before investing large amounts of time in a bioinformatics question, it is well-worth understanding the biological rationale for the question. In this instance that rationale appears to be lacking. If you found a comparison for example with gamma-coronaviruses, which was absent from many beta-coronaviruses that would be interesting. Here there is simply too much possibility of a chance similarity and given the size HHV1 that cannot be easily overlooked. However it is good that you are thinking and questioning, if you apply the same techniques, e.g. psi-blast, protein-blast into different questions ... that can work.
  
original_text: 7054: <p>Is it possible that the fusion with cell propriety of Human Herpes virus, I see <a href="https://www.ncbi.nlm.nih.gov/nuccore/X14112.1/" rel="nofollow noreferrer">X14112.1</a> in GenBank is due to protein UL36 (tegument of virus) starting in linear position 2685 ???</p>
  <pre><code>H R R A R S L A
  </code></pre>
  <p>there are similarities with SarsCov2 virus protein S in name MN908947.3 in GenBank position 681.</p>
  <pre><code>P R R A R S V A
  </code></pre>
  <p>It is strange but the now (21-12-2020) the new Sars2 Great Britain strain is more near to that UL36 piece, it seems already:</p>
  <pre><code>H R R A R S V A
  </code></pre>
  <p>Herpes virus protein UL36 and SarsCov2 virus protein S[1200 position], have  too</p>
  <pre><code>L Q E L G K
  </code></pre>
  <p>i find in internet they call it &quot;Glutaminase kidney isoform, mitochondrial&quot;</p>
   3848: <p>I can answer that ... I'm afraid no. What you are asking is whether there is any similarity in their cellular receptor binding or &quot;fusion loops&quot; because the motifs look a bit similar.</p>
  <p>These are very different viruses and you need to appreciate just how different they are,</p>
  <p><em>Human herpes</em> is a double stranded DNA virus resulting in a chronic infection. It has a vast genome of &gt;150kb, which includes cytokine mimics and proteins that we have no idea what they do. The protein you are referring to is likely a surface antigen in a virus covered in different surface antigens. However, this protein is involved in blocking the beta inferon response is considered a protease - not fusion loop and appears to have some sort of complex replication function involving the capsid. Finally, there is also the question of which human herpes 1 to 8. Here you are referring to HHV1 but for example HHV3 is chickenpox (okay its an acute not chronic infection) and HHV5 is cytomegliovirus (congenitcal infection).</p>
  <p><em>COVID-19</em> is a simple virus of a 30Kb genome of a single stranded positive sense RNA, causing an acute infection. I agree the Spike protein is much bigger than most RNA viruses, but the receptor-binding is tightly defined with ACE-2. It forms a classic RNA icosahedral virus, singly covered in Spike protein. I have no doubt it will go through conformational change like other RNA viruses in receptor binding but the protein involved is singularly involved in cell entry - thats its job.</p>
  <p><strong>Summary</strong>
  There are large differences between HHV1 and COVID-19 for,</p>
  <ol>
  <li>Viruses; DNA double stranded vs RNA single stranded</li>
  <li>Infections; chronic vs. acute</li>
  <li>Transmission; vertical/integration? direct contact vs. respiratory</li>
  <li>Ultimately very different proteins</li>
  <li>Finally very different functions</li>
  </ol>
  <p>At best this would be heavily  scrutinised as a virological assumption.</p>
  <p><em>Bioformatics</em> If you really wanted to follow this up you could compare the structures around these motifs, because COVID-19 is close to SARS and assess this possibility ... but you would need to be careful about the conformational changes Spike goes through in receptor-binding.</p>
  <p><strong>Advice</strong> before investing large amounts of time in a bioinformatics question, it is well-worth understanding the biological rationale for the question. In this instance that rationale appears to be lacking. If you found a comparison for example with gamma-coronaviruses, which was absent from many beta-coronaviruses that would be interesting. Here there is simply too much possibility of a chance similarity and given the size HHV1 that cannot be easily overlooked. However it is good that you are thinking and questioning, if you apply the same techniques, e.g. psi-blast, protein-blast into different questions ... that can work.</p>
  