Human Herpes Virus, fusion motif in protein vs. SARS-CoV-2? 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 ???
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there are similarities with SarsCov2 virus protein S in name MN908947.3 in GenBank position 681.
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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:
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Herpes virus protein UL36 and SarsCov2 virus protein S[1200 position], have  too
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i find in internet they call it &quot;Glutaminase kidney isoform, mitochondrial&quot;
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.
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 &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).
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.