Short Communication ISSN: 2640-9615 Volume 6 Theoretical Strategies in SARS-CoV-2 Human Host Treatment * Corresponding author: Yang I Pachankis, Department of Medicine, 2-28-4 Dexinyuan, 1001 Biqing N Rd, Chongqing, 402762, USA, E-mail: yang.pachankis@gmail.com Received: 09 Jan 2023 Accepted: 02 Mar 2023 Published: 08 Mar 2023 J Short Name: JCMI Copyright: ©2023 Pachankis YI, This is an open access article distrib- uted under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and build upon your work non-commercially. Citation: Pachankis YI, Theoretical Strategies in SARS-CoV-2 Human Host Treatment. J Clin Med Img. 2023; V6(28): 1-4 Journal of Clinical and Medical Images clinandmedimages.com 1 Pachankis YI* Department of Medicine, USA 1. Abstract The communication reports on the clinically tested hypothesis that SARS-CoV-2 Spike 1 (S1) and Spike 2 (S2) protein strands might pose pathogens independently in human physiology, and that they might extend inwards into the viral envelope structure. The hypo- thesis raises concern for vaccination as anti-SARS-CoV-2 strate- gic methodology. With the post-vaccination interventional trial, the communication reports on the treatment method developed and further improvements to be tested. 2. Theoretical Background Current SARS-CoV-2 vaccine strategies have been proven inef- cient [1]. HIV-1 vaccine developments target envelope proteins, and SARS-CoV-2’s hydrophobic Spike 2 (S2) protein is inverted in structure from HIV-1 gp41 [2,3,4,5]. It is not currently studied on the spike helix’s strand extension with the envelop and posi- tive-sense single-stranded RNA [5,6], but the structural similari- ties of S2 to HIV-1 gp41 in membrane fusion human pathogens correspond to the negative-sense paramyxovirus with the abnor- mally over-lengthed fusogenic single-strand virus [5,7]. Gp41en- velop protein has only recently been strategized in HIV-1 vaccine development, and SARS-CoV-2 vaccination and testing methods utilized its Spike 1 (S1) protein [8,9,10], with 10 to 20 times to SARS-CoV’s targeting on angiotensin-converting enzyme 2 (ACE2) [5,11]. Dissimilar to HIV-1’s gp120 target-cell recognition [5], SARS- CoV-2 S1 induces human pathogen severity by endocytosis, while S2 induces human immunological pathogens with vascular-neuro- nal infection potentials evidenced by Delta variant [12]. Signature symptomatic SARS-CoV-2 cases’ CT images show patient’s pri- mary lung infection starts with the innate immunity stem regions [7,13] and proliferates to whole lung infection with “white lung” imaging; post-vaccination pericarditis and myocarditis cases’ an- tibody-unbound S proteins inspired the hypothesis that S1 and S2 protein strands might pose pathogens independently in human physiology, if not contributed by quantitative factors of antibody levels against infection levels, and that they extend inwards into the viral envelope structure [14,15]. 3. Interventional Analysis The hypothesis has been tested in the interventional trial, and the data generated seen in tab. 1 is analyzed from adenosine triphos- phatase (ATP) synthesis [16,17]. The post-vaccination pericardi- tis adult case, diferentiated from the adolescent cases of platelet apoptosis instead of platelet binding [14], shares the same physio- logical symptoms and risks in other adult cases developing acute myocarditis and blood clots [16]. The data from continued inter- vention suggests that the use of ACE inhibitor in the treatment did not function against S1, but only reduced the risks in blood clot formation by platelet bindings with S2 proteins’ fusogenic activi- ties intervened by proton-pump inhibitor (PPI) [16]. The pericardi- tis cause is hence diagnosed to be over-sized platelet concentration with increased immune refex below the blood-brain barrier (BBB) contributed by the gateway refex [19,20], with corroboration by the electrocardiogram in (Figure 1) collected the same day as “continued” blood test result. The evidence suggests SARS-CoV-2 lung sediment may be contributed by S1 protein with ACE2 carrier and proton-motive force (PMF) [21], but the key lethal pathogen lies with S2 protein. Albeit Omicron variant showed less physio- logical pathogenic severity contributed by pathogenic fusion repli- cation, its increased six unique mutations in S2 are concerning for neuronal infections [11,12,22]. Keywords: Adenosine triphosphatase; Baflomycin; Pericarditis; Proton inhibition; Vaccination