COVID-19 Molecular Pathophysiology: Acetylation of Repurposing Drugs

Lee, Jong Hoon; Kanwar, Badar; Khattak, Asif; Balentine, Jenny; Nguyen, Ngoc Huy; Kast, Richard E.; Lee, Chul Joong; Bourbeau, Jean; Altschuler, Eric Lewin; Sergi, Consolato; Nguyen, Tuan Ngoc; Oh, Sangsuk; Sohn, Mun-Gi; Coleman, Michael D.

doi:10.3390/ijms232113260

Cited by 12 publications

(18 citation statements)

References 130 publications

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“…We de ne this up-regulation as acquired Mendelian up-regulation. NRP1 + ILC3s constitute the in ammatory cascade pathway with IFN1 or cGAS-STING through acetylation-deacetylation 9 .…”

Section: Discussionmentioning

confidence: 99%

“…Immune-to-brain communication occurs as glia, microglia, and astrocytes interpret and propagate in ammatory signals, in uencing physiological and behavioral changes 55 56 . In addition, activating the peripheral immune system affects physiological and clinical responses by the immunological memory engram pathway 9 . Jacqueline et al reported a relatively high incidence of cognitive impairment in processing speed, category uency, executive functioning, memory encoding, and recall several months after hospitalization in COVID-19 patients.…”

Section: The Cgas-sting-ifn-i Axis In Ad Pathogenesis By Vrdsmentioning

confidence: 99%

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The study of whether acquired Mendelian diseases are the origin of Alzheimer’s disease from viral respiratory diseases.

Lee

2023

Preprint

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We must study viral RNA infection, sustained interferon response, acetylcholine excess, and developing Alzheimer’s disease (AD). We analyzed viral respiratory disease (VRD) (+)/(−) and dapsone (DDS) (+)/(−) groups. ANOVA calculator, logistic regression analysis, and Mann-Whitney U Test Calculator were used to examine the association of VRDs, COPD, and anti-AD drugs (AADs) with AD. A total of 107 subjects from 2005 to 2021 developed COPD. The DDS (+) AAD (-) and DDS (-) AAD (+) groups were strongly positively correlated with all COPD subjects. COPD develops into AD without dapsone, and AAD exacerbates AD through COPD. Ten AD among ninety-three non-COPD patients occurred in 2010 since the endemic. Viral infections set a direct pathway into AD directly without COPD. The endemic causes bronchitis, COPD, and AD. Acquired Mendelian up-regulation might set a direct pathway into AD as an origin.

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“…We de ne this up-regulation as acquired Mendelian up-regulation. NRP1 + ILC3s constitute the in ammatory cascade pathway with IFN1 or cGAS-STING through acetylation-deacetylation 9 .…”

Section: Discussionmentioning

confidence: 99%

Section: The Cgas-sting-ifn-i Axis In Ad Pathogenesis By Vrdsmentioning

confidence: 99%

The study of whether acquired Mendelian diseases are the origin of Alzheimer’s disease from viral respiratory diseases.

Lee

2023

Preprint

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“…The recognized pathways invade the brainstem and involve transsynaptic transfer via peripheral, olfactory, or cranial nerves (Fig. 3) 41 .…”

Section: The Neuropilin-1 Pathwaymentioning

confidence: 99%

The picture theory of seven pathways associated with COVID-19 in the real world

Lee,

Sergi,

Kast

et al. 2024

Preprint

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces immune-mediated diseases. Interactions between the host and virus govern induction, resulting in multiorgan impacts In 2021, as normal life was challenging during the pandemic era, we analyzed SCI journals according to L. Wittgenstein's Tractatus Logi-co-Philosophicus. The pathophysiology of coronavirus disease 2019 (COVID-19) involves 1) the angiotensin-converting enzyme (ACE2) and Toll-like receptor (TLR) pathways starting with eight, from 2022.01.14., and rediscovered with nineteen, to 2024.01.10., 2) the neuropilin (NRP) pathway with seven and successful with twenty four, 3) the sterile alpha motif (SAM) and histidine-aspartate domain (HD)-containing protein 1 (SAMHD1) tetramerization pathway with two and successful with thirteen, 4) inflammasome activation pathways with five and successful with thirteen, 5) the cytosolic DNA sensor cyclic-GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) (cGAS–STING) signaling pathway with six and successful with eleven, 6) the spike protein pathway with fourteen and successful with twenty three, 7) the immunological memory engram pathway with thirteen and successful with eighteen, and 8) the excess acetylcholine pathway with three and successful with nine. We reconfirmed that COVID-19 involved seven (1–7) pathways and a new pathway involving excess acetylcholine. Therefore, it is necessary to therapeutically alleviate and block the pathological course harmoniously with modulating innate lymphoid cells (ILCs) if subsequent diverse SARS-CoV-2 variants are encountered in the future.

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“…Whether amyloid microclots could explain the elevated amyloid beta-42(Aβ-42) and amyloid beta-40 (Aβ 40) serum levels reported in chronic obstructive pulmonary disease patients [ 158 , 159 ] and the link with mild cognitive decline (MCI) is debatable. Other attempts to address some of the multiple pathogenic mechanisms (multiple organ dysfunction (MOD) and acute respiratory distress syndrome (ARDS)) also involve aspirin and dapsone [ 160 ]; the latter considered a second-line treatment of immune thrombocytopenia [ 161 ] and linked to the regulation of mild cognitive impairment (MCI) in Alzheimer’s disease (AD) [ 162 ].…”

Section: Diarylamidines Serine Proteasesmentioning

confidence: 99%

COVID-19 and Diarylamidines: The Parasitic Connection

Hulme

2023

IJMS

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As emerging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants (Omicron) continue to outpace and negate combinatorial vaccines and monoclonal antibody therapies targeting the spike protein (S) receptor binding domain (RBD), the appetite for developing similar COVID-19 treatments has significantly diminished, with the attention of the scientific community switching to long COVID treatments. However, treatments that reduce the risk of “post-COVID-19 syndrome” and associated sequelae remain in their infancy, particularly as no established criteria for diagnosis currently exist. Thus, alternative therapies that reduce infection and prevent the broad range of symptoms associated with ‘post-COVID-19 syndrome’ require investigation. This review begins with an overview of the parasitic–diarylamidine connection, followed by the renin-angiotensin system (RAS) and associated angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSSR2) involved in SARS-CoV-2 infection. Subsequently, the ability of diarylamidines to inhibit S-protein binding and various membrane serine proteases associated with SARS-CoV-2 and parasitic infections are discussed. Finally, the roles of diarylamidines (primarily DIZE) in vaccine efficacy, epigenetics, and the potential amelioration of long COVID sequelae are highlighted.

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COVID-19 Molecular Pathophysiology: Acetylation of Repurposing Drugs

Cited by 12 publications

References 130 publications

The study of whether acquired Mendelian diseases are the origin of Alzheimer’s disease from viral respiratory diseases.

The study of whether acquired Mendelian diseases are the origin of Alzheimer’s disease from viral respiratory diseases.

The picture theory of seven pathways associated with COVID-19 in the real world

COVID-19 and Diarylamidines: The Parasitic Connection

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