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. Author manuscript; available in PMC: 2020 Nov 13.
Published in final edited form as: J Allergy Infect Dis. 2020 Aug 19;1(2):38–48. doi: 10.46439/allergy.1.010

Figure 3: Upregulation of endolysosomal degradation pathway by 17β-estradiol.

Figure 3:

The virus infects the cell by binding spike proteins with ACE2 on cell membranes following priming by TMPRSS2. Following endolysosome escape, RNA can accumulate in the cytosol, where it participates in protein translation. Translated proteins produce a replication complex to make viral RNA. 17β-estradiol may enhance the endolysosome’s degradation of the virus by enhancing the fusion of endosomes and lysosomes, probably by increasing AMPK activity and other possible mechanisms. Moreover, 17β-estradiol-mediated AMPK activation may enhance ACE2 stability by inducing phosphorylation and reduce ARDS and pulmonary hypertension. (SARS-CoV2: Severe Acute Respiratory Syndrome-Coronavirus 2; ACE2: Angiotensin-Converting Enzyme 2; p-ACE2: Phosphor-Angiotensin-Converting Enzyme 2; TMPRSS2: Transmembrane Protease, Serine 2; Ang II: Angiotensin II; Ang 1–7: Angiotensin 1–7; AMPKα: Adenosine Monophosphate Kinase-α; ER: Endoplasmic Reticulum).