Table 1 Therapeutic options for COVID-19 with respect to lung cytokine storms by COVID-19
From: SARS-CoV-2 COVID-19 susceptibility and lung inflammatory storm by smoking and vaping
Treatment/ Prophylaxis Options | Rationale | Pros | Cons | Reference |
|---|---|---|---|---|
Targets from host’s immune system (IL6 blockers: Actemra, Tocilizumab. Monoclonal antibodies: Kevzara-sarilumab) | Preventing excessive inflammatory responses. | Modulation of host’s immunopathological responses would decrease risks of ARDS. | Immune-modulation could have adverse effects | [48] |
ACE inhibitors (e.g.Umifenovir) | ACE inhibitors may target the S1 domain and ACE2 interaction thus preventing virus entry. | ACE modulation has successfully been employed in treating conditions like hypertension, heart failure and atherosclerosis. | Role of ACE inhibitors in COVID-19 is not clear. | |
TMPRSS2 inhibitor (e.g.Camostat, Nafamostat) | TMPRSS2 inhibition could prevent the viral activation preventing virus entry. | TMPRSS2 inhibition may have little on-target side effect. | Proteases other than TMPRSS2 (e.g. Cathepsin L, TTSP) might have a role in viral activation. | |
Chloroquine/Hydroxychloroquine | It could prevent viral entry and have other immune-modulatory effects. | Its anti-inflammatory properties could help monitor immunopathological responses in patients. | It is associated with side effects like nausea, headache, blurred vision, vomiting, cramps, and diarrhea. | |
Anti-viral agents (e.g.remdesivir, favipiravir, ripavirin) | They target the viral replication by inhibiting the RNA polymerase enzyme. | These agents have shown promising results during initial clinical trials. | Use of antivirals has the risk of developing resistance amongst some patient populations. | |
Convalescent Plasma | It involves use of passive antibody therapy to provide viral neutralization. | It can be used for both prophylaxis or treatment. Its efficacy has been tested in previous infections like SARS, Ebola, and hepatitis. | It has a known risk of inadvertent infection due to blood transfer and antibody dependent enhancement of infection (ADE). | [56] |
Targets from viral structure (like; E protein, Mpro3CLpro, Furin-like cleavage site) | Targeting viral structure would prevent viral host-cell entry and replication. | This method would design SARS-CoV2-specific treatment | Finding a potential cure by this method might take some time before it reaches clinic. |