COVID-19 treatment: systemic agents
• Many systemic agents reduce risk
@CovidAnalysis, March 25, 2025
We do not provide medical advice. No treatment is
100% effective, and all may have side effects. Protocols combine multiple
treatments. Consult a qualified physician for personalized
risk/benefit analysis.
Over 8,000
compounds predicted to reduce COVID-19 risk. SARS-CoV-2 is easily
disabled.
SARS-CoV-2 infection and replication involves a complex
interplay of over 50 host and viral proteins and other
factors1-7, providing many therapeutic
targets.
Scientists have identified 8,859+
compounds8 potentially beneficial
for COVID-19. Hundreds of compounds inhibit SARS-CoV-2 in vitro,
including many with established pharmacokinetic profiles and proven safety.
c19early.org
| Efficacy confidence - Low-cost systemic agents | ||
| Hydroxychloroquine | p<0.0000000001 | |
| Ivermectin | p<0.0000000001 | |
| Metformin | p<0.0000000001 | |
| Curcumin | p=0.00000001 | |
| Antiandrogens | p=0.00000006 | |
| Melatonin | p=0.0000002 | |
| Colchicine | p=0.0000003 | |
| Probiotics | p=0.000001 | |
| Azvudine | p=0.000008 | |
| N-acetylcysteine | p=0.00003 | |
| Antihistamine H1RAs | p=0.00007 | |
| Fluvoxamine | p=0.0001 | |
| Nigella Sativa | p=0.0002 | |
| Famotidine | p=0.0003 | |
| Quercetin | p=0.002 | |
| Efficacy confirmed March 2020 (HCQ)(a),9 | ||
Hydroxychloroquine.
Most HCQ studies (89%) focused on late treatment. Early/preventive
trials show selective reporting—failing to report results at 3x the rate of
late treatment studies, suggesting suppresion of positive results.
11 In Silico981-991, 24 In Vitro981,992-1014, and 3 animal996,1006,1015 studies support the efficacy of hydroxychloroquine.
Viruses like SARS-CoV-2 that depend on low pH for endosomal
entry1016,1017 can be inhibited with endosomal
acidification inhibitors like
HCQ(c),993,1006,1017.
Direct clinical measurement shows that HCQ reaches therapeutic concentrations
in COVID-19 patients1018, and analysis of lung cells from COVID-19
patients shows inhibition in early target cell types1019.
Analysis of 422 controlled
clinical studies116-540 shows very
strong evidence for efficacy with early treatment
(p<0.0000000001,
38 studies) and
prophylaxis (p<0.0000000001,
118
studies), confirmed in multiple additional meta analyses417,1020-1027.
The largest HCQ/CQ RCT—the 4,652 patient Oxford/MORU COPCOV
RCT—shows 57% lower symptomatic PCR+ COVID-19 with
HCQ/CQ (p = 0.0002)(b),531.
In 2021 Naggie et al.483 showed that HCQ pre-exposure prophylaxis
significantly reduces COVID-19 cases based on 2 US RCTs. This is now known with
p=0.00004 from RCTs and
p=0.00000001 for observational studies.
HCQ shows poor results with late treatment and excessive dosage, and the
combination shows harm. In Vitro research supports the observed
results, with potential cardioprotective effects at lower doses, but
cardiotoxicity with excessive dosage997.
Studies for HCQ are inconsistent with the logical use of
antivirals. 89% of treatment studies have analyzed late treatment,
5+ days after the onset of symptoms541.
This makes it easy to generate meta analyses showing poor efficacy by
including large late treatment studies1028, although the results
are not relevant for recommended usage.
Results have not been reported for 37 RCTs1029-1065, and an
additional 65 HCQ RCTs were terminated with <30
patients1066-1124.
HCQ was the first treatment confirmed
effective1125, however alternatives
may offer advantages. Lung pharmacokinetics show high inter-individual
variability1018; dosage is relatively challenging, with dependence
on cholesterol1000, lung pH991, and renal
impairment991, delayed attainment of therapeutic
concentrations, and a relatively narrow range of regimens showing efficacy
while limiting side effects; and ~2.5%1126 of patients may have
contraindications.
Longer-term use of endosomal acidification modifiers for prophylaxis raises
concern for potential off-target effects, including disruption of cellular
processes, impaired lysosomal function, reduced immune
response1127, and altered cellular signaling.
Fake tablets are common in some locations1128,1129.
❝
There is a clear signal that IVM works in COVID patients ...
Ed Mills, Together Trial co-principal
investigator1130
Analysis of 105 clinical
studies10-114 shows very strong
evidence for efficacy (p<0.0000000001), confirmed in multiple additional meta analyses1220-1226.
Ivermectin shows efficacy in RCTs for prophylaxis,
early treatment, and late treatment.
The major RCTs claiming no benefit actually show positive results, despite
extreme bias1227.
The largest trial, with a design highly favoring
finding no efficacy, found superiority with probability > 0.999 for
recovery95. Improved recovery is very strongly associated
with lower mortality, p<0.0000000000195. The trial also
found 36% lower long COVID (p<0.0001) despite very suboptimal
use95.
Ivermectin also has the most carefully analyzed evidence base
in history, resulting in the retraction of a few studies which has improved
the quality of the evidence base, and improved the dose-response and treatment
delay-response relationships. However the analysis team focused only on issues
with positive
results1228,
showing very strong
bias1229,1230
and disregarding all flaws and fraud in the major trials
claiming no effect115.
For example, the main author claims the Together Trial was "incredibly
well-done" and a "masterpiece of science" despite the trial
reporting multiple impossible numbers, blinding being broken with external
sharing during the trial, randomization failure, refusal to share data despite
pledging to, no response from the authors, and many protocol violations.
Optimal use of ivermectin may involve synergy with combined treatments,
administration taking into account the lipophilic nature, and sublingual,
spray, or inhaled formulations for direct treatment to the respiratory tract.
Pharmacokinetics show significant inter-individual variability1231.
Injectable formulations may reduce variability and provide much faster onset
of action1181.
Liposomal formulations show increased antiviral activity and lower
cytotoxicity1174.
Synergistic results are seen with polytherapy1171,1173,1179.
Efficacy varies depending on the manufacturer1232, underdosed
and contaminated ivermectin is common1233-1236,
and fake tablets with no active ingredient have been
reported1237.
Metformin.
4 In Silico1136,1238-1240, 6 In Vitro549,625,1239,1241-1243, and 3 animal625,1241,1244 studies support the efficacy of metformin.
A systematic review and meta-analysis of 15 non-COVID-19 preclinical studies showed that metformin inhibits pulmonary inflammation and oxidative stress, minimizes lung injury, and improves survival in animal models of acute respiratory distress syndrome (ARDS) or acute lung injury (ALI)1245.
Metformin inhibits SARS-CoV-2 in vitro549,1243, minimizes LPS-induced cytokine storm in a mouse model1244, minimizes lung damage and fibrosis in a mouse model of LPS-induced ARDS625, may protect against SARS-CoV-2-induced neurological disorders1242, may be beneficial via inhibitory effects on ORF3a-mediated inflammasome activation1246, reduces UUO and FAN-induced kidney fibrosis625, increases mitochondrial function and decreases TGF-β-induced fibrosis, apoptosis, and inflammation markers in lung epithelial cells625, may reduce inflammation, oxidative stress, and thrombosis via regulating glucose metabolism1239, attenuates spike protein S1-induced inflammatory response and α-synuclein aggregation1241, may reduce COVID-19 severity and long COVID by inhibiting NETosis via suppression of protein kinase C activation1247, and may improve outcomes via modulation of immune responses with increased anti-inflammatory T lymphocyte gene expression and via enhanced gut microbiota diversity1248.
104 metformin clinical
studies414,420,542-643 show
efficacy, confirmed in multiple additional meta analyses1249-1270.
Efficacy has also been shown for influenza A1271.
Antiandrogens.
49 antiandrogen clinical
studies645-693 show
efficacy, confirmed in multiple additional meta analyses1272,1273.
Potential mechanisms include inhibition of TMPRSS2 expression, reduction of
androgen-mediated viral entry, modulation of the immune response, and
attenuation of inflammation.
Antihistamine H1RAs.
4 In Silico1274-1277, 7 In Vitro697,705,1275,1277-1280, and 2 animal1278,1281 studies support the efficacy of antihistamine H1RAs.
17 antihistamine H1RA clinical
studies695-711 show
efficacy.
Curcumin.
26 In Silico982,1133,1136,1164,1282-1303, 24 In Vitro994,1282,1283,1286,1288,1292,1297,1301,1304-1319 , and 1 animal1286 studies support the efficacy of curcumin.
In Silico studies predict inhibition of SARS-CoV-2 with curcumin or metabolites via binding to the spike(d),1133,1282,1286,1291,1293,1298,1301 (and specifically the receptor binding domain(e),1289,1292,1295), Mpro(f),1133,1282,1286,1288,1290-1292,1294-1296,1299,1301-1303,1316 , RNA-dependent RNA polymerase(g),1133,1282,1292,1300, PLpro(h),1133, ACE2(i),982,1293,1294, nucleocapsid(j),1164,1287, nsp10(k),1164, and helicase(l),1306 proteins.
In Vitro studies demonstrate inhibition of the spike(d),994 (and specifically the receptor binding domain(e),1319), Mpro(f),994,1297,1316,1318, ACE2(i),1319, and TMPRSS2(m),1319 proteins, and inhibition of spike-ACE2 interaction(n),1304.
Curcumin is predicted to inhibit the interaction between the SARS-CoV-2 spike protein receptor binding domain and the human ACE2 receptor for the delta and omicron variants1289, decreases pro-inflammatory cytokines induced by SARS-CoV-2 in peripheral blood mononuclear cells1315, alleviates SARS-CoV-2 spike protein-induced mitochondrial membrane damage and oxidative stress1283, may limit COVID-19 induced cardiac damage by inhibiting the NF-κB signaling pathway which mediates the profibrotic effects of the SARS-CoV-2 spike protein on cardiac fibroblasts1305, and inhibits SARS-CoV-2 ORF3a ion channel activity, which contributes to viral pathogenicity and cytotoxicity1311.
27 curcumin clinical
studies713-739 show
efficacy, confirmed in multiple additional meta analyses1320-1323.
Bioavailability.
Curcumin has low bioavailability and
stability1324. Extensive research has been done on advanced
formulations which has resulted in >50,000 times improved
bioavailability1325, and efficacy for COVID-19 may depend heavily on
the use of advanced formulations.
Melatonin.
3 In Silico1326-1328, 1 In Vitro1329, and 3 animal1328,1330,1331 studies support the efficacy of melatonin.
Melatonin may restore altered redox homeostasis in COVID-191332, modulates type III interferon responses and reduces inflammatory cytokine production in TLR3 receptor agonist stimulated viral inflammation while preserving tissue integrity1329, and negatively regulates genes critical for viral entry in lung tissue, including reduced expression of FURIN and components of the CD147 complex, while potentially disrupting TMPRSS2/ACE2-mediated entry mechanisms1328.
Melatonin reduces oxidative stress, inhibits NET formation, and protects tissues through anti-inflammatory and antioxidant actions1333.
18 melatonin clinical
studies741-758 show
efficacy, confirmed in multiple additional meta analyses1334-1339.
Potential mechanisms include antioxidant, anti-inflammatory, and
antithrombotic effects, immune modulation, regulation of autophagy, modulation
of the renin-angiotensin system, promotion of sleep and circadian rhythm, and
mitigation of cytokine storm.
Colchicine.
56 colchicine clinical
studies414,760-814 show
efficacy, confirmed in multiple additional meta analyses1340-1349.
Potential mechanisms include direct antiviral activity,
immunomodulatory and anti-inflammatory effects, cardioprotective effects, and
prevention of microvascular thrombosis.
Results are poor with very late treatment778—risks due
to side effects may exceed benefits.
Probiotics.
28 probiotics clinical
studies816-843 show
efficacy, confirmed in multiple additional meta analyses1350,1351.
Efficacy has also been shown for the common cold1352.
NAC.
1 In Silico1136, 7 In Vitro1305,1353-1358, and 1 animal1354 studies support the efficacy of N-acetylcysteine.
N-acetylcysteine shows dose-dependent inhibition of SARS-CoV-21353,1356,1358, shows anti-inflammatory and immunomodulatory effects against SARS-CoV-2-induced immune responses in combination with bromelain1355, suppressed virus-induced reactive oxygen species and blocked viral replication in a humanized mouse model and in human lung cells1354, and may limit COVID-19 induced cardiac damage by boosting cellular antioxidant defenses and potentially mitigating the oxidative stress caused by spike protein-induced ROS production in cardiac fibroblasts1305.
NAC may be beneficial for COVID-19 by replenishing glutathione stores and reinforcing the glutathione peroxidase-4 pathway to inhibit ferroptosis, an oxidative stress-induced cell death pathway implicated in COVID-191359.
NAC reinforces glutathione levels, reduces ROS, and minimizes ferroptosis and cytokine storm1333.
24 N-acetylcysteine clinical
studies878-901 show
efficacy, confirmed in another meta analysis1360.
Efficacy has also been shown for influenza1361.
Fluvoxamine.
2 In Silico1362,1363 and 2 In Vitro1363,1364 studies support the efficacy of fluvoxamine.
Fluvoxamine may inhibit SARS-CoV-2 cell entry by preventing the formation of ceramide platforms that facilitates viral uptake1362 and may help restore autophagic processes disrupted by NSP6, thereby reducing SARS-CoV-2 replication and improving host cellular defenses1364.
21 fluvoxamine clinical
studies903-923 show
efficacy, confirmed in multiple additional meta analyses1365-1372.
Potential mechanisms include ASM inhibition, σ-1 receptor activation,
antiplatelet effects, endolysosomal interference, HO-1 increase, reduced cytokine
storm, and elevated melatonin.
Azvudine.
1 In Silico1373, 1 In Vitro1373, and 1 animal1373 studies support the efficacy of azvudine.
32 azvudine clinical
studies845-876 show
efficacy, confirmed in multiple additional meta analyses1374-1377.
Nigella Sativa.
15 In Silico982,1378-1391, 5 In Vitro1382,1384,1392-1394, and 2 animal1389,1395 studies support the efficacy of nigella sativa.
14 nigella sativa clinical
studies925-938 show
efficacy, confirmed in multiple additional meta analyses1396,1397.
Potential mechanisms include direct antiviral activity, and immunomodulatory,
antioxidant, and anti-inflammatory action.
Famotidine.
30 famotidine clinical
studies409,414,940-966 show
efficacy.
Potential mechanisms include direct antiviral activity,
anti-inflammatory effects and reduced cytokine release, reduced acidity
altering conditions for viral replication, immune modulation, and
anticoagulant effects.
Quercetin.
46 In Silico982,984,1133,1282,1291,1294,1303,1398-1436 , 24 In Vitro1282,1304,1311,1316,1398,1399,1401,1411,1415,1417,1420,1434,1437-1448 , and 6 animal1401,1415,1443,1445,1449,1450 studies support the efficacy of quercetin.
In Silico studies predict inhibition of SARS-CoV-2, or minimization of side effects, with quercetin or metabolites via binding to the spike(d),984,1133,1282,1291,1294,1405,1406,1418,1420,1423,1431,1433,1434,1451 , Mpro(f),984,1133,1282,1291,1294,1303,1403,1405,1407,1409,1411,1413,1414,1416,1419,1423,1427,1429,1430,1434-1436 , RNA-dependent RNA polymerase(g),1133,1282,1399,1405,1425 , PLpro(h),1133,1430,1436, ACE2(i),982,1294,1418,1419,1430,1433 , TMPRSS2(m),1418, nucleocapsid(j),1133, helicase(l),1133,1422,1427, endoribonuclease(o),1431, NSP16/10(p),1402, cathepsin L(q),1421, Wnt-3(r),1418, FZD(s),1418, LRP6(t),1418, ezrin(u),1432, ADRP(v),984, NRP1(w),1433, EP300(x),1412, PTGS2(y),1419, HSP90AA1(z),1412,1419, matrix metalloproteinase 9(aa),1424, IL-6(ab),1417,1428, IL-10(ac),1417, VEGFA(ad),1428, and RELA(ae),1428 proteins, and inhibition of spike-ACE2 interaction(n),1398.
In Vitro studies demonstrate inhibition of the Mpro(f),1316,1411,1438,1442 protein, and inhibition of spike-ACE2 interaction(n),1304.
Animal studies demonstrate efficacy in K18-hACE2 mice(af),1445, db/db mice(ag),1443,1450, BALB/c mice(ah),1449, and rats1415.
Quercetin reduced proinflammatory cytokines and protected lung and kidney tissue against LPS-induced damage in mice1449, inhibits LPS-induced cytokine storm by modulating key inflammatory and antioxidant pathways in macrophages1401, and inhibits SARS-CoV-2 ORF3a ion channel activity, which contributes to viral pathogenicity and cytotoxicity1311.
12 quercetin clinical
studies968-979 show
efficacy, confirmed in multiple additional meta analyses1452,1453.
Potential mechanisms include direct antiviral activity, antioxidant and
anti-inflammatory activity, and immune support.
COVID-19 efficacy may depend heavily on advanced formulations for improved bioavailability.
Protocols typically combine multiple
treatments. No single treatment is guaranteed to be effective and safe for a specific individual.
Leading evidence-based protocols combine multiple treatments.
c19early.org
| Combined treatments increase efficacy | |
|---|---|
| Monotherapy | 33% [30‑36%] |
| Polytherapy | 68% [57‑77%] |
Complementary and
synergistic actions. There are many complementary mechanisms of action
across treatments, and studies show complementary and synergistic effects
with polytherapy80,1010,1171,1173,1179,1184,1454-1464 .
For example, Jitobaom et al.1173 showed >10x reduction in
IC50 with ivermectin and niclosamide, an RCT by Said et
al.1457 showed the combination of nigella sativa and vitamin D was
more effective than either alone, and an RCT by Wannigama et
al.914 showed improved results with fluvoxamine combined with
bromhexine, cyproheptadine, or niclosamide, compared to fluvoxamine alone.
Treatment efficacy may vary significantly across SARS-CoV-2 variants. For
example new variants may gain resistance to targeted
treatments1465-1471, and
the role of TMPRSS2 for cell entry differs across variants1472.
The efficacy of specific treatments varies depending on cell
type1473 due to differences in viral receptor expression, drug
distribution and metabolism, cell-specific mechanisms, and the relevance of
drug targets to specific cells.
Efficacy may also vary based on genetic
variants1474-1477.
Variable efficacy across SARS-CoV-2 variants, cell types, different tissues, and
host genetics, along with the complementary and synergistic actions of different
treatments, all point to greater efficacy with polytherapy.
In many studies, the standard of care given to all patients includes other
treatments—efficacy seen in these trials may rely in part on
synergistic effects.
Meta analysis of all early treatment trials shows 68% [57‑77%] lower risk
for studies using combined treatments, compared to 33% [30‑36%] for single
treatments.
SARS-CoV-2 evolution and the risk of
escape mutants suggests treatments with broader mechanisms of action and
polytherapy. SARS-CoV-2 can rapidly acquire mutations altering infectivity,
disease severity, and drug resistance even without selective
pressure1478. Antigenic drift can undermine more
variant-specific treatments like monoclonal antibodies and more specific
antivirals. Treatment with targeted antivirals may select for escape
mutations1479.
Less variant specific treatments and polytherapy targeting multiple viral and
host proteins may be more effective.
Systemic antivirals may be less
applicable to
low-risk infections. As SARS-CoV-2 has evolved, the frequency of
serious infections has reduced. Systemic antivirals may have a more limited
effect if infection does not spread beyond the upper respiratory tract.
Defined as ≥3 studies showing ≥10% improvement or >0% harm with statistical significance in meta analysis.
COPCOV has the largest number of treated patients of all HCQ/CQ RCTs.
The efficacy of endosomal entry inhibitors varies
across SARS-CoV-2 variants, depending on their reliance on the endosomal
pathway for entry. SARS-CoV-2 uses two major pathways for host cell entry:
endosomal entry via cathepsin proteases and TMPRSS2-mediated plasma membrane
fusion. Studies show increased reliance on TMPRSS2-mediated entry for the
Delta variant compared to the original strain. Conversely, Omicron variants
have shown significantly greater reliance on endosomal entry, suggesting
increased efficacy of endosomal acidification inhibitors. Specific
sub-variants may vary. A dual-inhibition strategy targeting both pathways
may be preferred.
The trimeric spike (S) protein is a glycoprotein that mediates viral entry by binding to the host ACE2 receptor, is critical for SARS-CoV-2's ability to infect host cells, and is a target of neutralizing antibodies. Inhibition of the spike protein prevents viral attachment, halting infection at the earliest stage.
The receptor binding domain is a specific region of the spike protein that binds ACE2 and is a major target of neutralizing antibodies. Focusing on the precise binding site allows highly specific disruption of viral attachment with reduced potential for off-target effects.
The main protease or Mpro, also known as 3CLpro or nsp5, is a cysteine protease that cleaves viral polyproteins into functional units needed for replication. Inhibiting Mpro disrupts the SARS-CoV-2 lifecycle within the host cell, preventing the creation of new copies.
RNA-dependent RNA polymerase (RdRp), also called nsp12, is the core enzyme of the viral replicase-transcriptase complex that copies the positive-sense viral RNA genome into negative-sense templates for progeny RNA synthesis. Inhibiting RdRp blocks viral genome replication and transcription.
The papain-like protease (PLpro) has multiple functions including cleaving viral polyproteins and suppressing the host immune response by deubiquitination and deISGylation of host proteins. Inhibiting PLpro may block viral replication and help restore normal immune responses.
The angiotensin converting enzyme 2 (ACE2) protein is a host cell transmembrane protein that serves as the cellular receptor for the SARS-CoV-2 spike protein. ACE2 is expressed on many cell types, including epithelial cells in the lungs, and allows the virus to enter and infect host cells. Inhibition may affect ACE2's physiological function in blood pressure control.
The nucleocapsid (N) protein binds and encapsulates the viral genome by coating the viral RNA. N enables formation and release of infectious virions and plays additional roles in viral replication and pathogenesis. N is also an immunodominant antigen used in diagnostic assays.
Non-structural protein 10 (nsp10) serves as an RNA chaperone and stabilizes conformations of nsp12 and nsp14 in the replicase-transcriptase complex, which synthesizes new viral RNAs. Nsp10 disruption may destabilize replicase-transcriptase complex activity.
The helicase, or nsp13, protein unwinds the double-stranded viral RNA, a crucial step in replication and transcription. Inhibition may prevent viral genome replication and the creation of new virus components.
Transmembrane protease serine 2 (TMPRSS2) is a host cell protease that primes the spike protein, facilitating cellular entry. TMPRSS2 activity helps enable cleavage of the spike protein required for membrane fusion and virus entry. Inhibition may especially protect respiratory epithelial cells, buy may have physiological effects.
The interaction between the SARS-CoV-2 spike protein and the human ACE2 receptor is a primary method of viral entry, inhibiting this interaction can prevent the virus from attaching to and entering host cells, halting infection at an early stage.
The endoribonuclease, also known as NendoU or nsp15, cleaves specific sequences in viral RNA which may help the virus evade detection by the host immune system. Inhibition may hinder the virus's ability to mask itself from the immune system, facilitating a stronger immune response.
The NSP16/10 complex consists of non-structural proteins 16 and 10, forming a 2'-O-methyltransferase that modifies the viral RNA cap structure. This modification helps the virus evade host immune detection by mimicking host mRNA, making NSP16/10 a promising antiviral target.
Cathepsin L is a host lysosomal cysteine protease that can prime the spike protein through an alternative pathway when TMPRSS2 is unavailable. Dual targeting of cathepsin L and TMPRSS2 may maximize disruption of alternative pathways for virus entry.
Wingless-related integration site (Wnt) ligand 3 is a host signaling molecule that activates the Wnt signaling pathway, which is important in development, cell growth, and tissue repair. Some studies suggest that SARS-CoV-2 infection may interfere with the Wnt signaling pathway, and that Wnt3a is involved in SARS-CoV-2 entry.
The frizzled (FZD) receptor is a host transmembrane receptor that binds Wnt ligands, initiating the Wnt signaling cascade. FZD serves as a co-receptor, along with ACE2, in some proposed mechanisms of SARS-CoV-2 infection. The virus may take advantage of this pathway as an alternative entry route.
Low-density lipoprotein receptor-related protein 6 is a cell surface co-receptor essential for Wnt signaling. LRP6 acts in tandem with FZD for signal transduction and has been discussed as a potential co-receptor for SARS-CoV-2 entry.
The ezrin protein links the cell membrane to the cytoskeleton (the cell's internal support structure) and plays a role in cell shape, movement, adhesion, and signaling. Drugs that occupy the same spot on ezrin where the viral spike protein would bind may hindering viral attachment, and drug binding could further stabilize ezrin, strengthening its potential natural capacity to impede viral fusion and entry.
The Adipocyte Differentiation-Related Protein (ADRP, also known as Perilipin 2 or PLIN2) is a lipid droplet protein regulating the storage and breakdown of fats in cells. SARS-CoV-2 may hijack the lipid handling machinery of host cells and ADRP may play a role in this process. Disrupting ADRP's interaction with the virus may hinder the virus's ability to use lipids for replication and assembly.
Neuropilin-1 (NRP1) is a cell surface receptor with roles in blood vessel development, nerve cell guidance, and immune responses. NRP1 may function as a co-receptor for SARS-CoV-2, facilitating viral entry into cells. Blocking NRP1 may disrupt an alternative route of viral entry.
EP300 (E1A Binding Protein P300) is a transcriptional coactivator involved in several cellular processes, including growth, differentiation, and apoptosis, through its acetyltransferase activity that modifies histones and non-histone proteins. EP300 facilitates viral entry into cells and upregulates inflammatory cytokine production.
Prostaglandin G/H synthase 2 (PTGS2, also known as COX-2) is an enzyme crucial for the production of inflammatory molecules called prostaglandins. PTGS2 plays a role in the inflammatory response that can become severe in COVID-19 and inhibitors (like some NSAIDs) may have benefits in dampening harmful inflammation, but note that prostaglandins have diverse physiological functions.
Heat Shock Protein 90 Alpha Family Class A Member 1 (HSP90AA1) is a chaperone protein that helps other proteins fold correctly and maintains their stability. HSP90AA1 plays roles in cell signaling, survival, and immune responses. HSP90AA1 may interact with numerous viral proteins, but note that it has diverse physiological functions.
Matrix metalloproteinase 9 (MMP9), also called gelatinase B, is a zinc-dependent enzyme that breaks down collagen and other components of the extracellular matrix. MMP9 levels increase in severe COVID-19. Overactive MMP9 can damage lung tissue and worsen inflammation. Inhibition of MMP9 may prevent excessive tissue damage and help regulate the inflammatory response.
The interleukin-6 (IL-6) pro-inflammatory cytokine (signaling molecule) has a complex role in the immune response and may trigger and perpetuate inflammation. Elevated IL-6 levels are associated with severe COVID-19 cases and cytokine storm. Anti-IL-6 therapies may be beneficial in reducing excessive inflammation in severe COVID-19 cases.
The interleukin-10 (IL-10) anti-inflammatory cytokine helps regulate and dampen immune responses, preventing excessive inflammation. IL-10 levels can also be elevated in severe COVID-19. IL-10 could either help control harmful inflammation or potentially contribute to immune suppression.
Vascular Endothelial Growth Factor A (VEGFA) promotes the growth of new blood vessels (angiogenesis) and has roles in inflammation and immune responses. VEGFA may contribute to blood vessel leakiness and excessive inflammation associated with severe COVID-19.
RELA is a transcription factor subunit of NF-kB and is a key regulator of inflammation, driving pro-inflammatory gene expression. SARS-CoV-2 may hijack and modulate NF-kB pathways.
A mouse model expressing the human ACE2 receptor under the control of the K18 promoter.
A mouse model of obesity and severe insulin resistance leading to type 2 diabetes due to a mutation in the leptin receptor gene that impairs satiety signaling.
A mouse model commonly used in infectious disease and cancer research due to higher immune response and susceptibility to infection.
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