Table 3.
The role of vital proteins of host and virus during infection and the possible efficacy of the drugs against SARS-CoV-2.
Proteins to target | The role of viral proteins during hijacking the host cells. | Drugs | Hypothesis to act against SARS-CoV-2 | Already tested against diseases | Adverse side effects | References |
---|---|---|---|---|---|---|
Viral Genome proteins | ||||||
RdRp | RNA-dependent RNA polymerase- replicates genome of the virus. | ribavirin and remdesivir | A nucleotide analogue that specifically inhibits replication of virus via blocking nucleotide synthesis of the virus. | Ebola Hepatitis C, RSV infection | Elevated levels of transaminases and renal injury. | [[59], [60], [61], [62], [63]] |
PLpro | Papain-like protease- proteolysis viral polyprotein to active viral protein. | lopinavir | Protease inhibitor | For HIV in combination with ritonavir | Nausea, vomiting, gastrointestinal disturbance, pancreatitis, cardiac abnormalities. | [60,62] |
3CLpro | Coronavirus protease- proteolysis viral polyprotein to active protein. | lopinavir | Protease inhibitor | HIV in combination with ritonavir | Nausea, vomiting, gastrointestinal disturbance, pancreatitis, cardiac abnormalities. | [60,62] |
S protein | Spike protein helps in holding virus to the host ACE2 receptor. | arbidol | Prevents binding of viral S protein to the host cells and blocks its entry. | Influenza | Elevated levels of transaminases, allergic reactions and gastrointestinal disorders. | [[64], [65], [66]] |
Host proteins | ||||||
ACE2 | Protein receptor binds with viral S protein allowing virus to enter into the host cells. | arbidol | Prevents binding of S protein to the ACE2 receptor and blocs its entry | Influenza | Elevated levels of transaminases, allergic reactions and gastrointestinal disorders. | [[64], [65], [66]] |
TMPRSS2 | Protease produced by the host potentiates priming of S protein of the virus, which facilitates binding. | Camostat mesylate | – | – | – | [67] |