The manuscript mainly aimed at providing clues on improving the innate immunity of coronavirus patients and safeguarding them from both new mutant strains and black
fungus infections. Coronavirus is readily mutating from one variant to another. Among the several variants, we selected SARS-CoV-2 B.1.1.7 in this study. Upon
infection of any virus, ideally, the phagocytic cells of the host engulf and destroy the virus by a mechanism called phagocytosis. However, compromised immunity impairs phagocytosis, and thus, restoring the immune system is crucial for a speedy recovery of infected patients. The autophagy and activation of Toll-like receptor-4 are the only ways to restore innate immunity. Recently, immunocompromised
COVID-19 patients have been suffering from the
coinfection of black fungus. Rhizomucor, a black fungus species, causes more than 75% of cases of
mucormycosis. Here, we present the results of molecular docking studies of sixty approved
antiviral drugs targeting receptors associated with the SARS-CoV-2 B 1.1.7 variant (PDB id: 7NEH), activating the innate immune system (PDB id: 5YEC and 5IJC). We also studied the twenty approved antifungal drugs with Rhizomucor miehei
lipase propeptide (PDB id: 6QPR) to identify the possible combination
therapy for patients coinfected with coronavirus and black fungus. The
ledipasvir showed excellent docking interactions with the 7NEH, 5YEC, and 5IJC, indicating that it is a perfect candidate for the treatment of
COVID-19 patients.
Itraconazole showed significant interaction with 6QPR of Rhizomucor miehei, suggesting that
itraconazole can treat black
fungus infections. In conclusion, the combination
therapy of
ledipasvir and
itraconazole can be a better alternative for treating
COVID-19 patients coinfected with black fungus.