The coronavirus disease 2019 (COVID-19), is a highly contagious transmittable disease caused by a recently discovered coronavirus, pathogenic SARS-CoV-2. Followed by the emergence of highly pathogenic coronaviruses in 2003 SARS-CoV, in 2012 MERS-CoV, now in 2019 pathogenic SARS-CoV-2, is associated with a global “pandemic” situation. In humans, the effects of these viruses are correlated with viral pneumonia, severe respiratory tract infections. It is believed that interaction between angiotensin converting enzyme 2 (ACE2) cell receptor and viral Spike protein mediates the coronavirus entry into human respiratory epithelial cells and establishes the host tropism. ACE2 receptor is highly expressed in airway epithelial cells. Along with viral-receptor interaction, proteolytic cleavability of S protein has been considered as the determinant of disease severity. Several studies highlight the occurrence of impaired host immune response and expression of excessive inflammatory response especially cytokines against viral infection. The mechanisms of SARS-CoV-2 induced acute lung injury are still undefined; however, the term cytokine storm has now been recognized to be closely associated with COVID-19. The levels of inflammatory mediators from cytokine storm cause damage to the host cells. In particular, the proinflammatory cytokine IL-6 appears to be the key mediator in early phase of virus-receptor interaction; however, secreted IL-6 might not be representative of lung inflammation. Understanding the cellular, and molecular factors involved in immune dysregulation and the high virulence capacity of COVID-19 will help in potential targeted therapy against it. “Drug repurposing” and “molecular docking analysis” is considered as an attractive alternative approach in analyzing suitable drug candidates to combat SARS-CoV-2 infection. Globally, extensive research is in progress to discover a new vaccine for novel COVID-19. Moreover, our review mainly focuses on the most state-of-the-art therapeutic approach mediated by “Mannose-binding lectin (MBL).” One of the most significant molecules of innate immunity is MBL. It plays a major role in the activation of the complement system as an ante-antibody prior to the response of any particular antibody. Recombinant human MBL can be used as immunomodulators against SARS-CoV-2.

Coronavirus disease 2019 (COVID-19) emerges as an expeditiously growing pandemic, in the human population caused by the highly transmissible RNA virus severe acute respiratory syndrome of coronavirus 2 (SARS-CoV-2). Prognosis of SARS-CoV-2 infection predominantly occurs at the angiotensin-converting enzyme 2 receptor and transmembrane protease serine type 2 positive (ACE2 + TMPRSS2)+ epithelial cells of the mucosal surface like nasal, oral mucosae, and/or the conjunctival surface of the eye where it has interacted along with the immune system. The primary host response towards the pathogen starts from an immune microenvironment of nasopharynx-associated lymphoid tissue (NALT) and mucosa-associated lymphoid tissue (MALT). The presence of exhausted lymphocytes, lymphopenia, pneumonia and cytokine storm is the hallmark of COVID-19. The multifaceted nature of co-morbidity factors like obesity and type 2 diabetes and its effects on immunity can alter the pathogenesis of SARS-CoV-2 infection. Adipose tissue is a crucial endocrine organ that secretes a plethora of factors like adipokines, cytokines, and chemokines that have a profound impact on metabolism and augments the expression of mucosal pro-inflammatory cytokines, like tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and the interleukin-12 (IL-12)/IL-23. Mucosal immunization could be a superior approach to activate mucosal and systemic immune responses against pathogenic invasion at mucosal surface entry ports. Mucosal vaccines are also able to generate strong systemic humoral immunity—required to neutralize any virus particle that dodges the primary immune response. To develop an efficient vaccine against mucosal pathogens, considering the designing of the delivery route, immunomodulatory features, and adjuvants are very important. In this article, we further provide evidence to understand the significant role of mucosal immunity, along with secretory and circulating immunoglobulin A (IgA) antibodies in generating a novel mucosal vaccine against COVID-19. Moreover, along with mucosal vaccines, we should look for combination treatment strategies with plant bioactive molecules. Glycan-binding lectins against viral proteins for targeted activation of mucosal immune response are one of such examples. This might play a promising role to halt this emerging virus.

A bio-mediated route for the synthesis of silver nanoparticles (AgNPs) is an area of interest in research of many scientists, and this work aims to study the electrocatalytic activity of these particles during electrochemical sensing of H 2 O 2 in a phosphate buffer media. The composite electrodes were fabricated using nearly spherical AgNPs and reduced graphene oxide (rGO) with the graphite (99.999% purity) support made of graphite paste. Graphene oxide (GO) was first synthesized using the modified Hummers method followed by rGO synthesis by chemical reduction of GO. rGO is consisting of about nine layers of rGO sheets of a wrinkled surface morphology with an intensity ratio of D to G band (I D /I G) of 1.17 and an interplanar d-spacing of 0.36 nm as evidenced by HRTEM micrograph. There was about 10 times increase in the cell current with the AgNPs-impregnated composite-electrode compared to without AgNPs impregnation, and an overpotential of H 2 O 2 reduction was found to be −1.373 V with a detection limit of 19.04 μM and 95.3% electrode stability with the graphite-rGO-AgNPs composite electrode. A nafion membrane cast on the rGO-AgNPs prevented the leakage of this composite from the electrode surface. The interference of various electroactive compounds on the amperometric response of the graphite-rGO-AgNPs electrode was also investigated.

Newly identified beta-coronavirus i.e. the 2019 novel coronavirus is associated with a contagious transmittable respiratory disease called COVID-19. This disease has been declared as a “pandemic” by the World Health Organization (WHO). The entry of coronavirus in the human respiratory epithelial cells depends upon the interaction between host cell receptor ACE2 and viral S-glycoprotein. However, this type of molecular recognition in between cell surface receptors and envelope glycoproteins are mediated by specific glycan epitopes and attribute to viral entry through membrane fusion. Glycans are essential biomolecules made by all living organisms, have roles in serving structure, energy storage, and system regulatory purposes. The glycan shield plays a crucial role in concealing the surface S protein from molecular recognition. The immunomodulatory properties of Glycan-binding proteins (GBPs) like Lectins, build them as an attractive candidates for vaccine adjuvant. Investigations involving the complement system activation by the lectin pathway in COVID-19 and diseases are in need of the hour. The innate immune response involving complement system could have varied biological effects against an array of microbial infections. The advances in glycoprotein style methods especially immunomodulatory action of some lectins are necessary to boost the effectiveness of treatment of COVID-19 and other pandemics.

In the COVID-19 pandemic, neurological complications have emerged as a significant cause of morbidity and mortality. A wide range of neurological manifestations ranging from cognitive or memory disturbances, headache, loss of smell or taste, confusion, and disabling strokes have been reported during and post COVID conditions. The COVID-19 virus can utilize two possible pathways for invasion into the brain, either through retrograde axonal transport (olfactory route) or by crossing the blood-brain barrier (BBB). Furthermore, the production of SARS-CoV-2-associated cytokines, such as interleukin (IL)-6, IL-17, IL-1b, and tumor necrosis factor (TNF), is able to disrupt the BBB. The neuroinvasive nature of SARS-CoV-2 has a more severe impact on patients with preexisting neurological manifestations such as Parkinson’s disease (PD). Pathological features of PD include selective loss of dopaminergic neurons in the substantia nigra pars compacta and aggregation of α-syn proteins present in neurons. Interaction between SARS-COV-2 infection and α-synuclein might have long-term implications on the onset of Parkinsonism by the formation of toxic protein clumps called amyloid fibrils—a hallmark of Parkinson’s. Molecular modeling is an emerging tool to predict potential inhibitors against the enzyme α-synuclein in neurodegenerative diseases by using plant bioactive molecules.