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Patients with asthma are susceptible to viral respiratory infections, due to weakened cellular immunity, chronic airway inflammation, and some other reasons. In fact, asthma was found to be a comorbidity to the Middle East respiratory syndrome coronavirus infection. Moreover, some asthma therapies like systemic corticosteroids used to manage severe asthma were found to be associated with severe acute respiratory syndrome coronavirus (SARS-CoV) viremia in the previous pandemic. However, from the epidemiological studies conducted so far across the globe, asthma patients are not exceptionally susceptible to COVID-19 compared to the general public; as opposed to the association seen with chronic obstructive pulmonary disease, diabetes, hypertension, obesity, and other known comorbidities of COVID-19. The bases for this interaction are not adequately understood. However, the heterogeneity of asthma disease as it relates to its various endotypes, altered angiotensin-converting enzyme (ACE2) expression in the airways, effect of rhinoviral infections, and effect of inhaled corticosteroids and biological response modifiers (BRMs), are the proposed mechanisms behind this interaction. Increased activity of ADAM 17 as induced by interleukin-13 at apical portion of pneumocytes may be responsible for the shedding of ACE2 on asthmatic airways. Furthermore, inhaled corticosteroids may prevent the occurrence of acute lung injury and, hence, acute respiratory distress by transrepression of pro-inflammatory pathways and transactivation of anti-inflammatory pathways. The antiviral effects of some inhaled corticosteroids whose molecular targets are not known may involve downregulation and competitive binding to the chaperone proteins heat shock proteins 90 and 70 between glucocorticoid receptor and nucleoprotein of SARS-CoV-2. MEDLINE was searched for terms such as asthma and COVID-19, antiviral effects of inhaled corticosteroids, BRM, and mechanisms of asthma-COVID-19 interaction. The reference lists of the obtained articles were also searched for additional literature.

Summary Filopodia are thin finger‐like protrusions at the surface of cells that are internally occupied with bundles of tightly parallel actin filaments. They play significant roles in cellular physiological processes, such as adhesion to extracellular matrix, guidance towards chemo‐attractants and in wound healing. Filopodia were recently reported to play important roles in viral infection including initial viral attachment to host cells, cell surfing, viral trafficking, internalization, budding, virus release and spread to other cells in a form that would avoid the host immune system. The detailed virus‐host protein interactions underlying most of these processes remain to be elucidated. This review will describe some reported virus‐host protein interactions on filopodia with the aim of identifying potential new anti‐virus therapeutic targets. Exploring this research area may lead to the development of novel classes of anti‐viral therapeutics that can block signalling pathways used by the virus to trigger filopodia formation. Successful compounds would inhibit initial virus attachment, formation of filopodia, expression of putative virus binding protein, extracellular virus trafficking, and budding.

Recent evidence has demonstrated that dengue virus requires active filopodia formation for a successful infection. However, the cellular factor involved in the interaction has not been fully elucidated. We used a combination of virus overlay protein binding assay and LC-MS/MS, and identified annexin II as a dengue virus serotype 2 (DENV2) interacting protein on Vero cells, upon filopodia induction. Flow cytometry analysis showed annexin II on the Vero cells surface increased when DENV2 was added. The amount of annexin II in the plasma membrane fraction was reduced as the infection progressed. Antibody-mediated inhibition of infection and siRNA-mediated knockdown of annexin II expression significantly reduced DENV2 infection and production levels. Collectively, we demonstrated that annexin II is one of the host factor involved in DENV2 binding on Vero cells.

Annexin A2 is a membrane scaffolding and binding protein, which mediated various cellular events. Its functions are generally affected by cellular localization. In the cytoplasm, they interacted with different phospholipid membranes in Ca2+ -dependent manner and play vital roles including actin binding, remodeling and dynamics, cytoskeletal rearrangement, and lipid-raft microdomain formation. However, upon cell exposure to certain stimuli, annexin A2 translocates to the external leaflets of the plasma membrane where annexin A2 was recently reported to serve as a virus receptor, play an important role in the formation of virus replication complex, or implicated in virus assembly and budding. Here, we review some of annexin A2 roles in virus infections and the potentiality of targeting annexin A2 in the design of novel and promising antivirus agent that may have a broader consequence in virus therapy.

Over the last few years, the increase in the number of multi-resistant (MR) enterobacteria has become a major clinical problem. This study detects the occurrence and prevalence of Metallo betalactamase production among some clinical bacterial isolates in Murtala Muhammad Specialist Hospital, Kano and Al-Madina Specialist Hospital Kaduna, Nigeria. A total of 200 clinical isolates comprising of E. coli (83), Klebsiella pneumoniae (52), Pseusomonas aeruginosa (28) and Proteus mirabilis (37) were screened phenotypically for carbapenemase and specifically for Metallo betalactamase using Modified Hodges Test and EDTA Disc Synergy Test respectively. The result showed that 67(33.5%) of the isolates were found to produce carbapenemase. High production occurred in 24(35.8%) and low production occurred in 43(64.2%) of the isolates. Highest prevalence of carbapenemase was found in Pseudomonas aeruginosa (38.55%) followed by E. coli (34.8%), Proteus mirabilis. (29.1%) and least prevalence in Klebsiella pneumoniae (25.0%). The prevalence of MBLs in the study was 24.5% with highest prevalence in E. coli (31.32%) followed by Proteus mirabilis. (21.6%), Pseudomonas aeruginosa (21.2%) and least among Klebsiella pneumoniae. (14.3%). Most of carbapenemase producers produce MBL type. Urine samples were found to be with the highest prevalence of 38.3% when compared with ear swab (12.0%). Prevalence of 67.9% and 76.9% were recorded for Murtala Muhammad specialist hospital Kano and Al-madina hospital Kaduna respectively. This showed that carbapenemase-mediated resistance occurred in the selected hospitals and uncontrolled spread may lead to treatment failure and frustration. Keywords : Metallobetalactamase, Carbapenemase, Enterobacteriaceae, prevalence, Hospital