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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.

Scrapie is a fatal prion protein disease stiffly associated with single nucleotide polymorphism (SNPs) of the prion protein gene (PRNP). The prevalence of this deadly disease has been reported in small ruminants, including goats. The Nigerian goats are hardy, trypano-tolerant, and contribute to the protein intake of the increasing population. Although scrapie has been reported in Nigerian goats, there is no study on the polymorphism of the PRNP gene. Herein, we evaluated the genetic and allele distributions of PRNP polymorphism in 132 Nigerian goats and compared them with publicly available studies on scrapie-affected goats. We utilized Polyphen-2, PROVEAN and AMYCO programs to examine structural variations produced by the non-synonymous SNPs. Our study revealed 29 SNPs in Nigerian goats, of which 14 were non-synonymous, and 23 were novel. There were significant differences (P 0.001) in the allele frequencies of PRNP codons 139, 146, 154 and 193 in Nigerian goats compared with scrapie-affected goats, except for Northern Italian goats at codon 154. Based on the prediction by Polyphen-2, R139S and N146S were 'benign', R154H was 'probably damaging', and T193I was 'possibly damaging'. In contrast, PROVEAN predicted 'neutral' for all non-synonymous SNPs, while AMYCO showed a similar amyloid propensity of PRNP for resistant haplotype and two haplotypes of Nigerian goats. Our study is the first to investigate the polymorphism of scrapie-related genes in Nigerian goats.

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.