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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.

Introduction: In a resource-constrained situation where HBV DNA viral load testing may not be available or be prohibitively expensive, the current study sought to assess the levels of white blood cells, red blood cells, haemoglobin, platelets count and other red cell indices, CD4+ T-cell count and ALT as an adjunct marker to viral load in HBV Management. Methods: A case-control cross-sectional study was conducted among 300 subjects (100 acute HBV patients, 100 chronic HBV patients, and 100 HBV-negative individuals). The haemostatic parameter, absolute CD4+ T-cell count, HBcAb-IgM, alanine aminotransferase (ALT) and HBV-DNA were measured using standard methods. Results: When compared to HBV-negative individuals, the median (interquartile range, IQR) of acute and chronic HBV-infected participants had significantly higher total WBC, granulocyte, and monocyte counts, but lower platelet, lymphocyte, and RBC counts. When compared to the HBV-negative group, the median (IQR) of acute and chronic HBV-infected participants had significantly lower haemoglobin, haematocrit, mean cell volume, mean cell haemoglobin, and mean cell haemoglobin concentration. ALT levels were highest in acute HBV participants (median 61.0 [IQR: 48.75-72.00]) and lowest in HBV negative controls (median 24.50 [IQR: 20.0-36.75]) (Krustal-Wallis test= 151.2, p Conclusion: Our findings highlight the impact of HBV infection on iron metabolism and the production of haematological precursor cells. As such these parameters could be used as adjunct markers for viral load in the management of HBV infection in a resource-constrained setting.