The age group of positive cases of H1N1 was between 21 and 30 years and age group of patients who died ranged from 40 to 45 year. This overview indicates that although the majority of hospitalized persons infected with novel influenza A (H1N1) recovered without complications, certain patients had severe and prolonged disease. It was also noted that 2009 influenza A (H1N1) infection - related clinical illness predominantly affects young patients. All hospitalized patients with novel influenza A (H1N1) infection should be monitored carefully and treated with antiviral therapy. Mandatory vaccination of health-care workers is especially important in emerging pandemic.

Background Low ADAMTS 13 Activity has been suggested as an interplaying factor in the pathogenesis of COVID-19, considering that it is a thrombo-inflammatory disease with high risk of microthrombosis. Objectives The study aimed to explore the correlation between ADAMTS13 activity and the pathophysiological pathway of COVID-19. Patients/Methods We carried out a retrospective observational study of 87 COVID-19 patients in Nmc Royal Hospital, Abu Dhabi, UAE. ADAMTS13 activity was measured and compared with patients' characteristics and clinical outcomes. Results Low ADAMTS13 level was associated with pneumonia (p=0.007), severity of COVID-19 (p<0.001), and mechanical ventilation rates (p=0.018). Death was more frequently observed among patients (5 patients) with low ADAMTS13 activity compared to normal activity (1 patient), as well as inflammatory markers. Decreased ADAMTS13 levels increased the risk of pneumonia, severity of COVID-19, need for mechanical ventilation, and use of anticoagulants ((OR= 4.75, 95%CI: [1.54-18.02], p=0.011), (OR= 6.50, 95%CI: [2.57-17.74], p<0.001), (OR= 4.10, 95%CI: [1.29-15.82], p=0.024), (OR=8.00, 95%CI: (3.13-22.16), p<0.001), respectively). The low ADAMTS13 activity group had a slightly longer time to viral clearance than the normal ADAMTS13 group, but it was not statistically significant. (20 days, 95% CI: [16-27] days, vs. 17 days, 95% CI: [13-22] days, p=0.08, Log rank= 3.1). Conclusion Low ADAMTS13 activity has been linked to pneumonia, COVID-19 severity, use of anticoagulants, and need for mechanical ventilation, but not to mortality. We propose rADAMTS13 as a novel treatment for severe COVID-19.

(1) Background: The association between ABO blood groups and COVID-19 outcomes was investigated in several studies. The results were controversial. This study aimed to explore the association between ABO blood groups and COVID-19 outcomes. (2) Methods: This retrospective study included 303 COVID-19 patients treated at the NMC Royal Hospital in the United Arab Emirates between 8 April 2020 and 30 June 2020. (3) Results: The mean age of patients included in the study was 39.3 ± 10.7 years, and 72.9% of patients were males. The prevalence of blood groups O, A, B, and AB was 40.3%, 27.7%, 25.1%, and 6.9%, respectively. The correlation between ABO blood groups and COVID-19 outcomes was insignificant except in the AB group, with significantly higher odds of disease severity. Increased age, higher body mass index (BMI), and being of male gender increased the risk for pneumonia among all blood groups. Both increased age and higher BMI increased the risk of mortality, and increased age increased the risk of disease severity. Troponin and platelet counts were significantly different in the A group compared to the non-A groups. Time to viral clearance was not different among blood groups. However, adjustment for Rh groups resulted in a significantly shorter time in the B group. (4) Conclusions: There was no significant association between ABO blood groups and COVID-19 outcomes, with the exception of group AB.

(1) Background: Severe COVID-19 outcomes are associated with cytokine release syndrome, characterized by the release of several immune modulators, including Interleukin-6 (IL-6). Tocilizumab (TCZ) is an IL-6 receptor antagonist used to treat rheumatic arthritis. The study aimed to evaluate the efficacy and safety of TCZ against COVID-19. (2) Methods: This was a retrospective study including 49 severe COVID-19 patients who received TCZ therapy in NMC Royal Hospital, UAE. (3) Results: Before Tocilizumab administration, the median temperature was 37.0 (IQR 36.0–39.6), and after day seven, the median reduced to 36.5 (IQR 35.8–37.9), p > 0.001. Thirty (61.2%) patients were admitted to the ICU, of which, eight (16.3%) were on WHO scale 4, sixteen (32.6%) on scale 5, and six (20.0%) on scale 6. TCZ reduced inflammatory markers over time, including CRP, D-Dimer, Ferritin, and Fibrinogen. By the end of week seven, 14 patients died (28.6%) while 35 (71.4%) improved and were discharged. (4) Conclusions: The study showed limited improvements in COVID-19 outcomes with TCZ therapy and highlighted the importance of D-Dimer monitoring for possible risk of thrombosis. Additionally, it could be recommended to upgrade the anti-coagulation dose to therapeutic levels once TCZ therapy is decided upon.

Endothelial dysfunction is one of the key cornerstone complications of emerging and re-emerging viruses which lead to vascular leakage and a high mortality rate. The mechanism that regulates the origin of endothelial dysregulation is not completely elucidated. Currently, there are no potential pharmacological treatments and curable management for such diseases. In this sense, mesenchymal stromal/stem cells (MSCs) has been emerging to be a promising therapeutic strategy in restoring endothelial barrier function in various lung disease, including ALI and ARDS. The mechanism of the role of MSCs in restoring endothelial integrity among single-strand RNA (ssRNA) viruses that target endothelial cells remains elusive. Thus, we have discussed the therapeutic role of MSCs in restoring vascular integrity by (i) inhibiting the metalloprotease activity thereby preventing the cleavage of tight junction proteins, which are essential for maintaining membrane integrity (ii) possessing antioxidant properties which neutralize the excessive ROS production due to virus infection and its associated hyper host immune response (iii) modulating micro RNAs that regulate the endothelial activation and its integrity by downregulating the inflammatory response during ssRNA infection.