Background Coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2, previously named 2019-nCov), a novel coronavirus that emerged in China in December 2019 and was declared a global pandemic by World Health Organization by March 11th, 2020. Severe manifestations of COVID-19 are caused by a combination of direct tissue injury by viral replication and associated cytokine storm resulting in progressive organ damage. Discussion We reviewed published literature between January 1st, 2000 and June 30th, 2020, excluding articles focusing on pediatric or obstetric population, with a focus on virus-host interactions and immunological mechanisms responsible for virus associated cytokine release syndrome (CRS). COVID-19 illness encompasses three main phases. In phase 1, SARS-CoV-2 binds with angiotensin converting enzyme (ACE)2 receptor on alveolar macrophages and epithelial cells, triggering toll like receptor (TLR) mediated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ƙB) signaling. It effectively blunts an early (IFN) response allowing unchecked viral replication. Phase 2 is characterized by hypoxia and innate immunity mediated pneumocyte damage as well as capillary leak. Some patients further progress to phase 3 characterized by cytokine storm with worsening respiratory symptoms, persistent fever, and hemodynamic instability. Important cytokines involved in this phase are interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. This is typically followed by a recovery phase with production of antibodies against the virus. We summarize published data regarding virus-host interactions, key immunological mechanisms responsible for virus-associated CRS, and potential opportunities for therapeutic interventions. Conclusion Evidence regarding SARS-CoV-2 epidemiology and pathogenesis is rapidly evolving. A better understanding of the pathophysiology and immune system dysregulation associated with CRS and acute respiratory distress syndrome in severe COVID-19 is imperative to identify novel drug targets and other therapeutic interventions.

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introduction: The objectives of this study were to identify and assess the impact of capacity-building biosafety initiatives and programs that have taken place in the broader Middle East and North Africa (BMENA) region between 2001 and 2013, to highlight gaps that require further development, and to suggest sustainable ways to build cooperative regional biosafety opportunities.Methods: A cross-sectional study was conducted with two aspects (1) thorough desktop review of literature for all biosafety/biosecurity-related activities in the study countries, such as seminars, conferences, workshops, policy documents, technology transfer, sustained scientific endeavors between countries, etc. and (2) an online survey of scientists in countries in the region to get first-hand information about biosafety and biosecurity initiatives and gaps in their country.results: A total of 1832 initiatives of biosafety/biosecurity were recorded from 97 web links; 70.68% (n = 1295) initiatives were focused on raising general awareness among the scientific community about biosafety/biosecurity/biocontainment. The most frequent areas of interest were biorisk management in biomedical and biotechnology laboratories 13% (n = 239), followed by living modified organisms (LMOs) 9.17% (n = 168). Hands-on training accounted for 2.67% (n = 49) of initiatives. Online survey results confirmed desktop review findings; however, the response rate was 11%.

In 1942, 53% of medically treated patients with cirrhosis were dead 6 months after the onset of ascites. Only 30% survived 1 year. This dismal outlook has improved only slightly with advances in medicine. Yet, some internists reject the peritoneovenous shunt (PVS) for this fatal condition even if they are aware that a diminished blood volume causes the abnormal sodium retention responsible for ascites. Their objections are based on life-threatening complications of PVS, especially post shunt coagulopathy (PSC). Blood shed into the peritoneal cavity becomes incoagulable. Such blood is immediately coagulated by a protocoagulant (soluble collagen) and concurrently lysed by tissue plasminogen activator (TPA) secreted by the peritoneal serosa. Wide zones of lysis surround peritoneal tissue placed on fibrin plates. Large volumes of ascitic fluid infused into circulating blood simulates the fate of blood shed into the peritoneal cavity with lysis playing the major role. Addition of ascitic fluid to normal platelet-rich plasma in vitro initiates clot lysis on thromboelastogram (TEG). Epsilon-aminocaproic acid (EACA) counteracts this lysis. EACA and clotting factors normalize the TEG and arrest PSC. Disposal of ascitic fluid at surgery prevents or ameliorates PSC. Mild PSC was encountered only twice in 150+ consecutive patients (1.3%) with only one case being clinically significant (0.6%). Severe PSC occurred seven times in 98 early shunt patients whose ascitic fluid was not discarded. Severe PSC requires shunt interruption and control of bleeding with clotting factors and EACA. Peritoneal lavage with saline prevents the recurrence of PSC on reopening the shunt. In four patients, EACA and clotting factors were adequate to arrest coagulopathy. Three earlier patients died of PSC before its cause and treatment were understood. Proper management eliminates this life-threatening complication, and PSC cannot be considered a deterrent to PVS. Disseminated intravascular coagulopathy (DIC) is produced in experimental animals only by the injection of thrombin or thromboplastin. PSC is a distinct entity differing from DIC; EACA and not heparin is the antidote for PSC.

Blood transfusions represent a small but significant source of malaria transmission. Most blood banks rely solely on donor questioning to exclude malaria patients from donating blood. No guidelines exist for in vitro screening of donor blood for malaria in endemic areas. Possible laboratory screening techniques include: microscopy; enzyme-linked immunosorbent assay (ELISA) antibody testing; polymerase chain reaction (PCR) testing; and rapid diagnostic antigen tests. However, all these modalities have diagnostic limitations. Based on a best evidence review, we present recommendations using an algorithmic approach to blood screening for malaria in Pakistan. This algorithm considers regional endemicity for malaria, as well as a detailed donor history, in order to decide whether donor blood should be tested with rapid antigen testing. We hope this algorithm will assist in the development of future national guidelines for screening blood for malaria that will reduce the risk of blood-borne transmission.