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The pandemic of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) suggests a novel type of disease spread dynamics. We here study the case where infected agents recover and only develop immunity if they are continuously infected for some time τ. For large τ, the disease model is described by a statistical field theory. Hence, the phases of the underlying field theory characterise the disease dynamics: (i) a pandemic phase and (ii) a response regime. The statistical field theory provides an upper bound of the peak rate of infected agents. An effective control strategy needs to aim to keep the disease in the response regime (no 'second' wave). The model is tested at the quantitative level using an idealised disease network. The model excellently describes the epidemic spread of the SARS-CoV-2 outbreak in the city of Wuhan, China. We find that only 30% of the recovered agents have developed immunity. [ABSTRACT FROM AUTHOR]

In 2019 in Wuhan province, China, an outbreak of atypical pneumonia was reported with similar symptoms to Severe Acute Respiratory Syndrome (SARS), an outbreak reported in 2003, and Middle East Respiratory Syndrome (MERS) reported in Saudi Arabia in 2012. This emerging disease was caused by a novel coronavirus "Severe Acute Respiratory Syndrome Coronavirus 2" (SARS-CoV-2) or also called COVID-19. Which causes severe respiratory problems and various extrapulmonary manifestations. At the moment, the high mortality of COVID-19 has been related to the male sex, older adults (>60 years), and preexisting comorbidities of diabetes, obesity, hypertension, and heart problems. Diabetes is a disease characterized by insulin resistance and loss of ß cell function in the pancreas, with an impaired immune system due to chronic inflammation. In patients with severe COVID-19 infection, altered secretion of pro-inflammatory cytokines has been observed, if this infection occurs in a diabetic patient who already has an inflammatory state per se, an exacerbated inflammation and multiorgan failure with fatal consequences can be triggered. Several authors hypothesis suggest that hyperglycemia increases the viral replication in patients "diabetic with COVID-19 infection" is necessary to keep adequate glycemic control. Treatments for COVID-19 had focused on decreasing symptoms, the use of antivirals, anti-inflammatory drugs, monoclonal antibodies and COVID-19 convalescent plasma has shown variable results. A vaccine is needed to control this viral infection, at the moment more than 150 candidates have been developed with efficiency ranges from 70 to 95%, however, the long-term immunity in vaccinated people is still unknown. This review focus on the characteristics of SARS-CoV-2 infection and the immune response in diabetic patients facing COVID-19. [ABSTRACT FROM AUTHOR]

In humans, coronaviruses can cause infections of the respiratory system, with damage of varying severity depending on the virus examined: ranging from mild-to-moderate upper respiratory tract diseases, such as the common cold, pneumonia, severe acute respiratory syndrome, kidney failure, and even death. Human coronaviruses known to date, common throughout the world, are seven. The most common—and least harmful—ones were discovered in the 1960s and cause a common cold. Others, more dangerous, identified in the early 2000s and cause more severe respiratory tract infections. Among these the SARS-CoV, isolated in 2003 and responsible for the severe acute respiratory syndrome (the so-called SARS), which appeared in China in November 2002, the coronavirus 2012 (2012-nCoV) cause of the Middle Eastern respiratory syndrome (MERS) from coronavirus, which exploded in June 2012 in Saudi Arabia, and actually SARS-CoV-2. On December 31, 2019, a new coronavirus strain was reported in Wuhan, China, identified as a new coronavirus beta strain ß-CoV from group 2B, with a genetic similarity of approximately 70% to SARS-CoV, the virus responsible of SARS. In the first half of February, the International Committee on Taxonomy of Viruses (ICTV), in charge of the designation and naming of the viruses (i.e., species, genus, family, etc.), thus definitively named the new coronavirus as SARS-CoV-2. This article highlights the main knowledge we have about the biomolecular and pathophysiologic mechanisms of SARS-CoV-2. [ABSTRACT FROM AUTHOR]

Since its identification in Wuhan, China, in December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has resulted in 46 million cases and more than one million deaths worldwide, as of 30 October 2020. Limited data exist on the magnitude and durability of antibodies generated by natural infection with SARS-CoV-2 and whether they can provide long-lasting immunity from reinfection. Vaccination has proven the most effective measure for controlling and preventing pandemics and, thus, development of a vaccine against COVID-19 is a top priority. However, the doses required to induce effective, long-lasting antibody responses against SARS-CoV-2 remain undetermined. Here, we present the development of SARS-CoV-2 vaccine candidates encoding the viral spike (S) gene, generated using plasmid (p)DNA technology, and we demonstrate the eliciting of S-specific antibodies in mice after three and four doses. The magnitude of binding and neutralizing antibody responses with three doses of synthetic, codon-optimized, full-length S (S.opt.FL) vaccine is comparable to that generated after four doses, suggesting that three doses are sufficient to elicit robust immune responses. Conversely, four doses of S1.opt pDNA vaccine, containing the S globular head, are required to elicit high levels of neutralizing antibodies. Furthermore, the S.opt.FL pDNA vaccine induces the highest serum levels of interferon (IFN)-γ, a marker for activation of cellular immune responses. Overall, our data show that three doses of S.FL pDNA vaccine elicit potent neutralizing antibody responses, with preclinical data that support the immunogenicity of these COVID-19 vaccine candidates and provide justification for further translational studies. [ABSTRACT FROM AUTHOR]