Paramount efforts worldwide are seeking to increase understanding of the basic virology of SARS-CoV-2, characterize the spectrum of complications associated with COVID-19, and develop vaccines that can protect from new and recurrent infections with SARS-CoV-2. While we continue learning about this new virus, it is clear that 1) the virus is spread via the respiratory route, primarily by droplets and contact with contaminated surfaces and fomites, as well as by aerosol formation during invasive respiratory procedures; 2) the airborne route is still controversial; and 3) that those infected can spread the virus without necessarily developing asymptomatic). With the number of SARS-CoV-2 infections increasing globally, the possibility of co-infections and/or co-morbidities is becoming more concerning. Co-infection with Human Immunodeficiency Virus (HIV) is one such example of polyparasitism of interest. This military-themed comparative review of SARS-CoV-2 and HIV details their virology and describes them figuratively as separate enemy armies. HIV, an old enemy dug into trenches in individuals already infected, and SARS-CoV-2 the new army, attempting to attack and capture territories, tissues and organs, in order to provide resources for their expansion. This analogy serves to aid in discussion of three main areas of focus and draw attention to how these viruses may cooperate to gain the upper hand in securing a host. Here we compare their target, the key receptors found on those tissues, viral lifecycles and tactics for immune response surveillance. The last focus is on the immune response to infection, addressing similarities in cytokines released. While the majority of HIV cases can be successfully managed with antiretroviral therapy nowadays, treatments for SARS-CoV-2 are still undergoing research given the novelty of this army.

Background Multi-System Inflammatory Syndrome in Children (MIS-C) is a systemic inflammatory condition where various body organs, such as the heart, kidney, gastrointestinal organs, become inflamed. Several cases have been reported in children linking MIS-C with Novel Corona Virus Disease-2019 (COVID-19); however, few cases have been reported in adults (MIS-A). Case Summary A case of a 20-year-old male patient with a history of COVID-19 infection two months before presentation who presented with fever and acute right lower quadrant pain. Workup revealed right-sided mesenteric lymphadenopathy and mild colitis that was non-responsive to antibiotics. The patient was found to have significantly elevated inflammatory markers. He also developed myocarditis resulting in acute systolic heart failure with reduced ejection fraction. The diagnosis of MIS-A was made by exclusion. The patient showed improvement with intravenous immunoglobulin and pulse steroids. Based on available literature, MIS-C was defined till the age of 21; however, we think it is a misnomer for adults more than 18. Hence, we prefer to use MIS-A for our patient. Conclusion It is essential to diagnose and treat patients with the multi-system inflammatory syndrome at an early stage; the management of these patients, especially with heart disease, should include immune-modulatory therapy as well as guideline-directed therapy.

Objective:The prognostic value of changes in neutrophil-to-lymphocyte ratios (NLR) in cardiac arrest survivors receiving targeted temperature management (TTM) is unknown. The current study investigated NLR in postcardiac arrest (PCA) patients undergoing TTM.Methods:This retrospective single-center study included 95 patients (59 males, age: 55.0±17.0 years) with in-hospital and out-of-hospital cardiac arrests who underwent TTM for PCA syndrome within 6 h of cardiac arrest. Hypothermia was maintained for 24 h at a target temperature of 33°C. NLR was calculated as the absolute neutrophil count divided by the absolute lymphocyte count.Results:Of the 95 patients, 59 (62%) died during hospital stay. Fewer vasopressors were used in patients who survived. Out-of-hospital cardiac arrest was more frequent in decedents (p=0.005). Length of stay in the hospital and intensive care unit were significantly longer in patients who survived (p=0.0001 and p=0.001, respectively). NLR on admission and during rewarming did not differ between survivors and decedents. NLR during cooling was significantly higher in decedents (p=0.014). Delta NLR cut-off of 13.5 best separated survivors and decedents (AUC=0.68, 95%CI: 0.57–0.79, p=0.003 with a sensitivity and specificity of 64% and 67%, respectively). In multivariate logistic regression analysis, larger increase in NLR was significantly associated with decreased survival (OR:0.96, 95%CI:0.94–0.99, p=0.008).Conclusion:Changes in NLR are an independent determinant of survival in patients with return of spontaneous circulation PCA treated with TTM. An NLR change can be used to predict survival in these patients.

Abnormal regulation of DNA methylation and its readers has been associated with a wide range of cellular dysfunction. Disruption of the normal function of DNA methylation readers contributes to cancer progression, neurodevelopmental disorders, autoimmune disease and other pathologies. One reader of DNA methylation known to be especially important is MeCP2. It acts a bridge and connects DNA methylation with histone modifications and regulates many gene targets contributing to various diseases; however, much remains unknown about how it contributes to cancer malignancy. We and others previously described novel MeCP2 post-translational regulation. We set out to test the hypothesis that MeCP2 would regulate novel genes linked with tumorigenesis and that MeCP2 is subject to additional post-translational regulation not previously identified. Herein we report novel genes bound and regulated by MeCP2 through MeCP2 ChIP-seq and RNA-seq analyses in two breast cancer cell lines representing different breast cancer subtypes. Through genomics analyses, we localize MeCP2 to novel gene targets and further define the full range of gene targets within breast cancer cell lines. We also further examine the scope of clinical and pre-clinical lysine deacetylase inhibitors (KDACi) that regulate MeCP2 post-translationally. Through proteomics analyses, we identify many additional novel acetylation sites, nine of which are mutated in Rett Syndrome. Our study provides important new insight into downstream targets of MeCP2 and provide the first comprehensive map of novel sites of acetylation associated with both pre-clinical and FDA-approved KDACi used in the clinic. This report examines a critical reader of DNA methylation and has important implications for understanding MeCP2 regulation in cancer models and identifying novel molecular targets associated with epigenetic therapies.