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Despite anti-retroviral therapy, HIV-1 infection increases the risk of pneumonia and causes oxidative stress and defective alveolar macrophage (AM) immune function. We have previously determined that HIV-1 proteins inhibit antioxidant defenses and impair AM phagocytosis by suppressing nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Given its known effects on Nrf2, we hypothesize miR-144 mediates the HIV-1 induced suppression of Nrf2.

Primary AMs isolated from HIV-1 transgenic (HIV-1 Tg) rats and wild type littermates (WT) as well as human monocyte-derived macrophages (MDMs) infected ex vivo with HIV-1 were used. We modulated miR-144 expression using a miR-144 mimic or an inhibitor to assay its effects on Nrf2/ARE activity and AM functions in vitro and in vivo.

MiR-144 expression was increased in AMs from HIV-1 Tg rats and in HIV-1-infected human MDMs compared to cells from WT rats and non-infected human MDMs, respectively. Increasing miR-144 with a miR-144 mimic inhibited the expression of Nrf2 and its downstream effectors in WT rat macrophages and consequently impaired their bacterial phagocytic capacity and H
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scavenging ability. These effects on Nrf2 expression and AM function were reversed by antagonizing miR-144 ex vivo or in the airways of HIV-1 Tg rats in vivo, but this protection was abrogated by silencing Nrf2 expression.

Our results suggest that inhibiting miR-144 or interfering with its deleterious effects on Nrf2 attenuates HIV-1-mediated AM immune dysfunction and improves lung health in individuals with HIV.
Our results suggest that inhibiting miR-144 or interfering with its deleterious effects on Nrf2 attenuates HIV-1-mediated AM immune dysfunction and improves lung health in individuals with HIV.Physical inactivity is a well-established risk factor for cardiovascular disease (CVD) incidence and mortality. In the last decade, there is also emerging evidence of the role of sedentary behaviors (sitting) as a risk factor for CVD. Therefore, there is increasing interest in understanding the independent and joint effects of physical activity and sedentary behavior on CVD risk. Higher levels of moderate-to-vigorous physical activity and less time spent in sedentary behavior are associated with a decreased risk of CVD. There is also preliminary evidence that higher levels of light-intensity physical activity are associated with lower all-cause mortality rates; however, the cardio-protective effects of light-intensity physical activity are yet to be determined. The results from several studies have demonstrated that the effects of sedentary behavior on CVD risk is more pronounced among individuals who are physically inactive, compared to those who are more active. Further, high levels (60-75 min per day) of moderate-to-vigorous physical activity appear to eliminate the increased risk of CVD associated with excessive sedentary behavior. Replacing sedentary behavior with any intensity of physical activity will produce health benefits; however, the greatest benefits occur when replacing sedentary behavior with moderate-to-vigorous intensity physical activity.The COVID-19 pandemic has put a serious strain on health treatments as well at the economies of many nations. Unfortunately, there is not currently available vaccine for SARS-Cov-2/COVID-19. Various types of patients have delayed treatment or even routine check-ups and we are adapting to a virtual world. In many cases, surgeries are delayed unless they are essential. This is also true with regards to cancer treatments and screening. Interestingly, some existing drugs and nutraceuticals have been screened for their effects on COVID-19. Certain FDA approved drugs, vitamin, natural products and trace minerals may be repurposed to treat or improve the prevention of COVID-19 infections and disease progression. This review article will summarize how the treatments of various cancer patients has changed during the COVID-19 era as well as discuss the promise of some existing drugs and other agents to be repurposed to treat this disease.The rapid onset and worldwide spread of the COVID-19 epidemic (caused by SARS-CoV-2 coronavirus) has been associated with a profound impact in clinical practice also in the hematologic setting. First of all, given the immunosuppressive effect of many therapies that are normally administered to patients with hematological diseases, with a consequent increased risk of contracting a more severe viral infection, it has been necessary to reconsider in each individual patient the urgency and priority of the treatments foreseen by the normal standards of care. In particular, as regards allogeneic (and to a lesser extent autologous) hematopoietic cell transplantation and CAR T-cell therapy, specific recommendations have been issued by the transplant community on the criteria to be used to decide whether or not to postpone these procedures and on the clinical management of recipients and donors exposed to COVID-19. As to cytotoxic chemotherapy and other antineoplastic therapies, criteria have been proposed to decide, in the various clinical situations, which treatments were not deferrable and which instead could be postponed or replaced by less aggressive therapies. In the outpatient clinics, various organizational solutions for telemedicine have been adopted, resorting to telephone interviews and/or Information Technology, with the aim of reducing the influx of patients while maintaining an adequate control of their clinical condition. The collection of blood by the transfusion centers has been the subject of organizational measures, in order to avoid the transmission of COVID 19 while maintaining a sufficient blood collection for clinical needs. Finally, some hematologic laboratory alterations have been identified, such as thrombocytopenia, lymphopenia and coagulation abnormalities, useful for the prognostic evaluation of infected patients.Pandemic coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and poses an unprecedented challenge to healthcare systems due to the lack of a vaccine and specific treatment options. Accordingly, there is an urgent need to understand precisely the pathogenic mechanisms underlying this multifaceted disease. There is increasing evidence that the immune system reacts insufficiently to SARS-CoV-2 and thus contributes to organ damage and to lethality. #link# In this review, we suggest that the overwhelming production of reactive oxygen species (ROS) resulting in oxidative stress is a major cause of local or systemic tissue damage that leads to severe COVID-19. It increases the formation of neutrophil extracellular traps (NETs) and suppresses the adaptive arm of the immune system, i.e. T cells that are necessary to kill virus-infected cells. This creates a vicious cycle that prevents a specific immune response against SARS-CoV-2. The key role of oxidative stress in the pathogenesis of severe COVID-19 implies that therapeutic counterbalancing of ROS by antioxidants such as vitamin C or NAC and/or by antagonizing ROS production by cells of the mononuclear phagocyte system (MPS) and neutrophil granulocytes and/or by blocking of TNF-α can prevent COVID-19 from becoming severe.
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