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Background Availability of highly active antiretroviral therapy (HAART) for HIV has prolonged life expectancy of patients but has also increased the incidence of non-AIDS comorbid conditions. Among these, there are cardiovascular diseases, and aortic involvement has been described in patients with HIV in the form of aortitis, aneurysms, or dissections. Our study aims to describe aortic pathology occurring in patients with HIV, focusing on clinical and surgical presentation, management, and outcome, through a review of cases published in literature. Methods MEDLINE ( www.ncbi.nlm.nih.gov/pubmed ) database was reviewed for “aortitis” OR “aortic aneurysm” OR “aortic dissection” AND HIV. Research was restricted to English language. Only case reports were included. Data on patients' age, sex, traditional risk factors, timing from HIV diagnosis, pharmacological details, coinfection (syphilis, hepatitis C virus [HCV], and hepatitis B virus [HBV]), anatomical localization of lesion, presence of inflammatory involvement, rapid growing or rupture, and surgical treatment and outcomes were collected and summarized in tables. Results Forty articles (51 cases) were included in the study. The mean age of patients was 48.8 ± 8.3 years. Male sex was preponderant (43 cases, 84.3%). Among traditional risk factors, hypertension and smoking were the most frequently reported ones (14 and 13 cases, respectively), followed by vasculopathy involving other arterial districts, dyslipidemia, diabetes, and drug addiction. In 3 cases, HIV was diagnosed in the same time as aortic pathology, whereas in most cases, aortic event occurred after five years from HIV diagnosis. In 30.5% of cases for which data on pharmacologic management were available, no treatment or poor adherence was reported. Coinfection occurred in some cases (syphilis in 6, HCV in 5, and HBV in 3). As for anatomical involvement, isolated thoracic lesions were more frequent (24, 47.1%), followed by abdominal and thoracoabdominal lesions. The etiology ranged from bacterial mycotic aneurysms to tertiary syphilis, postsurgical complications, or atherosclerosis. In 3 cases, HIV vasculitis was directly suggested, and in another 2, no other potential etiology had been diagnosed through cultural tests. Open surgical treatment was carried out in 30 cases (58.8%), and in addition, 10 endovascular (19.6%) and 2 hybrid procedures were described. Inflammatory features occurred in 7 cases, and a rapid evolution of lesions in 6. In 9 cases (17.6%), rupture occurred. Mortality was reported in 8 cases (15.7%). Conclusions Aortic pathology may occur in patients with HIV. The entanglement of different patterns of pathological involvement of the aortic wall, secondary to immune dysregulation, infectious process, or atherosclerotic damage that may co-occur in one single case, results in a very challenging management of the condition. Because of the increased life expectancy of patients and immigration from regions with both high HIV and coinfection prevalence, the incidence of aortic pathology could increase in the upcoming years, suggesting the urgent need for further studies to optimize management in these very complex cases.

Highlights • SARS-CoV-2 infected patients have a differential IFN response. • IFN-stimulated genes levels are reduced in critically-ill patients. • SARS-CoV-2 viral load correlated to IFN-stimulated genes levels., The natural course of type I and III interferon (IFN) response in the respiratory tract of COVID-19 patients needs to be better defined. We showed that type I/III IFNs, IFN-regulatory factor 7 (IRF7), and IFN stimulated genes (ISGs), are highly expressed in the oropharyngeal cells of SARS-CoV-2 positive patients compared to healthy controls. Notably, the subgroup of critically-ill patients that required invasive mechanical ventilation had a general decrease in expression of IFN/ISG genes. Heterogeneous patterns of IFN-I/III response in the respiratory tract of COVID-19 patients may be associated to COVID-19 severity.

The diagnosis of coronavirus disease 2019 (COVID-19) relies on nasopharyngeal swab, which shows a 20–30% risk of false negativity [1]. Bronchoalveolar lavage (BAL) is reported to be useful in patients with pulmonary interstitial infiltrates on high-resolution computed tomography (HRCT). We investigated the usefulness of BAL in symptomatic patients with positive HRCT and a repeatedly negative swab test (‘grey zone’).

The aims were to describe efficacy and tolerability of regimens containing dolutegravir (DTG) in advanced ART-naive people living with HIV (PLHIV) from the clinical practice. The frequency of Immune Reconstitution Inflammatory Syndrome (IRIS), the estimated time of discontinuation of the first ART regimen and the time to reach virological suppression in a multicenter cohort of AIDS-presenters or late-presenters with CD4

Summary Objectives increased incidence of acute coronary events, high rate of abnormal surrogate markers of atherosclerosis and increased amount of coronary calcium have been described in HIV infected population. To expand knowledge on coronary artery disease (CAD) in HIV patients, cardiac CT scan was performed in asymptomatic subjects with low cardiovascular (CV) risk. Methods A cross-sectional study using dual-source CT (MDCT) coronary angiography.was conducted in HIV-infected subjects with the following characteristics: Framingham Risk Score (FRS) ≤10, absence of metabolic syndrome, negative echocardiographic and ECG stress-test. A luminal narrowing exceeding 50% was defined as a clinically significant coronary stenosis. Calcium score was quantified using the Agatston Calcium Score method. Results Fifty-five subjects were enrolled. Significant coronary stenoses, requiring coronary angiography, were found in 16/55 (29.1%). At multivariate analysis older age was the only variable independently associated with the presence of significant luminal narrowing ( p = 0.011). Conclusions MDCT showed an unexpected, age-associated high rate of significant coronary stenosis in asymptomatic HIV positive subjects with low CV risk. These findings suggest that aggressive screening programs for coronary artery disease may be appropriate in this population; further studies are recommended to assess the appropriateness of MDCT for this purpose.

Objective To determine the functions of in vitro primed Natural Killer (NK) cells in Human Immunodeficiency Virus (HIV-1) infection and the role of IL-2, IL-12 and IL-15 in enhancing the NK survival and activity in terms of viral suppression and of purging of HIV provirus. Methods Peripheral Blood Mononuclear Cells (PBMCs) and CD4+ T lymphocytes cells obtained from eight healthy donors were infected in vitro with HIV-1 and p24 was measured with and without IL-2, IL-12 and IL-15. We studied the effect of NK pulsed in vitro with IL-2, IL-12 and IL-15 on HIV replication by measurement of p-24 and DNA-provirus load when added into the culture of PBMCs and CD4+ T lymphocytes cells infected in vitro. We evaluated the effect of NK cells pulsed with IL-2, IL-12 and IL-15 on HIV replication and DNA-load into the culture of CD4+ T lymphocytes cells and PBMCs by trans-well chamber. Results We found high levels of p24 in the supernatants of PBMCs and CD4+ T lymphocytes cells cultured with IL-2, IL-12, and IL-15. We observed a significant reduction of p24 in the culture both of infected PBMCs and CD4+ T lymphocytes cells in which was added NK pulsed with IL-15. We did not obtain the some results with NK pulsed with IL-2 and IL-12. We observed a power effect of NK pulsed with IL-15 on HIV-DNA. The trans-well chamber experiments showed that the effect of NK is both direct and both mediated by realizing of soluble factors. Conclusions This study highlights some important effects of IL 15 on NK in HIV patients anyway our results are preliminary and descriptive and others studies will be needed to provide rationale for immune therapies.

Several lines of evidence documented a renewed interest in the role of natural killer (NK) cells in the innate immune control of HIV infection and disease progression. To further assess the role of NK cells as target for immunotherapy in HIV infection, we evaluated the priming effect of interleukin (IL)-15 on freshly isolated human peripheral NK cells, from viremic and aviremic HIV-infected patients, measuring the production of IFN-gamma and CC chemokines. In vitro IL-15 priming induced a significant increase of IFN-gamma production in both viremic and aviremic patients. IL-15 stimulated NK cells producing CC chemokine quantities that are reported to be capable of inhibiting HIV infection and replication. This priming effect is observed both in viral suppressed patients after antiretroviral therapy, and in viremic subjects with progressive HIV infection. The combination of IL-15 plus IL-12 is the most potent costimulus for CD69 expression and production of CC chemokines by NK cells. These findings indicate that NK cells are an important target for immunotherapeutic agents and provide additional pre-clinical data supporting the great potential of IL-15 in the immune-based interventions in HIV disease.

Interleukin (IL)-15 is a cytokine that has lymphocyte stimulatory activity similar to that of IL-2, and plays important immunoregulatory functions during HIV disease. To evaluate the role of IL-15 in HIV infection the following patients were studied: 18 antiretroviral-naive patients with advanced disease; 19 patients with continuous viral suppression and immunological response after 48-120 weeks of highly active antiretroviral therapy (HAART); and 12 patients with evidence of virological and immunological HAART treatment failure. Nineteen healthy blood donors were included as controls. The production of IL-15 by human peripheral blood monocytes stimulated with lipopolysaccharide and Mycobacterium avium complex, the priming effect of IL-15 on IFN-gamma production from purified CD4(+) and CD8(+) T cells, and the ability of IL-15 to stimulate the beta-chemokine release from purified CD4(+) and CD8(+) T cells were analyzed. In the present work IL-15 production by human peripheral blood monocytes was significantly increased in HIV-infected patients with long-term virological and immunological response to HAART. IL-15 enhanced the in vitro priming of CD4(+) and CD8(+) T cells for IFN-gamma production, also in patients receiving HAART. Finally, IL-15 had positive effects on RANTES, MIP-1alpha, and MIP-1beta release by CD4(+) and CD8(+) T cells. In conclusion IL-15 could affect the immune response of HIV-infected patients by augmenting and/or modulating IFN-gamma production and beta-chemokine release. These data about functional properties of IL-15 could provide new implications for immune-based therapies in HIV infection.

Increased levels of soluble cell adhesion molecules (sCAM) have been reported in HIV-1 infection and may possibly contribute to altering the adhesion mechanisms of phagocytic cells. We evaluated the effect of highly active antiretroviral therapy (HAART) on plasma levels of sL-selectin, sE-selectin, intercellular cell adhesion molecule-1 (sICAM-1), sICAM-3, and vascular cell adhesion molecule-1 (sVCAM-1). Study participants included 22 HIV-1-infected patients with a CD4+ T-cell count/μl below 500 who were started on a HAART regimen and followed up for 9 months. After the initiation of therapy, plasma sL-selectin concentrations progressively decreased to normal ranges in the majority of our patients (P < 0.001), while no changes in sE-selectin were found. In all patients sICAM-1 remained relatively constant at significantly elevated concentrations during the 9 months of therapy. A significant reduction in plasma concentrations of both sICAM-3 and sVCAM-1 was found; however, the levels of these sCAM were not normalized by HAART and remained significantly elevated throughout the study (P < 0.001). The reduced release of sL-selectin could improve the ability of phagocitic cells to migrate in response to chemotactic stimuli after starting HAART. On the other hand, the persistent elevation of sICAM-1, sICAM-3, and sVCAM-1 could reflect continuous HIV-1-mediated immune activation, despite adequate control of plasma HIV-1 replication by therapy.