Thoracic adipose tissue contributes to severe virus infection of the lung.

OBJECTIVE: Obesity is an independent risk factor for severe influenza virus and COVID-19 infections. There might be an interplay between adipose tissue and respiratory pathogens, although the mechanism is unknown. Proinflammatory factors secreted by the adipose tissue are often discussed to serve as indirect contributor to virus infection. However, the direct potential of adipose tissue to serve as a viral niche has not yet been investigated. METHODS: Two murine obesity models (DIO and ob/ob) were infected with influenza A virus (IAV) and monitored for 3 weeks. p.i. Lung and adipose tissue were harvested, and the viral load was analysed. Direct replication of IAV in vitro was investigated in human derived primary adipocytes and macrophages. The indirect impact of the secretory products of adipocytes during infection was analysed in a co-culture system with lung fibroblasts. Moreover, lung and adipose tissue was harvested from deceased patients infected with SARS-CoV-2 omicron variant. Additionally, replication of SARS-CoV-2 alpha, delta, and omicron variants was investigated in vitro in adipocytes and macrophages. RESULTS: Both murine obesity models presented high IAV titers compared to non-obese mice. Interestingly, adipose tissue adjacent to the lungs was a focal point for influenza virus replication in mice. We further detected IAV replication and antiviral response in human adipocytes. Co-cultivation of adipocytes and lung fibroblasts led to increased IL-8 concentration during infection. Though we observed SARS-CoV-2 in the thoracic adipose tissue of COVID-19 patients, no active replication was found in adipocytes in vitro. However, SARS-CoV-2 was detected in the macrophages and this finding was associated with increased inflammation. CONCLUSIONS: Our study revealed that thoracic adipose tissue contributes to respiratory virus infection. Besides indirect induction of proinflammatory factors during infection, adipocytes and macrophages within the tissue can directly support viral replication.

Stabbed by motorcycle? Reconstruction of an unusual traffic accident.

The reconstruction of traffic accidents involving powered two-wheelers (PTWs) frequently proves to be a challenging task. A case in which a fatal head-on crash of a PTW with a small truck where only minor vehicles damage was observed but resulted in isolated fatal chest trauma is discussed here. External examination of the corpse revealed two lacerations on the back, at the first glance implying sharp trauma. Based on the accident traces, the technical expert assumed an emergency break of the PTW rider resulting in a rotation of the PTW in terms of a wheelie on the front wheel. The first contact between the PTW rider and the tail end of the small truck probably occurred with the upper side of the helmet, and then, the back handle of the PTW caused the stab-like injuries followed by compression of the rider between the small truck or asphalt and the PTW. Based on the few accident traces available, neither a reconstruction of the pre-impact velocity nor a detailed reconstruction of the PTW rider kinematics was possible. However, using an interdisciplinary approach, the principal collision position as well as the injury mechanisms could be reconstructed.

Pulmonary Artery Calcification in a 57-Year-Old Man.

CASE PRESENTATION: A 57-year-old man was admitted to our hospital via the ED presenting in reduced general condition because of an infection of unknown origin, generalized edema, and dyspnea at rest (peripheral capillary oxygen saturation, 89%) that required 2 L/min intranasal oxygen. Anamnesis was complicated by an infection-triggered delirium, but his wife reported an increasing physical decay that had led to bed confinement. The BP was reduced at 88/55 mm Hg with a normal heart rate of 86 beats/min. Lung auscultation showed mild bipulmonal rales. Previous comorbidities were a BMI of 42 kg/m2, an insulin-dependent type 2 diabetes mellitus with a severe diabetes-related chronic kidney disease stage G4A3, and systemic arterial hypertension.

Complicated Long Term Vaccine Induced Thrombotic Immune Thrombocytopenia-A Case Report.

BACKGROUND AND OBJECTIVES: Vaccine induced thrombotic thrombocytopenia (VITT) may occur after COVID-19 vaccination with recombinant adenoviral vector-based vaccines. VITT can present as cerebral sinus and venous thrombosis (CSVT), often complicated by intracranial hemorrhage. Today it is unclear, how long symptomatic VITT can persist. Here, we report the complicated long-term course of a VITT patient with extremely high titers of pathogenic anti-platelet factor 4 (PF4)-IgG antibodies. METHODS: Clinical and laboratory findings are presented, including the course of platelet counts, D-Dimer levels, clinical presentation, imaging, SARS-CoV-2-serological and immunological, platelet activating anti-PF4-IgG, as well as autopsy findings. RESULTS: The patient presented with extended superior sagittal sinus thrombosis with accompanying bifrontal intracerebral hemorrhage. Repeated treatment with intravenous immune globuline (IVIG) resolved recurrent episodes of thrombocytopenia. Moreover, the patient's serum remained strongly positive for platelet-activating anti-PF4-IgG over three months. After a period of clinical stabilization, the patient suffered a recurrent and fatal intracranial hemorrhage. CONCLUSIONS: Complicated VITT with extremely high anti-PF4-IgG titers over three months can induce recurrent thrombocytopenia despite treatment with IVIG and anticoagulation. Plasma exchange, immunoadsorption, and /or immunosuppressive treatment may be considered in complicated VITT to reduce extraordinarily high levels of anti-PF4-IgG. Long-term therapy in such cases must take the individual bleeding risk and CSVT risk into account.