Pleomorphic hyalinizing angiectatic tumor: FNA analysis of a rare entity and review of the literature.

INTRODUCTION: The fine-needle aspiration (FNA) cytopathology of pleomorphic hyalinizing angiectatic tumor (PHAT) is the subject of a very limited number of reports. We undertook a review of our FNA experience with this neoplasm. MATERIALS AND METHODS: A search was made of our files for PHAT FNA cases with histopathologic confirmation. FNA biopsy smears and cell blocks were performed and examined using standard techniques. RESULTS: Two primary cases of histologically proven PHAT [both male, ages 56 and 60 years] met study inclusion. FNA sites included buttock and foot. A misdiagnosis of sarcoma was made in each case. Ancillary immunohistochemical testing performed in 1 case suggested angiosarcoma. Cytologic smears showed only modest cellularity with a dual population of bland spindle cells and isolated large pleomorphic cells, many harboring nuclear pseudoinclusions. Smear background was clean, and mitoses absent. CONCLUSIONS: The imitative cytopathology of PHAT with a pleomorphic sarcoma remains a pitfall in FNA specimens. Awareness of this entity and its lack of hypercellularity, necrosis, and cohesive groups of atypical cells in smears should assist the cytopathologist in avoiding a misdiagnosis of malignancy.

Influenza A virus modulates ACE2 expression and SARS-CoV-2 infectivity in human cardiomyocytes.

Influenza A virus (IAV) and SARS-CoV-2 virus are both acute respiratory viruses currently circulating in the human population. This study aims to determine the impact of IAV infection on SARS-CoV-2 pathogenesis and cardiomyocyte function. Infection of human bronchial epithelial cells (HBEC), A549 cells, lung fibroblasts (HLF), monocyte derived macrophages (MDMs), cardiac fibroblasts (HCF) and hiPSC-derived cardiomyocytes with IAV enhanced the expression of ACE2, the SARS-CoV-2 receptor. Similarly, IAV infection increased levels of ACE2 in the lungs of mice and humans. Of interest, we detected heavily glycosylated form of ACE2 in hiPSC-CMs and poorly glycosylated ACE2 in other cell types. Also, prior IAV infection enhances SARS-CoV-2 spike protein binding and viral entry in all cell types. However, efficient SARS-CoV-2 replication was uniquely inhibited in cardiomyocytes. Glycosylation of ACE2 correlated with enzymatic conversion of its substrate Ang II, induction of eNOS and nitric oxide production, may provide a potential mechanism for the restricted SARS-CoV-2 replication in cardiomyocytes.