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1.
EuropePMC; 2021.
Preprint in English | EuropePMC | ID: ppcovidwho-292556

ABSTRACT

Neurological manifestations are common in COVID-19, the disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Despite some reports of detection of SARS-CoV-2 in the brain and cerebrospinal fluid of patients with COVID-19, it is still unclear whether the virus can infect the central nervous system (CNS), and which neuropathological alterations can be ascribed to viral tropism rather than immune-mediated mechanisms. Available autopsy reports are often conflictual, reporting a heterogeneous spectrum of neuropathological alterations, while viral proteins and RNA were detected only in sparse cells within the brainstem;furthermore, there appears to be no consistent correlation between viral invasion and neuropathological alterations to date. Here, we assess the neuropathological changes occurring in 24 patients who died following a diagnosis of SARS-CoV-2 infection in Italy during the COVID-19 pandemic (from March 2020 to May 2021) and 10 age-matched controls with comparable medical conditions. Aside from a wide spectrum of neuropathological alterations, including astrogliosis, sparse lympho-monocytic infiltrations and several instances of small vessel thromboses, we identified 5 COVID-19 subjects presenting SARS-CoV-2-immunoreactive neurons within the boundaries of the solitary tract nucleus, nucleus ambiguus and substantia nigra in the brainstem. In these subjects, viral RNA was also detected by real-time RT-PCR. Quantification of reactive microglia revealed an anatomically segregated pattern of inflammation targeting mainly the medulla oblongata and the mesencephalon, and was significantly higher when compared to controls. However, SARS-CoV-2 direct invasion did not appear to correlate with the severity of neuropathological changes. The results of this study support the neuroinvasive potential of SARS-CoV-2 by demonstrating the presence of viral proteins and genome sequences within the human brainstem, but further investigation is required to identify the link between invasion and consequent neuropathological alterations in humans.

2.
Front Immunol ; 12: 736529, 2021.
Article in English | MEDLINE | ID: covidwho-1515533

ABSTRACT

Various authors have hypothesized carotid body (CB) involvement in Coronavirus Disease 2019 (COVID-19), through direct invasion or indirect effects by systemic stimuli ('cytokine storm', angiotensin-converting enzyme [ACE]1/ACE2 imbalance). However, empirical evidence is limited or partial. Here, we present an integrated histopathological and virological analysis of CBs sampled at autopsy from four subjects (2 males and 2 females; age: >70 years old) who died of COVID-19. Histopathological, immunohistochemical and molecular investigation techniques were employed to characterize Severe Acute Respiratory Syndrome - Coronavirus 2 (SARS-CoV2) viral invasion and inflammatory reaction. SARS-CoV2 RNA was detected in the CBs of three cases through Real-Time Reverse Transcription Polymerase Chain Reaction (RT-PCR). In these cases, positive immunostaining for Nucleocapsid and Spike protein were also demonstrated, mainly at the level of large roundish cells consistent with type I cells, confirming direct CB invasion. In these cases, T lymphocytes showed focal aggregations in the CBs, suggestive of local inflammatory reaction. Blood congestion and microthrombosis were also found in one of the positive cases. Intriguingly, microthrombosis, blood congestion and microhaemorrages were also bilaterally detected in the CBs of the negative case, supporting the possibility of COVID-19 effects on the CB even in the absence of its direct invasion. SARS-CoV-2 direct invasion of the CB is confirmed through both immunohistochemistry and RT-PCR, with likely involvement of different cell types. We also reported histopathological findings which could be ascribed to local and/or systemic actions of SARS-CoV-2 and which could potentially affect chemoreception.


Subject(s)
COVID-19 , Carotid Body , SARS-CoV-2 , Aged , Autopsy , COVID-19/pathology , COVID-19/virology , Carotid Body/pathology , Carotid Body/virology , Coronavirus Nucleocapsid Proteins/metabolism , Female , Humans , Male , Phosphoproteins/metabolism , RNA, Viral/analysis , SARS-CoV-2/genetics , Spike Glycoprotein, Coronavirus/metabolism
3.
Anat Sci Educ ; 14(6): 739-751, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1400749

ABSTRACT

The world has been turned upside down by a global health emergency caused by the Covid-19. Given the high contagiousness of the virus and the need to contain its spread, social distancing rules, self-isolation policies, and geographical lockdowns have been enforced globally. Over the pandemic emergency the majority of the planned in-person meetings and congresses of national and international anatomical societies have been postponed or canceled. It is unclear what the future holds, but times of crisis often present possibilities for re-thinking old ways to achieve a more critical approach. It has become increasingly clear that traditional in-person congress formats of scientific societies need to be reevaluated. Over the past year and a half, two types of congressional modalities have been trialed to address the challenge of the pandemic as far as scientific meetings are concerned: the fully virtual congress, in which case the conference program is live streamed to all of the attendees, and the hybrid congress, in which case some of the attendees physically participate at the congress's venue while others interact via a virtual platform. The current study set out to investigate the technical difficulties, social challenges, costs and sustainability, logistics and management issues linked to holding various types of congresses in the post-Covid world. Anatomical societies throughout the world are actively striving to reshape their response to the current global emergency and to uncover new types of conference modalities in the effort to keep scientific exchange alive and flourishing in the post-Covid era.


Subject(s)
Anatomy , COVID-19 , Anatomy/education , Communicable Disease Control , Humans , Pandemics , SARS-CoV-2
4.
Front Immunol ; 12: 676828, 2021.
Article in English | MEDLINE | ID: covidwho-1320577

ABSTRACT

In coronavirus disease 2019 (COVID-19), ulcerative lesions have been episodically reported in various segments of the gastrointestinal (GI) tract, including the oral cavity, oropharynx, esophagus, stomach and bowel. In this report, we describe an autopsy case of a COVID-19 patient who showed two undiagnosed ulcers at the level of the anterior and posterior walls of the hypopharynx. Molecular testing of viruses involved in pharyngeal ulcers demonstrated the presence of severe acute respiratory syndrome - coronavirus type 2 (SARS-CoV-2) RNA, together with herpes simplex virus 1 DNA. Histopathologic analysis demonstrated full-thickness lympho-monocytic infiltration (mainly composed of CD68-positive cells), with hemorrhagic foci and necrosis of both the mucosal layer and deep skeletal muscle fibers. Fibrin and platelet microthrombi were also found. Cytological signs of HSV-1 induced damage were not found. Cells expressing SARS-CoV-2 spike subunit 1 were immunohistochemically identified in the inflammatory infiltrations. Immunohistochemistry for HSV1 showed general negativity for inflammatory infiltration, although in the presence of some positive cells. Thus, histopathological, immunohistochemical and molecular findings supported a direct role by SARS-CoV-2 in producing local ulcerative damage, although a possible contributory role by HSV-1 reactivation cannot be excluded. From a clinical perspective, this autopsy report of two undiagnosed lesions put the question if ulcers along the GI tract could be more common (but frequently neglected) in COVID-19 patients.


Subject(s)
COVID-19/complications , Hypopharynx/pathology , SARS-CoV-2/isolation & purification , Ulcer/pathology , Aged , Antigens, CD/metabolism , Antigens, Differentiation, Myelomonocytic/metabolism , Autopsy , Blood Platelets/metabolism , Blood Platelets/pathology , COVID-19/mortality , COVID-19/pathology , COVID-19/physiopathology , Gastrointestinal Tract/pathology , Herpesvirus 1, Human/genetics , Herpesvirus 1, Human/isolation & purification , Humans , Hypopharynx/virology , Immunohistochemistry , Inflammation/immunology , Inflammation/metabolism , Inflammation/virology , Lymphocytes/metabolism , Monocytes/metabolism , Mucous Membrane/pathology , Muscle, Skeletal/pathology , Necrosis/pathology , SARS-CoV-2/genetics , Spike Glycoprotein, Coronavirus/metabolism , Thrombosis/pathology , Ulcer/virology
5.
FEBS J ; 287(17): 3681-3688, 2020 09.
Article in English | MEDLINE | ID: covidwho-960853

ABSTRACT

In coronavirus disease 2019 (COVID-19), higher morbidity and mortality are associated with age, male gender, and comorbidities, such as chronic lung diseases, cardiovascular pathologies, hypertension, kidney diseases, diabetes mellitus, and obesity. All of the above conditions are characterized by increased sympathetic discharge, which may exert significant detrimental effects on COVID-19 patients, through actions on the lungs, heart, blood vessels, kidneys, metabolism, and/or immune system. Furthermore, COVID-19 may also increase sympathetic discharge, through changes in blood gases (chronic intermittent hypoxia, hyperpnea), angiotensin-converting enzyme (ACE)1/ACE2 imbalance, immune/inflammatory factors, or emotional distress. Nevertheless, the potential role of the sympathetic nervous system has not yet been considered in the pathophysiology of COVID-19. In our opinion, sympathetic overactivation could represent a so-far undervalued mechanism for a vicious circle between COVID-19 and comorbidities.


Subject(s)
COVID-19/metabolism , Coronary Disease/metabolism , Diabetes Mellitus/metabolism , Hypertension/metabolism , Kidney Failure, Chronic/metabolism , Obesity/metabolism , Respiratory Insufficiency/metabolism , Sympathetic Nervous System/metabolism , COVID-19/mortality , COVID-19/pathology , COVID-19/virology , Comorbidity , Coronary Disease/mortality , Coronary Disease/pathology , Coronary Disease/virology , Diabetes Mellitus/mortality , Diabetes Mellitus/pathology , Diabetes Mellitus/virology , Female , Humans , Hypertension/mortality , Hypertension/pathology , Hypertension/virology , Kidney Failure, Chronic/mortality , Kidney Failure, Chronic/pathology , Kidney Failure, Chronic/virology , Male , Obesity/mortality , Obesity/pathology , Obesity/virology , Respiratory Insufficiency/mortality , Respiratory Insufficiency/pathology , Respiratory Insufficiency/virology , SARS-CoV-2/metabolism , SARS-CoV-2/pathogenicity , Severity of Illness Index , Sex Factors , Survival Analysis , Sympathetic Nervous System/physiopathology , Sympathetic Nervous System/virology
6.
Am J Physiol Lung Cell Mol Physiol ; 319(4): L620-L626, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-696494

ABSTRACT

The carotid body (CB) plays a contributory role in the pathogenesis of various respiratory, cardiovascular, renal, and metabolic diseases through reflex changes in ventilation and sympathetic output. On the basis of available data about peripheral arterial chemoreception and severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), a potential involvement in the coronavirus disease 2019 (COVID-19) may be hypothesized through different mechanisms. The CB could be a site of SARS-CoV-2 invasion, due to local expression of its receptor [angiotensin-converting enzyme (ACE) 2] and an alternative route of nervous system invasion, through retrograde transport along the carotid sinus nerve. The CB function could be affected by COVID-19-induced inflammatory/immune reactions and/or ACE1/ACE2 imbalance, both at local or systemic level. Increased peripheral arterial chemosensitivity and reflex sympatho-activation may contribute to the increased morbidity and mortality in COVID-19 patients with respiratory, cardiovascular, renal, or metabolic comorbidities.


Subject(s)
Carotid Body/metabolism , Central Nervous System/virology , Coronavirus Infections/pathology , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/pathology , Angiotensin-Converting Enzyme 2 , Betacoronavirus , COVID-19 , Carotid Sinus/innervation , Carotid Sinus/virology , Humans , Pandemics , Renin-Angiotensin System/physiology , SARS-CoV-2
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