PT  - JOURNAL ARTICLE
AU  - Sreekala Nampoothiri
AU  - Florent Sauve
AU  - Gaëtan Ternier
AU  - Daniela Fernandois
AU  - Caio Coelho
AU  - Monica Imbernon
AU  - Eleonora Deligia
AU  - Romain Perbet
AU  - Vincent Florent
AU  - Marc Baroncini
AU  - Florence Pasquier
AU  - François Trottein
AU  - Claude-Alain Maurage
AU  - Virginie Mattot
AU  - Paolo Giacobini
AU  - S. Rasika
AU  - Vincent Prevot
TI  - The hypothalamus as a hub for putative SARS-CoV-2 brain infection
AID  - 10.1101/2020.06.08.139329
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.06.08.139329
4099  - http://biorxiv.org/content/early/2020/06/09/2020.06.08.139329.short
4100  - http://biorxiv.org/content/early/2020/06/09/2020.06.08.139329.full
AB  - Most patients with COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), display neurological symptoms, and respiratory failure in certain cases could be of extra-pulmonary origin. With reports detecting SARS-CoV-2 in some post-mortem patient brains, the routes, targets and consequences of brain infection merit investigation. Hypothalamic neural circuits play key roles in sex differences, diabetes, hypertension, obesity and aging, all risk factors for severe COVID-19, besides being connected to brainstem cardiorespiratory centers. Here, human brain gene-expression analyses reveal that the hypothalamus and associated regions express angiotensin-converting enzyme 2 and transmembrane proteinase, serine 2, which mediate SARS-CoV-2 cellular entry, in correlation with several genes or pathways involved in physiological functions or viral pathogenesis. Immunolabeling in human and animal brains suggests that the hypothalamus could be central to SARS-CoV-2 brain invasion through multiple routes, and that sex hormones and metabolic diseases influence brain susceptibility.Competing Interest StatementThe authors have declared no competing interest.