Post by Nadica (She/Her) on Nov 13, 2024 3:49:43 GMT
SARS-CoV-2 targets pericytes to restrict blood flow within the brain - Published Dec 20, 2022
The SARS-CoV-2 virus targets multiple organs including the brain. In the early stages of the COVID-19 pandemic, many acutely infected patients who needed hospitalization had signs and symptoms of neurological disease. A 1-year follow-up study of SARS-CoV-2 patients found an increased risk of stroke, cognitive decline and mental health disorders.1 However, the nature of the link between SARS-CoV-2 infection and neurological damage remains obscure. Neuropathological assessment has not provided convincing evidence of widespread active replication of virus within the brain, although brain infarcts consistent with hypoxic-ischaemic injury, and foci of cerebral haemorrhage, are common.2 Single-cell mapping indicates that ACE-2, a regulatory enzyme belonging to the renin-angiotensin system (RAS) and the receptor for SARS-CoV-2, is largely absent from neuronal cells within the cerebral cortex and is instead predominantly expressed within cerebral vascular mural cells, known as pericytes,3 which are major regulators of small-vessel calibre. In this issue of Brain, Hirunpattarasilp and co-workers4 now show that SARS-CoV-2 infection of brain pericytes causes the internalization of ACE-2, resulting in exaggerated angiotensin-II(Ang-II)-mediated pericyte contraction and consequent capillary constriction, which can be blocked by losartan, an Ang-II receptor type 1 (AT1R) antagonist.
The SARS-CoV-2 virus targets multiple organs including the brain. In the early stages of the COVID-19 pandemic, many acutely infected patients who needed hospitalization had signs and symptoms of neurological disease. A 1-year follow-up study of SARS-CoV-2 patients found an increased risk of stroke, cognitive decline and mental health disorders.1 However, the nature of the link between SARS-CoV-2 infection and neurological damage remains obscure. Neuropathological assessment has not provided convincing evidence of widespread active replication of virus within the brain, although brain infarcts consistent with hypoxic-ischaemic injury, and foci of cerebral haemorrhage, are common.2 Single-cell mapping indicates that ACE-2, a regulatory enzyme belonging to the renin-angiotensin system (RAS) and the receptor for SARS-CoV-2, is largely absent from neuronal cells within the cerebral cortex and is instead predominantly expressed within cerebral vascular mural cells, known as pericytes,3 which are major regulators of small-vessel calibre. In this issue of Brain, Hirunpattarasilp and co-workers4 now show that SARS-CoV-2 infection of brain pericytes causes the internalization of ACE-2, resulting in exaggerated angiotensin-II(Ang-II)-mediated pericyte contraction and consequent capillary constriction, which can be blocked by losartan, an Ang-II receptor type 1 (AT1R) antagonist.