 Whether SARS-CoV-2 is able to invade the nervous system remains unknown ; however. it is clear that many people with COVID-19 exhibit neurological or mental health issues. The virus is not detected in the CNS of the majority of COVID-19 people with neurological issues. However, SARS-CoV-2 has been detected at low levels in the brains of those who have died from COVID-19, but these results need to be confirmed. Loss of smell results from infection of the support cells of the olfactory epithelium, with subsequent damage to the olfactory neurons. SARS-CoV-2 could cause respiratory failure through affecting the brain stem as other coronaviruses have been found to invade the CNS. While virus has been detected in cerebrospinal fluid of autopsies, the exact mechanism by which it invades the CNS remains unclear and may first involve invasion of peripheral nerves given the low levels of ACE2 in the brain. The virus may also enter the bloodstream from the lungs and cross the blood-brain barrier to gain access to the CNS, possibly within an infected white blood cell. Tropism and multiple organ injuries in SARS-CoV-2 infection  The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium as well as endothelial cells and enterocytes of the small intestine.  The virus can cause acute myocardial injury and chronic damage to the cardiovascular system. An acute cardiac injury was found in 12\% of infected people admitted to the hospital in Wuhan, China, and is more frequent in severe disease. Rates of cardiovascular symptoms are high, owing to the systemic inflammatory response and immune system disorders during disease progression, but acute myocardial injuries may also be related to ACE2 receptors in the heart. ACE2 receptors are highly expressed in the heart and are involved in heart function. A high incidence of thrombosis and venous thromboembolism have been found in people transferred to Intensive care units (ICU) with COVID-19 infections, and may be related to poor prognosis. Blood vessel dysfunction and clot formation (as suggested by high D-dimer levels caused by blood clots) are thought to play a significant role in mortality, incidences of clots leading to pulmonary embolisms, and ischaemic events within the brain have been noted as complications leading to death in people infected with SARS-CoV-2. Infection appears to set off a chain of vasoconstrictive responses within the body, constriction of blood vessels within the pulmonary circulation has also been posited as a mechanism in which oxygenation decreases alongside the presentation of viral pneumonia. Furthermore, microvascular blood vessel damage has been reported in a small number of tissue samples of the brainswithout detected SARS-CoV-2and the olfactory bulbs from those who have died from COVID-19.   Another common cause of death is complications related to the kidneys. Early reports show that up to 30\% of hospitalized patients both in China and in New York have experienced some injury to their kidneys, including some persons with no previous kidney problems.Coronavirus: Kidney Damage Caused by COVID-19, Johns Hopkins Medicine, C. John Sperati, updated 14 May 2020.
Nervous system Whether SARS-CoV-2 is able to invade the nervous system remains unknown . However, it is clear that many people with COVID-19 exhibit neurological or mental health issues. The virus is not detected in the CNS of the majority of COVID-19 people with neurological issues. However, SARS-CoV-2 has been detected at low levels in the brains of those who have died from COVID-19, but these results need to be confirmed. Loss of smell results from infection of the support cells of the olfactory epithelium, with subsequent damage to the olfactory neurons. SARS-CoV-2 could cause respiratory failure through affecting the brain stem as other coronaviruses have been found to invade the CNS. While virus has been detected in cerebrospinal fluid of autopsies, the exact mechanism by which it invades the CNS remains unclear and may first involve invasion of peripheral nerves given the low levels of ACE2 in the brain. The virus may also enter the bloodstream from the lungs and cross the blood-brain barrier to gain access to the CNS, possibly within an infected white blood cell. Tropism and multiple organ injuries in SARS-CoV-2 infection Gastrointestinal tract The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium as well as endothelial cells and enterocytes of the small intestine. Cardiovascular system The virus can cause acute myocardial injury and chronic damage to the cardiovascular system. An acute cardiac injury was found in 12\% of infected people admitted to the hospital in Wuhan, China, and is more frequent in severe disease. Rates of cardiovascular symptoms are high, owing to the systemic inflammatory response and immune system disorders during disease progression, but acute myocardial injuries may also be related to ACE2 receptors in the heart. ACE2 receptors are highly expressed in the heart and are involved in heart function. A high incidence of thrombosis and venous thromboembolism have been found in people transferred to Intensive care units (ICU) with COVID-19 infections, and may be related to poor prognosis. Blood vessel dysfunction and clot formation (as suggested by high D-dimer levels caused by blood clots) are thought to play a significant role in mortality, incidences of clots leading to pulmonary embolisms, and ischaemic events within the brain have been noted as complications leading to death in people infected with SARS-CoV-2. Infection appears to set off a chain of vasoconstrictive responses within the body, constriction of blood vessels within the pulmonary circulation has also been posited as a mechanism in which oxygenation decreases alongside the presentation of viral pneumonia. Furthermore, microvascular blood vessel damage has been reported in a small number of tissue samples of the brainswithout detected SARS-CoV-2and the olfactory bulbs from those who have died from COVID-19. COVID-19 was also found to cause substantial – including morphological and mechanical – changes to blood cells – such as increased sizes – sometimes persisting for months after hospital discharge. Other organs Another common cause of death is complications related to the kidneys. Early reports show that up to 30\% of hospitalized patients both in China and in New York have experienced some injury to their kidneys, including some persons with no previous kidney problems.Coronavirus: Kidney Damage Caused by COVID-19, Johns Hopkins Medicine, C. John Sperati, updated 14 May 2020.
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Nervous system
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; however.
. However,
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Gastrointestinal tract
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Cardiovascular system
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COVID-19 was also found to cause substantial – including morphological and mechanical – changes to blood cells – such as increased sizes – sometimes persisting for months after hospital discharge.
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Other organs