<unk>  pathogenesis The SARS-CoV-2 virus can infect a wide range of cells and systems of the body.<unk>  is most known for affecting the upper respiratory tract (sinuses, nose, and throat) and the lower respiratory tract (windpipe and lungs). The lungs are the organs most affected by<unk>  because the virus accesses host cells via the receptor for the enzyme angiotensin-converting enzyme 2 (ACE2), which is most abundant on the surface of type II alveolar cells of the lungs. The virus uses a special surface glycoprotein called a "spike" to connect to the ACE2 receptor and enter the host cell. Respiratory tract Following viral entry,<unk>  infects the ciliated epithelium of the nasopharynx and upper airways. Nervous system One common symptom, loss of smell, results from infection of the support cells of the olfactory epithelium, with subsequent damage to the olfactory neurons. The involvement of both the central and peripheral nervous system in<unk>  has been reported in many medical publications. It is clear that many people with<unk>  exhibit neurological or mental health issues. The virus is not detected in the CNS of the majority of<unk>  patients with neurological issues. However, SARS-CoV-2 has been detected at low levels in the brains of those who have died from<unk> , but these results need to be confirmed. 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 Research conducted when Alpha was the dominant variant has suggested<unk>  May cause brain damage. It is currently unknown if such damage is temporary or permanent, and whether Omicron has similar effects. Observed individuals infected with<unk>  (most with mild cases) experienced an additional 0.2% to 2% of brain tissue lost in regions of the brain connected to the sense of smell compared with uninfected individuals, and the overall effect on the brain was equivalent on average to at least one extra year of normal aging; infected individuals also scored lower on several cognitive tests. All effects were more pronounced among older ages. 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<unk>  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 (arterioles and capillaries) 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<unk> .<unk>  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. Autopsies of people who died of<unk>  have found diffuse alveolar damage, and lymphocyte-containing inflammatory infiltrates within the lung. Immunopathology adaptive immune response to SARS-CoV-2 Although SARS-CoV-2 has a tropism for ACE2-expressing epithelial cells of the respiratory tract, people with severe<unk>  have symptoms of systemic hyperinflammation. Clinical laboratory findings of elevated IL2, IL7, IL6, granulocyte-macrophage colony-stimulating factor (GMCSF), interferon gamma-induced protein10 (IP10), monocyte chemoattractant protein1 (MCP1), macrophage inflammatory protein 1alpha (MIP1alpha), and tumour necrosis factor (TNFα) indicative of cytokine release syndrome (CRS) suggest an underlying immunopathology. Additionally, people with<unk>  and acute respiratory distress syndrome (ARDS) have classical serum biomarkers of CRS, including elevated C-reactive protein (CRP), lactate dehydrogenase (LDH), D-dimer, and ferritin. Systemic inflammation results in vasodilation, allowing inflammatory lymphocytic and monocytic infiltration of the lung and the heart. In particular, pathogenic GM-CSF-secreting T cells were shown to correlate with the recruitment of inflammatory IL-6-secreting monocytes and severe lung pathology in people with<unk> . Lymphocytic infiltrates have also been reported at autopsy. Viral and host factors Virus proteins Renin-Angiotensin-Aldosterone System (RAAS) Multiple viral and host factors affect the pathogenesis of the virus. The S-protein, otherwise known as the spike protein, is the viral component that attaches to the host receptor via the ACE2 receptors. It includes two subunits: S1 and S2. S1 determines the virus-host range and cellular tropism via the receptor-binding domain. S2 mediates the membrane fusion of the virus to its potential cell host via the H1 and HR2, which are heptad repeat regions. Studies have shown that S1 domain induced IgG and IgA antibody levels at a much higher capacity. It is the focus spike proteins expression that are involved in many effective<unk>  vaccines. The M protein is the viral protein responsible for the transmembrane transport of nutrients. It is the cause of the bud release and the formation of the viral envelope. The N and E protein are accessory proteins that interfere with the host's immune response. Host factors Human angiotensin converting enzyme 2 (hACE2) is the host factor that SARS-COV2 virus targets causing<unk> . Theoretically, the usage of angiotensin receptor blockers (ARB) and ACE inhibitors upregulating ACE2 expression might increase morbidity with<unk> , though animal data suggest some potential protective effect of ARB; however no clinical studies have proven susceptibility or outcomes. Until further data is available, guidelines and recommendations for hypertensive patients remain. The effect of the virus on ACE2 cell surfaces leads to leukocytic infiltration, increased blood vessel permeability, alveolar wall permeability, as well as decreased secretion of lung surfactants. These effects cause the majority of the respiratory symptoms. However, the aggravation of local inflammation causes a cytokine storm eventually leading to a systemic inflammatory response syndrome. Among healthy adults not exposed to SARS-CoV-2, about 35% have CD4+ T cells that recognize the SARS-CoV-2 S protein (particularly the S2 subunit) and about 50% react to other proteins of the virus, suggesting cross-reactivity from previous common colds caused by other coronaviruses. It is unknown whether different persons use similar antibody genes in response to<unk> . Host cytokine response immune response during virus infection The severity of the inflammation can be attributed to the severity of what is known as the cytokine storm. Levels of interleukin1B, interferon-gamma, interferon-inducible protein 10, and monocyte chemoattractant protein1 were all associated with<unk>  disease severity. Treatment has been proposed to combat the cytokine storm as it remains to be one of the leading causes of morbidity and mortality in<unk>  disease. A cytokine storm is due to an acute hyperinflammatory response that is responsible for clinical illness in an array of diseases but in<unk> , it is related to worse prognosis and increased fatality. The storm causes acute respiratory distress syndrome, blood clotting events such as strokes, myocardial infarction, encephalitis, acute kidney injury, and vasculitis. The production of IL-1, IL-2, IL-6, TNF-alpha, and interferon-gamma, all crucial components of normal immune responses, inadvertently become the causes of a cytokine storm. The cells of the central nervous system, the microglia, neurons, and astrocytes, are also involved in the release of pro-inflammatory cytokines affecting the nervous system, and effects of cytokine storms toward the CNS are not uncommon. Pregnancy response There are many unknowns for pregnant women during the<unk>  pandemic. Given that they are prone to suffering from complications and severe disease infection with other types of coronaviruses, they have been identified as a vulnerable group and advised to take supplementary preventive measures. Physiological responses to pregnancy can include: * Immunological: The immunological response to<unk> , like other viruses, depends on a working immune system. It
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