COVID-19

==== Host factors ====
Human [[angiotensin converting enzyme 2]] (hACE2) is the host factor that SARS-CoV-2 virus targets causing COVID‑19. Theoretically, the usage of [[Angiotensin II receptor blocker|angiotensin receptor blockers]] (ARB) and [[ACE inhibitor]]s upregulating ACE2 expression might increase [[morbidity]] with COVID‑19, 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.<ref>{{#invoke:cite journal || vauthors = Kai H, Kai M | title = Interactions of coronaviruses with ACE2, angiotensin II, and RAS inhibitors-lessons from available evidence and insights into COVID-19 | journal = Hypertension Research | volume = 43 | issue = 7 | pages = 648–654 | date = July 2020 | pmid = 32341442 | pmc = 7184165 | doi = 10.1038/s41440-020-0455-8 }}</ref>

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]].<ref>{{#invoke:cite journal || vauthors = Chen HX, Chen ZH, Shen HH | title = [Structure of SARS-CoV-2 and treatment of COVID-19] | journal = Sheng Li Xue Bao | volume = 72 | issue = 5 | pages = 617–630 | date = October 2020 | pmid = 33106832 }}</ref>

Among healthy adults not exposed to SARS-CoV-2, about 35% have [[CD4+ T cell|CD4<sup>+</sup> T cells]] that recognise the SARS-CoV-2 [[Peplomer|S protein]] (particularly the S2 subunit) and about 50% react to other proteins of the virus, suggesting [[cross-reactivity]] from previous [[common cold]]s caused by other coronaviruses.<ref>{{#invoke:cite journal ||vauthors=Jeyanathan M, Afkhami S, Smaill F, Miller MS, Lichty BD, Xing Z |date=4 September 2020 |title=Immunological considerations for COVID-19 vaccine strategies |journal=Nature Reviews Immunology |volume=20 |issue=10 |pages=615–632 |doi=10.1038/s41577-020-00434-6 |pmid=32887954 |pmc=7472682 |issn=1474-1741}}</ref>

It is unknown whether different persons use similar antibody genes in response to COVID‑19.<ref>{{#invoke:cite journal || vauthors = Zhang Q, Ju B, Ge J, Chan JF, Cheng L, Wang R, Huang W, Fang M, Chen P, Zhou B, Song S, Shan S, Yan B, Zhang S, Ge X, Yu J, Zhao J, Wang H, Liu L, Lv Q, Fu L, Shi X, Yuen KY, Liu L, Wang Y, Chen Z, Zhang L, Wang X, Zhang Z  | title = Potent and protective IGHV3-53/3-66 public antibodies and their shared escape mutant on the spike of SARS-CoV-2 | journal = Nature Communications | volume = 12 | issue = 1 | pages = 4210 | date = July 2021 | pmid = 34244522 | pmc = 8270942 | doi = 10.1038/s41467-021-24514-w | bibcode = 2021NatCo..12.4210Z | s2cid = 235786394 }}</ref>