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It is well known that people of old age or with respiratory problems are more vulnerable by the effects of COVID-19. However, I wasn't able to find information on any similar trends on catching the disease in the first place.

So what are the factors predicting the most significant differences in the chance of catching COVID-19?

I'm looking for predictors of the immune system response, whether that would be smoking, age or gender, not obvious notions such as "people from populated areas".

I know the role of ethnicity is much debated but since there's no conclusive evidenence yet, I'm not interested in its role.

Evidence suggests higher death rates from COVID-19 including among racialised groups might be linked to higher levels of a cell surface receptor molecule known as ACE2. But this can result from taking drugs for diabetes and hypertension, which takes us back to the point about the social causes of such diseases. (The Conversation)

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    $\begingroup$ might be worth looking at this for starters. I imagine that occupation is likely one of the biggest predictors of catching covid-19 - ons.gov.uk/employmentandlabourmarket/peopleinwork/… $\endgroup$ – user438383 Jul 30 '20 at 13:00
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    $\begingroup$ @AlexReynolds Can you make this into a full answer? $\endgroup$ – Chris Jul 31 '20 at 6:38
  • $\begingroup$ @AlexReynolds I'm looking for biological, not behavioral determinants. $\endgroup$ – Probably Jul 31 '20 at 16:31
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There are populations that might be more vulnerable due to genetics surrounding the ACE2 receptor. For instance, men are more likely than women to get severe cases of COVID-19:

A growing body of evidence reveals that male sex is a risk factor for a more severe disease, including death. Indeed, globally, ~60% of deaths from COVID-19 are reported in men7,8, and a recent cohort study of 17 million adults in England reported a strong correlation between male sex and risk of death from COVID-19 (hazard ratio 1.99, 95% confidence interval 1.88-2.10)8

The ACE2 gene lies on the X chromosome. In addition to polymorphisms distributed by ethnicity, women have two X chromosomes and may gain some protection from differences in their two alleles of the ACE2 gene, which could make viral binding more difficult, or alter the signaling pathways which result in the subsequent autoimmune response that damages internal organs:

In addition to differential polymorphisms which may explain susceptibility and even outcome in different ethnic populations, the fact that ACE2 is localized to Xp22.2 may help explain the observed male-associated risk. As such, even in the absence of variation in this gene, the monoallelic versus biallelic presence of this gene may impact the natural history and prognosis of COVID-19 in males.

Additionally, in some ethnic populations, expression of the ACE2 gene (as measured by mRNA levels) is lower in women than in men, which may account for reduced infectivity or disease severity in women:

In the normal human lung, ACE2 is expressed on type I and II alveolar epithelial cells. Among them, 83% of the type II alveolar cells have ACE2 expression. Men had a higher ACE2 level in their alveolar cells than women. Asians have a higher level of ACE2 expression in their alveolar cells than the White and African American populations. The binding of SARS‐CoV‐2 on ACE2 causes an elevated expression of ACE2, which can lead to damages on alveolar cells. Damages to alveolar cells can, in turn, trigger a series of systemic reactions and even death.

This aspect of research seems to be ongoing. Region-specific behavior does seem to be the main driver for new infections, however: Ignoring public health guidelines and reopening economies early, calling the virus a hoax, giving healthcare workers garbage bags for PPE, etc. etc. Biology takes a backseat, when governments deliberately put people in harm's way.

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