The common [cold] coronaviruses are pretty common:
Four HCoVs (HCoV 229E, NL63, OC43, and HKU1) are endemic globally and account for 10% to 30% of upper respiratory tract infections in adults.
To pick a more detailed study in (ahem) Ghana:
This study sought to determine whether human coronaviruses (HCoVs) are associated with upper respiratory tract infections among older children and adults in Ghana. We conducted a case control study among older children and adults in three rural areas of Ghana using asymptomatic subjects as controls. [...]
Out of 1,213 subjects recruited, 150 (12.4%) were positive for one or more viruses. Of these, single virus detections occurred in 146 subjects (12.0%) and multiple detections occurred in 4 (0.3%). Compared with control subjects, infections with HCoV-229E (OR = 5.15, 95%CI = 2.24–11.78), HCoV-OC43 (OR = 6.16, 95%CI = 1.77–21.65) and combine HCoVs (OR = 2.36, 95%CI = 1.5 = 3.72) were associated with upper respiratory tract infections. HCoVs were found to be seasonally dependent with significant detections in the harmattan season (mainly HCoV-229E) and wet season (mainly HCoV-NL63).
Occasionally there are substantial outbreaks of common cold, e.g. as observed in Japan:
we conducted a longitudinal survey
between 2010 and 2013 in Yamagata, Japan, to clarify
the epidemiology of HCoVs using RT-PCR methods
[...]. In 2011, we
found that the monthly detection frequencies of HCoVNL63 were higher than 20% in January and February
(28.5% and 25.3%, respectively), whereas those of the
other HCoVs (HCoV-229E, -OC43, -HKU1) did not exceed 20%. In light of these findings, we continued
the HCoV surveillance and, thus, captured data from
the largest outbreak of HCoV-OC43 reported in the last
6 years. During the 2014–2015 influenza season in
Yamagata, Japan, the monthly detection frequencies
were approximately 30–40%.
Those percentages are from people reporting symptoms (and then swabbed.) The graph below (from the same paper) nicely shows the seasonality.
Monthly distribution of clinical specimens (A) and HCoVs (B) detected from patients with acute respiratory
infections between January 2014 and March 2015, in Yamagata, Japan.
Question 2 is rather meaningless because immunity to common coronaviruses is short lived. See (also) this answer (esp. the 2nd table) to a related question putting the common coronaviruses immunity duration in perspective; reproducing just the table below (the relevant line for common coronavirus is the 1st below the break, i.e. 1st in the 2nd section of the table).
And I've managed to track down one of the primary studies on 229E long-term immunity (or rather lack thereof)
Although after 1 year concentrations of specific serum IgG and nasal IgA were
still significantly raised in the infected group, they were much lower than at the
maximum. [...] When challenged after 1 year all of the original uninfected group were infected and 6/9 of the infected group were reinfected. [...] In the infected group there were considerable individual differences. Some lost their antibody, particularly serum antibody, completely by 1 year, some did not.
And it's basically impossible not be exposed to a strain of the common cold coronaviruses at one point; one study on newborns found that interval to be 3.5 years, but that's probably an overestimation for adults.
all of the children had maternal anti-NL63 and anti-229E antibodies at birth that disappeared within 3 months [...] on average, HCoV-NL63 and HCoV-229E seroconversion occurs before children reach the age of 3.5 years.
The real question is whether Covid-19 will behave like the common coronaviruses or more like SARS and MERS for which it is suspected (from the detection of antibodies), but not certain that immunity lasts longer.
For the SARS and MERS coronaviruses, antibodies appear to persist for several years, but no studies have intentionally attempted to re-infect people, since these are deadly diseases.