Only a few studies have addressed the role of the genetic variability at SFTPA1, and SFTPA2 in infectious diseases [28] [29] [30] [31] . In bacterial infections, homozygosity for the 1A 1 haplotype was reported to be associated with meningococcal disease [30] . Noteworthy, 6A 2 -1A 0 was protective against acute otitis media (AOM) in children [32] . Haplotypes 6A 2 and 1A 0 may also be involved in protection against respiratory syncytial virus (RSV) disease [29, 33] . Considering the high difference in the frequencies with the corresponding alternative alleles and haplotypes, it is tempting to speculate that 6A 2 , 1A 0 and 6A 2 -1A 0 could have been maintained at high frequencies partly by their protective effect against respiratory infections. The 6A and 6A-1A haplotypes were found to be associated with an increased risk of wheeze and persistent cough, presumably triggered by respiratory infections or environmental contaminants, among infants at risk for asthma [27] . Regarding SP-D, the SFTPD aa11-T allele was associated with severe RSV bronchiolitis [34] , whereas the SFTPD aa11-C variant was associated with tuberculosis [30] .