It was previously reported that the SFTPD aa11 SNP is in LD with SFTPA1 and SFTPA2 [25] . A protective effect of the 6A 2 to 1A 0 haplotype was even higher when this haplotype co-segregates with the SFTPD aa11-C allele. Likewise, one haplotype containing 6A 2 -1A 0 and the G allele of the SFTPD aa160 SNP could be protective against severe RSV disease [29] . Haplotypes at SFTPA1 are in LD with SFTPD aa11 in our population, but only a marginal LD between SFTPA2 and SFTPD aa11 was observed. In addition, no LD between 6A 2 to A 0 and SFTPD aa11 was found in controls (D' = 0.09) or CAP patients (D' = 0.024) in our study. These findings suggest that the protective effect of the co-segregation of SFTPD aa11-C with 6A 2 to 1A 0 on CAP susceptibility may rather reflect genetic interactions. Alternatively, the SFTPD aa11 SNP may be a marker of other SNPs in LD with SFTPA1 and SFTPA2. The gene of another collecting, the mannose-binding lectin (MBL), is located at 10q11.2-q21. We have previously observed that MBL deficiency predisposes to higher severity and poor outcome in CAP [56] , and LD of the SP genes with MBL2 cannot be ruled out.