Expansion of a natural killer (NK) cell population that expresses NKG2C has been associated with cytomegalovirus and other viral infections. It has been suggested that this cell population may play a role in infection control. Deletion of the NKG2C gene (homozygous or heterozygous) has been reported with high prevalence in European and Asian populations. However, the effect of NKG2C genotype on NK cell responses to infection remains poorly defined. We determined the prevalence of the NKG2C deletion in a Mexican population (n = 300) and in a group of patients (n = 131) to assess whether NKG2C genotype affects the incidence of symptomatic viral infections caused by influenza or respiratory syncytial virus. The frequency of the NKG2C deletion haplotype in Mexican mestizos was significantly lower (10.3%) than that reported in other populations (17.5-21.9%). No difference in the prevalence of NKG2C deletion was observed in subjects with viral infections compared with the reference population. In addition, no differences in clinical characteristics and infection outcome were observed between patients with and without the NKG2C gene deletion. Our results indicate that copy number variation in the NKG2C gene has no impact on the severity of respiratory viral infections.

Respiratory syncytial virus (RSV) is the leading cause of severe lower respiratory tract infection in infants. Reduced numbers of NK cells have been reported in infants with severe RSV infection; however, the precise role of NK cells during acute RSV infection is unclear. In this study the NK and T cell phenotypes, LILRB1 gene polymorphisms and KIR genotypes of infants hospitalized with RSV infection were analyzed. Compared to controls, infants with acute RSV infection showed a higher proportion of LILRB1þ T cells; in addition, a subgroup of infants with RSV infection showed an increase in LILRB1þ NK cells. No differences in NKG2C, NKG2A, or CD161 expression between RSV infected infants and controls were observed. LILRB1 genotype distribution of the rs3760860 A>G, and rs3760861 A>G single nucleotide polymorphisms differed between infants with RSV infection and healthy donors, whereas no differences in any of the KIR genes were observed. Our results suggest that LILRB1 participates in the pathogenesis of RSV infection. Further studies are needed to define the role of LILRB1þ NK in response to RSV and to confirm an association between LILRB1 polymorphisms and the risk of severe RSV infection.