RESULTS: HbAA and HbGA levels ranged from 3 to 910 and from 4 to 756 pmol/g hemoglobin, respectively, with smokers having the highest levels overall.
Hemoglobin adducts of acrylamide (HbAA) and glycidamide (HbGA) are well-established biomarkers of exposure to these chemicals (Dybing et al.
To date, no data on internal acrylamide and glycidamide exposure acquired by use of HbAA and HbGA in the general U.S.
In conclusion, our data and that of others show that rotavirus infection might be correlated with genetic factors, such as HBGAs. Further studies will be required to determine the exact role of HBGA ligands and other ligands in rotavirus infection.
Recent findings showed that human blood group antigens (HBGAs) might be involved in rotavirus attachment to intestinal cells (3,4,5,6).
The interaction between rotavirus particles and HBGAs might constitute the first step in the attachment to the cell before internalization of the virus particle, after binding with integrins (4,5).
Our observed lack of HBGA
carbohydrates on the surface of the intestinal cells that participate in NV binding to mammalian cells further highlights that this model is likely not a sufficient model system to study NV replication because the cells do not express the putative NV receptor.
SaV-positive specimens were compared with specimens from a control group of children who tested negative for SaV, which was matched in terms of sex, age group, clinical status, and HBGAs
using 2-tailed significance with Fisher exact tests.
Compared with recent GII.4 variants, GII.4 New Orleans had several amino acid substitutions, which were located near protruding regions (aa 294 and 396) and HBGA interaction sites (aa 339-341) (Figure 4).
Compared with known GII.4 viruses, GII.4 New Orleans had several changes in key amino acids in the P2 region of VP1 and around the sites that have been shown to be important in HBGA binding (20).
Because the host genetic observation of this outbreak was unexpected, attempts were made to compare the HBGA frequencies of the participating persons with those of the population in Sweden.
However, this possibility is unlikely to influence the main findings of this study, namely the secretor- and HBGA-independent infection pattern, because symptomatic persons were found in all HBGA groups.