Acute gastroenteritis is one of the most common diseases worldwide. Ten to 70% of the outbreaks are food-borne seafood associated. However, no data has been collected to determine viral contamination in harvesting areas. We determined the occurrence of human enteric calicivirus (HECV) and AECV, in market oysters along the U.S. coasts during different seasons. Samples from bays approved for human consumption were positive for HuNoVs GII.4, and AECV (PoNoV, PoSaV, BoNoV). Different seasonal and state distributions were detected. Simultaneous detection of HECV and AECV strains raises concerns for possible human co-infection, favoring the opportunity for recombination and emergence of new strains.The major source of water and food contamination is the discharge of waste into waters. Causative agents of gastroenteritis are excreted by the fecal route from healthy or unhealthy animals. We determined the presence of swine enteric viruses in feces and evaluated 5 technologies (cESTs) for animal waste treatment. Porcine SaVs, PoNoVs, RV-A and RV-C were detected before treatment. After treatment infectious particles were not detected, nor were clinical signs or seroconversion detected in inoculated Gn pigs. This is the first study to evaluate the impact of cESTs on virus detection and viability in manure and suggest that infectious virus would not be present in the field after treatment. Different from RVs, HECV do not growth in cell culture except for PoSaV/Cowden strain and murine NoV. The PoSaV/Cowden growths in LLC-PK cells in presence of intestinal content (IC), from Gn pigs or bile acids. This requires down-regulation of STAT1/Interferon (IFN) by the PKA pathway. We measured gene expression of LLC-PK cells infected with PoSaV/Cowden in the presence of IC. Based on a threshold of 1.5-fold change, at 4h PI, 29 genes were up-regulated and, at 8h PI, 83 genes were up- and 7 were down-regulated in infected cells. Late up-regulation of immune response genes suggest block or delay of IFN response. Up-regulation of genes involved in apoptosis suggests that PoSaV/Cowden may trigger apoptosis for cell release or spread. Our study may serve as a foundation for further analysis to understand the mechanism of SaV infection and potentially NoVs.