Human parvovirus B19 (B19V) causes various human diseases, ranging from childhood benign infection to arthropathies, severe anemia and fetal hydrops, depending on the health state and hematological status of the patient. To counteract B19V blood-borne contamination, evaluation of B19 DNA in plasma pools and viral inactivation/removal steps are performed, but nucleic acid testing does not correctly reflect B19V infectivity. There is currently no appropriate cellular model for detection of infectious units of B19V. We describe here an improved cell-based method for detecting B19V infectious units by evaluating its host transcription. We evaluated the ability of various cell lines to support B19V infection. Of all tested, UT7/Epo cell line, UT7/Epo-STI, showed the greatest sensitivity to B19 infection combined with ease of performance. We generated stable clones by limiting dilution on the UT7/Epo-STI cell line with graduated permissiveness for B19V and demonstrated a direct correlation between infectivity and S/G2/M cell cycle stage. Two of the clones tested, B12 and E2, reached sensitivity levels higher than those of UT7/Epo-S1 and CD36+ erythroid progenitor cells. These findings highlight the importance of cell cycle status for sensitivity to B19V, and we propose a promising new straightforward cell-based method for quantifying B19V infectious units.

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New Findings What is the central question of this study?Do Fog2Rb−/Rb− mice present a defect of small intestine homeostasis? What is the main finding and its importance?The importance of interactions between FOG‐2 and pRb in adipose tissue physiology has previously been demonstrated. Here it is shown that this interaction is also intrinsic to small intestine homeostasis and exerts extrinsic control over mouse metabolism. Thus, this association is involved in maintaining small intestine morphology, and regulating crypt proliferation and lineage differentiation. It therefore affects mouse growth and adaptation to a high‐fat diet. Abstract GATA transcription factors and their FOG cofactors play a key role in tissue‐specific development and differentiation, from worms to humans. We have shown that GATA‐1 and FOG‐2 contain an LXCXE pRb‐binding motif. Interactions between retinoblastoma protein (pRb) and GATA‐1 are crucial for erythroid proliferation and differentiation, whereas the LXCXE pRb‐binding site of FOG‐2 is involved in adipogenesis. Fog2‐knock‐in mice have defective pRb binding and are resistant to obesity, due to efficient white‐into‐brown fat conversion. Our aim was to investigate the pathophysiological impact of FOG‐2–pRb interaction on the small intestine and mouse growth. Histological analysis of the small intestine revealed architectural changes in Fog2Rb−/Rb− mice, including villus shortening, with crypt expansion and a change in muscularis propria thickness. These differences were more marked in the proximo‐distal part of the small intestine and were associated with an increase in crypt cell proliferation and disruption of the goblet and Paneth cell lineage. The small intestine of the mutants was unable to adapt to a high‐fat diet, and had significantly lower plasma lipid levels on such a diet. Fog2Rb−/Rb− mice displayed higher levels of glucose‐dependent insulinotropic peptide release, and lower levels of insulin‐like growth factor I release on a regular diet. Their intestinal lipid absorption was impaired, resulting in restricted weight gain. In addition to the intrinsic effects of the mutation on adipose tissue, we show here an extrinsic relationship between the intestine and the effect of FOG‐2 mutation on mouse metabolism. In conclusion, the interaction of FOG‐2 with pRb coordinates the crypt–villus axis and controls small intestine homeostasis.