AASLD ABSTRACTS OF PAPERS .,)3 THE EFFEC7 OF LIVER MACllOPHAGE SOURCE ON V1RUS- MACROPHAGE INTERACTIONS IN A MODEL OF MURINE VIRAL HEPATITIS. PS L.ltham and 5B SepelaK,

.,)3 THE EFFEC7 OF LIVER MACllOPHAGE SOURCE ON V1RUSMACROPHAGE INTERACTIONS IN A MODEL OF MURINE VIRAL HEPATITIS. PS L.ltham and 5B SepelaK, Depts. of MedicIne and Pathology, UnIversity of Maryland, Baltimore, MD Most experimental models of viral hepaUtis In mice extrapolate the role of Kupffer cell-vU'llS Interaction [rom s.tudies usmg non-hepatiC sources of rnacrophages lMos). This study was rteslgned to compare the viral mteractlon of liver macrophages (Kupffer cells) with Mos from pentoneal exudate ;PE), and peripheral blood (monocyte") usin~ a Phlebovlrus of the Bunyaviridiae, Punta Toro VI1'US (PI1V). PRY causes an age-dependent lethal hepatIC necrosIs 10 3 week old C57BL!6 mIce 3-4 days after s.c. inoculation, but 8 week old mIce survIve with mmimal hepatic necrosis. Methods: Mos were derived from 3 week old (susceptible) and 8 week old (resIstant) C57BL/6 mice and Isolated from liver by collagenase perfusion and centrifugal elutriation, from PE by lavage after thlOglycolate, and from blood by Perc 011 gradient centrifugation. Mo Monolayers were infected with PRV (MOl 0.05) after 24 hours of culture in the presence of anti-interferon. PRV titers in supematant were measured as plaque-forming units in Vero Kidney cells. Results: PRY could replicate to a variable extent in Mos from both age groups and all sources, however, only Kupffer cells expressed an age-related susceptibility to the virus in vitro (P<0.05). ConcIUSions: Inherent age-related differences in ?TV-liver macrophage interactions are uniquely expressed in Kupffer cells vs Mos from other sources. The results suggest that the nature of Kupffer cell-virus interactions cannot be presumed from studies using other macrophage populations.