Macrophage tropism of rabbit hemorrhagic disease virus is associated with vascular pathology

• Published in: Virus research Vol. 60; no. 1; pp. 21 - 28
• Main Authors: Ramiro-Ibáñez, Fernando, Martı́n-Alonso, José M., Garcı́a Palencia, Pilar, Parra, Francisco, Alonso, Covadonga
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01-03-1999
• Subjects: Animals; Antigens, Viral - immunology; Caliciviridae Infections - immunology; Caliciviridae Infections - pathology; Caliciviridae Infections - virology; DIC; Endothelium, Vascular - pathology; Hemorrhagic Disease Virus, Rabbit - immunology; Hemorrhagic Disease Virus, Rabbit - physiology; Liver - immunology; Liver - pathology; Macrophages - immunology; Macrophages - virology; Monocytes - immunology; Monocytes - virology; Rabbit hemorrhagic disease virus; Rabbits; RHDV tropism and pathogenesis; Tropism; Viral hemorrhagic fevers; RHDV tropism and pathogenesis; Viral hemorrhagic fevers; DIC
• ISSN: 0168-1702; 1872-7492
• DOI: 10.1016/S0168-1702(98)00144-0

To delineate the interactions between rabbit hemorrhagic disease virus (RHDV) and host cells, organ and cellular targets of infection were identified in vivo. Viral specific antigens were detected by immunohistochemistry in liver, lung, spleen and lymph nodes cells. Also, intravascular infected cells were detected in most organs including kidneys, myocardium, thymus and central nervous system. To further characterize infected target cells, viral proteins and cell-specific surface antigens were identified simultaneously in double labeling experiments. Numerous lymphoid organ macrophages, from the splenic red pulp, circulating monocytes, alveolar macrophages and Kupffer cells were double labeled, demonstrating that cells of the mononuclear phagocyte lineage are major hosts for RHDV. Double labeling for other specific cell markers were negative. The distribution of viral antigens in these tissues coincided with those areas where cells presented morphology of apoptosis. Association of intravascular monocyte infection and apoptosis, could represent a possible mechanism to develop disseminated intravascular coagulation.