Neonatal Infection with Mouse Thymic Virus: Spleen and Lymph Node Necrosis
Departments of Pathology and Microbiology, Box 662, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, U.S.A. Mouse thymic virus (TA) is a naturally occurring herpesvirus of laboratory and wild mice, which produces massive thymic necrosis when inoculated into ne...
Saved in:
Published in | Journal of general virology Vol. 57; no. 1; pp. 139 - 147 |
---|---|
Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
England
Soc General Microbiol
01.11.1981
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Departments of Pathology and Microbiology, Box 662, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, U.S.A.
Mouse thymic virus (TA) is a naturally occurring herpesvirus of laboratory and wild mice, which produces massive thymic necrosis when inoculated into newborn mice. Our histopathological study showed necrosis not only of the thymus but also of the spleen and lymph nodes which was noticeable by day 7 and complete by day 14. Both spleen and lymph nodes regenerated to an almost normal histological pattern by day 70. The results show that TA infects multiple lymphoid tissues causing massive necrosis in all, and is not limited to a single site, the thymus. TA infection was found to be a persistent herpesvirus infection in both the lymph nodes and spleen. During the period of acute infection, as necrosis increased, the response of cell suspensions of lymph nodes to the T cell mitogens concanavalin A and phytohaemagglutinin was virtually non-existent. Activity returned to normal as the histological repair progressed.
Keywords: mouse thymic virus, T cell depletion, spleen and lymph node necrosis
Received 10 April 1981;
accepted 12 June 1981. |
---|---|
Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0022-1317 1465-2099 |
DOI: | 10.1099/0022-1317-57-1-139 |