Mouse hepatitis virus infection suppresses modulation of mouse spleen T-cell activation

• Published in: Immunology Vol. 75; no. 3; pp. 542 - 545
• Main Authors: COOK-MILLS, J. M, MINSHI, H. G, PERLMAN, R. L, CHAMBERS, D. A
• Format: Journal Article
• Language: English
• Published: Oxford Blackwell 01-03-1992
• Subjects: Animals; Biological and medical sciences; Concanavalin A - immunology; DNA - biosynthesis; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Hepatitis, Viral, Animal - immunology; Immune Tolerance - immunology; Immunobiology; Lymphocyte Activation - immunology; Male; Mice; Mice, Inbred BALB C; Modulation of the immune response (stimulation, suppression); Norepinephrine - immunology; Spleen - immunology; T-Lymphocytes - immunology; Immune response; Rodentia; Aminoacid derivative hormone; Activation; Host virus relation; Murine hepatitis virus; Infection; Virus; Vertebrata; Immunosuppression; Coronavirus; Mammalia; Mouse; Animal; Viral disease; T-Lymphocyte; Norepinephrine; Coronaviridae; Neuroimmunomodulation
• ISSN: 0019-2805; 1365-2567

Natural infection by mouse hepatitis virus (MHV) can affect interpretation of immunological studies in mice. MHV, a collective term describing a group of corona viruses, is found in natural infections in over 70% of laboratory mouse populations in the U.S.A. and Canada. Natural outbreaks of MHV in our animal colony afforded us the opportunity to study MHV-induced immunosuppression as well as the effects of MHV infection on neurotransmitter immunomodulation. Concanavalin A (Con A)-stimulated DNA synthesis by spleen T lymphocytes from MHV-infected mice was 20-50% that of non-infected mice. The MHV infection also altered neurotransmitter modulation of spleen T-lymphocyte activation. In contrast to noradrenaline ablation of Con A-activated DNA synthesis by spleen lymphocytes from non-infected mice, DNA synthesis by the infected group was not inhibited by noradrenaline or dibutyryl-cAMP. These effects of MHV infection were specific for spleen T lymphocytes since MHV infection did not alter Con A stimulation of thymocytes, lipopolysaccharide stimulation of spleen B lymphocytes, or noradrenaline inhibition of thymocyte and B-cell DNA synthesis. MHV infection also did not alter spleen T-lymphocyte subset proportions. Thus, MHV infection inhibits spleen T-lymphocyte activation and blocks in vitro catecholamine and cAMP regulation of spleen T-cell activation but does not affect activation of thymic cells or spleen B cells.