Effect Of Measles Virus Infection Research Articles

Variability in Immune Response to Pathogens: Using Measles Vaccine to Probe Immunogenetic Determinants of Response

“The measles had not prevailed on the Faroes since 1781; they broke out early in April, 1846. … of the 7,782 inhabitants, about 6,000 were taken with measles … 225 persons in all died … of the many old people still living on the Faroes who had had the measles in 1781, not one … was attacked the second time.” [P. L. Panum, Observations Made during the Epidemic of Measles on the Faroe Islands in the Year 1846]

Effect of Measles Virus Infection on MHC Class II Expression and antigen Presentation in Human Monocytes

We studied the effect of measles virus (MV) infection on the expression of MHC class II molecules and on the antigen-presenting function in human peripheral blood monocytes in vitro. The expression of HLA-DR. -DQ, and -DP molecules was up to 10-fold higher in MV-infected than that in uninfected monocytes. This effect did not change upon stimulation of monocytes with LPS, and was not mediated by IFNγ. In contrast to results obtained with peripheral monocytes. MV infection in a human monocytic cell line. THP-1, did not enhance the basic MHC class II expression, but strongly inhibited the IFN-γ-induced expression. High levels of MHC class II expression in MV-infected monocytes were associated with capacity to present MV antigens, but the capacity to present unrelated antigens was strongly reduced. These results indicate how MV infection in monocytes may suppress the antigen-medicated T cell proliferation, still allowing the expansion of MV-specific T cell clones.

Accumulation of radiolabelled fatty acids in the neutral lipid fraction of measles virus persistently infected BGM cells

The effect of measles virus infection (acute and persistent) on fatty acid metabolism has been studied in BGM (African green monkey kidney) cells. In persistently infected cells, there was an increase in the incorporation of radiolabelled fatty acids into the neutral lipid fraction. Compared to uninfected cells, the increase was up to 2-fold for palmitic, stearic and oleic acids and 8–14 fold for arachidonic acid. The lipid metabolism in measles virus acutely infected cells was unmodified. The radiolabelled fatty acids incorporated into the neutral lipids in persistently infected cells were principally associated with the triglyceride fraction. The implications of a virus-induced modification of lipid metabolism are discussed.

Measles virus inhibits acquisition of lymphocyte functions but not established effector functions

The effect of measles-virus infection on effector activities of human lymphocytes and on the generation of certain effector activities was studied in vitro. Addition of measles virus to allogeneic mixed lymphocyte cultures resulted in a strongly depressed cytolytic activity in a subsequent cell-mediated lympholysis assay. Late addition of measles virus did not inhibit cytotoxic effector function, although effector cells were probably infected. Similarly, measles-virus infection did not affect the ability of lymphocytes to mediate antibody-dependent cellular cytotoxicity. Addition of measles virus to lymphocytes with, or shortly after, exposure of the cells to the polyclonal activator pokeweed mitogen resulted in abolition of the synthesis of immunoglobulins in vitro. When the virus was added late, the rate of Ig secretion was only partially inhibited. Finally, when lymphocytes were cultured without stimulus in medium supplemented with fetal bovine serum, a population of inhibitory cells was generated. Measles virus was able to prevent the generation of such inhibitory cells. In conclusion, measles virus inhibited acquisition of various effector functions, but the activities of committed lymphocytes were generally not affected.

The Effect of Measles Virus Infection on T and B Lymphocytes in the Mouse

Abstract The effect of measles virus infection on T and B lymphocytes in the mouse has been studied with a system of cell cooperation for production of an anti-hapten response. The effect of virus was studied by infecting helper cell or antibody-forming precursor cell donors with measles virus at various times before cell transfer into recipient mice and measuring the anti-hapten response after challenge with carrier-hapten conjugates. These studies indicate that measles virus produces a significant reduction in the anti-hapten response. This reduction in antibody formation is caused predominately by measles virus suppression of T helper cell function and possibly by a lesser effect on B cell function. The suppression of T cells is transient and corresponds to the time during which measles antigen can be demonstrated in the mouse spleens. Although infectious virus cannot be recovered from the lymphocytes, the suppression of T cells could only be demonstrated after inoculation with a virus strain capable of replicating in the mouse. These findings suggest that the virus may be present in a non-infectious or defective form. The effect of measles virus in T cells does not appear to be due to a depletion of T cells. The possible mechanisms for the suppressive effect are discussed.