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fected with LDV. A number of viruses, including the Rauscher and Friend viruses and those causing measles and rubella, have been shown to inhibit blast transformation of lymphocytes (Dent, 1972).

Not all viruses exert depressant effects on the immune system. Several, such as LDV and VEEV, can act as adjuvants and potentiate the immune response to certain antigens.

A number of mechanisms have been postulated to explain the immunodepressive effect of certain virus infections (Allison, 1972; Notkins et al., 1970). These include (1) virus-induced changes in the uptake and processing of antigens, possibly by alteration of cell surfaces; (2) depression of nucleic acid and protein (antibody) synthesis; (3) destruction of antibody-producing cells or their precursors; (4) alteration of thymic function; (5) acceleration of immunoglobulin catabolism; (6) antigenic compe- tition; and (7) lymphocytolysis as a result of increased adrenocortical secretion. Possible explanations of the immunologic enhancement associated with virus infections include (1) altered uptake and pro- cessing of antigens; (2) increase in the number of antibody-producing cells or their precursors; and (3) enhanced metabolism of antibody-producing cells.

should be studied in greater detail, with morphologic changes perhaps serving as an indication of functional alterations. Since differences in terminology often make it difficult to assess reports of pathological changes in lymphoid tissue, all modifications of the lymphoid organs should be described according to standardized criteria. Efforts at standardization are currently being supported by the World Health Organization.

(3) An attempt should be made to ascertain whether viruses can in fact exert selective effects on immune function, e.g., by depressing 7S versus 19S antibody, or by affecting T cell function as opposed to B cell function (Allison et al., 1971). The possibility should also be looked into that the immune response to the virus may itself be impaired if the infecting virus damages more or less selectively the cells responding to the viral antigens. If this proves to be the case, virus-induced immunodepression might conceivably be highly instrumental in prolonging certain virus infections, such as murine leukaemia, hepatitis, sub- acute sclerosing panencephalitis, or infections caused by LDV, LCMV, or ADV.


The effects of virus infections on immune function may have several important pathological repercus- sions. Virus-induced immunodepression might allow certain infections to persist, thereby adding to the antigenic load and increasing the likelihood of immunopathological consequences (e.g.. immune- complex disease). Moreover, depression of the im- mune response might trigger or enhance the growth of certain tumours. Virus-induced potentiation of immune response might also have immunopatho- logical consequences, such as the development of autoimmune disorders (WHO Scientific Group on Factors Regulating the Immune Response, 1970).


(1) A systematic evaluation of the effects of viruses on immune function should be undertaken. A num- ber of viruses should be studied and a standard set of immune function tests should be employed. Among the factors that deserve special investigation are antigen types (e.g., thymus-dependent versus non-thymus-dependent), antigen dose, and the time relationship between infection and antigen adminis- stration.

(2) The effects of virus infection on different cell types (e.g., macrophages, T and B lymphocytes)

It is well known that the persistence of antigen— antibody complexes in the circulating blood can lead to serum sickness, as manifested by glomerulo- nephritis, polyarteritis, urticaria, arthralgia, and arthritis. Recently, it has been shown in animals that viruses can persist in the bloodstream in the form of virus—antibody complexes, and that the deposition of these complexes in the kidney can produce an immune-complex type of glomerulonephritis.

Infectious virus—antibody complexes have been detected in the blood of animals with murine leukae- mias and those infected with LDV, ADV, and LCMV (Mellors et al., 1969; Oldstone & Dixon, 1969; Notkins et al., 1966; Porter et al., 1969; Oldstone & Dixon, 1971b, respectively). Prelimi- nary evidence suggests that infectious complexes also exist in the bloodstream of horses infected with equine infectious anaemia virus (EIAV) (McGuire et al., 1971). Immunopathological studies have re- vealed the 'presence of viral antigens, specific antiviral antibody, and complement in the kidneys of these animals (Oldstone & Dixon, 1971b).

Severe glomerulonephritis has been found in LCMV carrier mice (Hotchin & Collins, 1964; Oldstone & Dixon, 1969, 1971b). The severity of the disease appears to be related to the strain of


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